Models that contain the Modeling Application : NEURON ()

(NEURON is a simulation environment for developing and exercising models of neurons and networks of neurons. It is particularly well-suited to problems where cable properties of cells play an important role, possibly including extracellular potential close to the membrane), and where cell membrane properties are complex, involving many ion-specific channels, ion accumulation, and second messengers. It evolved from a long collaboration between Michael Hines and John W. Moore at the Department of Neurobiology, Duke University. Their express goal was to create a tool designed specifically for solving the equations that describe nerve cells.) Re-display model names without descriptions

	Models	Description
1.	2 Distinct Classes of L2 and L3 Pyramidal Neurons in Human Temporal Cortex (Deitcher et al 2017)
		"There have been few quantitative characterizations of the morphological, biophysical, and cable properties of neurons in the human neocortex. We employed feature-based statistical methods on a rare data set of 60 3D reconstructed pyramidal neurons from L2 and L3 in the human temporal cortex (HL2/L3 PCs) removed after brain surgery. Of these cells, 25 neurons were also characterized physiologically. Thirty-two morphological features were analyzed (e.g., dendritic surface area, 36 333 ± 18 157 µm2; number of basal trees, 5.55 ± 1.47; dendritic diameter, 0.76 ± 0.28 µm). ... A novel descriptor for apical dendritic topology yielded 2 distinct classes, termed hereby as “slim-tufted” and “profuse-tufted” HL2/L3 PCs; the latter class tends to fire at higher rates. Thus, our morpho-electrotonic analysis shows 2 distinct classes of HL2/L3 PCs."
2.	2D model of olfactory bulb gamma oscillations (Li and Cleland 2017)
		This is a biophysical model of the olfactory bulb (OB) that contains three types of neurons: mitral cells, granule cells and periglomerular cells. The model is used to study the cellular and synaptic mechanisms of OB gamma oscillations. We concluded that OB gamma oscillations can be best modeled by the coupled oscillator architecture termed pyramidal resonance inhibition network gamma (PRING).
3.	3D model of the olfactory bulb (Migliore et al. 2014)
		This entry contains a link to a full HD version of movie 1 and the NEURON code of the paper: "Distributed organization of a brain microcircuit analysed by three-dimensional modeling: the olfactory bulb" by M Migliore, F Cavarretta, ML Hines, and GM Shepherd.
4.	3D olfactory bulb: operators (Migliore et al, 2015)
		"... Using a 3D model of mitral and granule cell interactions supported by experimental findings, combined with a matrix-based representation of glomerular operations, we identify the mechanisms for forming one or more glomerular units in response to a given odor, how and to what extent the glomerular units interfere or interact with each other during learning, their computational role within the olfactory bulb microcircuit, and how their actions can be formalized into a theoretical framework in which the olfactory bulb can be considered to contain "odor operators" unique to each individual. ..."
5.	3D-printer visualization of NEURON models (McDougal and Shepherd, 2015)
		"... We introduce the use of 3D printing as a technique for visualizing traced morphologies. Our method for generating printable versions of a cell or group of cells is to expand dendrite and axon diameters and then to transform the tracing into a 3D object with a neuronal surface generating algorithm like Constructive Tessellated Neuronal Geometry (CTNG). ..."
6.	A 1000 cell network model for Lateral Amygdala (Kim et al. 2013)
		1000 Cell Lateral Amygdala model for investigation of plasticity and memory storage during Pavlovian Conditioning.
7.	A 3D population model of midget retinal ganglion cells at the human fovea (Italiano et al, 2022)
		A robust means of generating eccentricity-dependent and morphologically realistic and three-dimensional populations of midget retinal ganglion cells at the central human retina (specifically, at the (para-)foveal region).
8.	A cerebellar model of phase-locked tACS for essential tremor (Schreglmann et al., 2021)
		This model is a supplementary material for Schreglmann, Sebastian R., et al. "Non-invasive suppression of essential tremor via phase-locked disruption of its temporal coherence" Nature Communications (2021). The model demonstrates that phase-locked transcranial alternating current stimulation (tACS) is able to disrupt the tremor-related oscillations in the cerebellum, and its efficacy is highly dependent on the relative phase between the stimulation and tremor.
9.	A cortico-cerebello-thalamo-cortical loop model under essential tremor (Zhang & Santaniello 2019)
		We investigated the origins of oscillations under essential tremor (ET) by building a computational model of the cortico-cerebello-thalamo-cortical loop. It showed that an alteration of amplitudes and decay times of the GABAergic currents to the dentate nucleus can facilitate sustained oscillatory activity at tremor frequency throughout the network as well as a robust bursting activity in the thalamus, which is consistent with observations of thalamic tremor cells in ET patients. Tremor-related oscillations initiated in small neural populations and spread to a larger network as the synaptic dysfunction increased, while thalamic high-frequency stimulation suppressed tremor-related activity in thalamus but increased the oscillation frequency in the olivocerebellar loop.
10.	A detailed Purkinje cell model (Masoli et al 2015)
		The Purkinje cell is one of the most complex type of neuron in the central nervous system and is well known for its massive dendritic tree. The initiation of the action potential was theorized to be due to the high calcium channels presence in the dendritic tree but, in the last years, this idea was revised. In fact, the Axon Initial Segment, the first section of the axon was seen to be critical for the spontaneous generation of action potentials. The model reproduces the behaviours linked to the presence of this fundamental sections and the interplay with the other parts of the neuron.
11.	A fast model of voltage-dependent NMDA Receptors (Moradi et al. 2013)
		These are two or triple-exponential models of the voltage-dependent NMDA receptors. Conductance of these receptors increase voltage-dependently with a "Hodgkin and Huxley-type" gating style that is also depending on glutamate-binding. Time course of the gating of these receptors in response to glutamate are also changing voltage-dependently. Temperature sensitivity and desensitization of these receptor are also taken into account. Three previous kinetic models that are able to simulate the voltage-dependence of the NMDARs are also imported to the NMODL. These models are not temperature sensitive. These models are compatible with the "event delivery system" of NEURON. Parameters that are reported in our paper are applicable to CA1 pyramidal cell dendrites.
12.	A Fast Rhythmic Bursting Cell: in vivo cell modeling (Lee 2007)
		One of the cellular mechanisms underlying the generation of gamma oscillations is a type of cortical pyramidal neuron named fast rhythmic bursting (FRB) cells. After cells from cats' primary visual cortices were filled with Neurobiotin, the brains were cut, and the cells were photographed. One FRB cell was chosen to be confocaled, reconstructed with Neurolucida software, and generated a detailed multi-compartmental model in the NEURON program. We explore firing properties of FRB cells and the role of enhanced Na+ conductance.
13.	A focal seizure model with ion concentration changes (Gentiletti et al., 2022)
		Computer model was used to investigate the possible mechanisms of seizure initiation, progression and termination. The model was developed by complementing the Hodgkin-Huxley equations with activity-dependent changes in intra- and extracellular ion concentrations. The model incorporates a number of ionic mechanisms such as: active and passive membrane currents, inhibitory synaptic GABAA currents, Na/K pump, KCC2 cotransporter, glial K buffering, radial diffusion between extracellular space and bath, and longitudinal diffusion between dendritic and somatic compartments in pyramidal cells.
14.	A Layer V CCS type pyramidal cell, inhibitory synapse current conduction (Kubota Y et al., 2015)
		A layer V crossed-corticostriatal (CCS) ‘slender untufted’ pyramidal cell model of rat frontal cortex was built using Neurolucida tracing as well as 3D reconstructed dendrites of serial electron micrographs to give the model as authentic morphology as possible.
15.	A Markov model of human Cav2.3 channels and their modulation by Zn2+ (Neumaier et al 2020)
		The Markov model for Cav2.3 channel gating in the absence of trace metals was developed based on channel structure, previous modeling studies and the ability to fit the data. Model parameters were optimized by fitting the model to macroscopic currents recorded with various electrophysiological protocols from HEK-293 cells stably transfected with human Cav2.3+ß3 channel subunits. The effects of Zn2+ were implemented by assuming that Zn2+ binding to a first site (KZn=0.003 mM) leads to electrostatic modification and mechanical slowing of one of the voltage-sensors while Zn2+-binding to a second, intra-pore site (KZn=0.1 mM) blocks the channel and modifies the opening and closing transitions.
16.	A Model Circuit of Thalamocortical Convergence (Behuret et al. 2013)
		“… Using dynamic-clamp techniques in thalamic slices in vitro, we combined theoretical and experimental approaches to implement a realistic hybrid retino-thalamo-cortical pathway mixing biological cells and simulated circuits. … The study of the impact of the simulated cortical input on the global retinocortical signal transfer efficiency revealed a novel control mechanism resulting from the collective resonance of all thalamic relay neurons. We show here that the transfer efficiency of sensory input transmission depends on three key features: i) the number of thalamocortical cells involved in the many-to-one convergence from thalamus to cortex, ii) the statistics of the corticothalamic synaptic bombardment and iii) the level of correlation imposed between converging thalamic relay cells. In particular, our results demonstrate counterintuitively that the retinocortical signal transfer efficiency increases when the level of correlation across thalamic cells decreases. …”
17.	A model for a nociceptor terminal and terminal tree (Barkai et al., 2020)
		This model was used to study how the architecture of the nociceptor terminal tree affects the input-output relation of the primary nociceptive neurons. The model shows that the input-output properties of the nociceptive neurons depend on the length, the axial resistance, and location of individual terminals and that activation of multiple terminals by a capsaicin-like current allows summation of the responses from individual terminals, thus leading to increased nociceptive output.
18.	A model for interaural time difference sensitivity in the medial superior olive (Zhou et al 2005)
		This model simulates responses of neurons to interaural time difference (ITD) in the medial superior olive (MSO) of the mammalian brainstem. The model has a bipolar cell structure and incorporates two anatomic observations in the MSO: (1) the axon arises from the dendrite that receives ipsilateral inputs and (2) inhibitory synapses are located primarily on the soma in adult animals. Fine adjustment of the best ITD is achieved by the interplay of somatic sodium currents and synaptic inhibitory currents. The model suggests a mechanism for dynamically "fine-tuning" the ITD sensitivity of MSO cells by the opponency between depolarizing sodium currents and hyperpolarizing inhibitory currents.
19.	A model of closed-loop motor unit including muscle spindle feedback (Kim, 2020)
		Persistent inward current generating ion channels are located over spinal motoneurons and actively recruited during normal behaviors. Constructing a realistic computational model of closed-loop motor unit, a motoneuron and muscle fibers that it innervates including muscle spindle afferents, the study reveals functional linkage between persistent inward current location, motoneuron discharge pattern and muscle force output at various muscle lengths. This systematic analysis may provide useful insights into interplay of spinal and muscular mechanisms in control of movements.
20.	A model of optimal learning with redundant synaptic connections (Hiratani & Fukai 2018)
		This is a detailed neuron model of non-parametric near-optimal latent model acquisition using multisynaptic connections between pre- and postsynaptic neurons.
21.	A model of slow motor unit (Kim, 2017)
		Cav1.3 channels in motoneuron dendrites are actively involved during normal motor activities. To investigate the effects of the activation of motoneuron Cav1.3 channels on force production, a model motor unit was built based on best-available data. The simulation results suggest that force potentiation induced by Cav1.3 channel activation is strongly modulated not only by firing history of the motoneuron but also by length variation of the muscle as well as neuromodulation inputs from the brainstem.
22.	A model of the T-junction of a C-fiber sensory neuron (Sundt et al. 2015)
		The effect of geometry and ionic mechanisms on spike propagation through the T-junction of an unmyelinated sensory neuron.
23.	A model of unitary responses from A/C and PP synapses in CA3 pyramidal cells (Baker et al. 2010)
		The model was used to reproduce experimentally determined mean synaptic response characteristics of unitary AMPA and NMDA synaptic stimulations in CA3 pyramidal cells with the objective of inferring the most likely response properties of the corresponding types of synapses. The model is primarily concerned with passive cells, but models of active dendrites are included.
24.	A model of ventral Hippocampal CA1 pyramidal neurons of Tg2576 AD mice (Spoleti et al. 2021)
		Gradual decline in cognitive and non-cognitive functions are considered clinical hallmarks of Alzheimer's Disease (AD). Post-mortem autoptic analysis shows the presence of amyloid ß deposits, neuroinflammation and severe brain atrophy. However, brain circuit alterations and cellular derailments, assessed in very early stages of AD, still remain elusive. The understanding of these early alterations is crucial to tackle defective mechanisms. In a previous study we proved that the Tg2576 mouse model of AD displays functional deficits in the dorsal hippocampus and relevant behavioural AD-related alterations. We had shown that these deficits in Tg2576 mice correlate with the precocious degeneration of dopamine (DA) neurons in the Ventral Tegmental Area (VTA) and can be restored by L-DOPA treatment. Due to the distinct functionality and connectivity of dorsal versus ventral hippocampus, here we investigated neuronal excitability and synaptic functionality in the ventral CA1 hippocampal sub-region of Tg2576 mice. We found an age-dependent alteration of cell excitability and firing in pyramidal neurons starting at 3 months of age, that correlates with reduced levels in the ventral CA1 of tyrosine hydroxylase – the rate-limiting enzyme of DA synthesis. Additionally, at odds with the dorsal hippocampus, we found no alterations in basal glutamatergic transmission and long-term plasticity of ventral neurons in 8-month old Tg2576 mice compared to age-matched controls. Last, we used computational analysis to model the early derailments of firing properties observed and hypothesize that the neuronal alterations found could depend on dysfunctional sodium and potassium conductances, leading to anticipated depolarization-block of action potential firing. The present study depicts that impairment of cell excitability and homeostatic control of firing in ventral CA1 pyramidal neurons is a prodromal feature in Tg2576 AD mice.
25.	A multi-compartment model for interneurons in the dLGN (Halnes et al. 2011)
		This model for dLGN interneurons is presented in two parameterizations (P1 & P2), which were fitted to current-clamp data from two different interneurons (IN1 & IN2). The model qualitatively reproduces the responses in IN1 & IN2 under 8 different experimental condition, and quantitatively reproduces the I/O-relations (#spikes elicited as a function of injected current).
26.	A network model of the vertebrate retina (Publio et al. 2009)
		In this work, we use a minimal conductance-based model of the ON rod pathways in the vertebrate retina to study the effects of electrical synaptic coupling via gap junctions among rods and among AII amacrine cells on the dynamic range of the retina. The model is also used to study the effects of the maximum conductance of rod hyperpolarization activated current Ih on the dynamic range of the retina, allowing a study of the interrelations between this intrinsic membrane parameter with those two retina connectivity characteristics.
27.	A network of AOB mitral cells that produces infra-slow bursting (Zylbertal et al. 2017)
		Infra-slow rhythmic neuronal activity with very long (> 10 s) period duration was described in many brain areas but little is known about the role of this activity and the mechanisms that produce it. Here we combine experimental and computational methods to show that synchronous infra-slow bursting activity in mitral cells of the mouse accessory olfactory bulb (AOB) emerges from interplay between intracellular dynamics and network connectivity. In this novel mechanism, slow intracellular Na+ dynamics endow AOB mitral cells with a weak tendency to burst, which is further enhanced and stabilized by chemical and electrical synapses between them. Combined with the unique topology of the AOB network, infra-slow bursting enables integration and binding of multiple chemosensory stimuli over prolonged time scale. The example protocol simulates a two-glomeruli network with a single shared cell. Although each glomerulus is stimulated at a different time point, the activity of the entire population becomes synchronous (see paper Fig. 8)
28.	A neurite to measure ePSP and AP amplitude after passive spread (DeMaegd & Stein, 2021)
		Increasing temperatures overwhelmingly shunts dendritic electrical spread in a crustacean motor neuron (LG) leading to the disruption of a vital pattern generator. LG recieves synaptic input from a descending projection neuron (MCN1) via a chemical and electrical synapse. Warmer temperatures increase leak conductances in the neurite and increase the synaptic input. Here, we modelled the conflicting influence of temperature at the MCN1-LG synapse and LG neurite to determine the resulting ePSP and AP amplitude measured at different distanced from the synaptic input after passive progation through the neurite.
29.	A set of reduced models of layer 5 pyramidal neurons (Bahl et al. 2012)
		These are the NEURON files for 10 different models of a reduced L5 pyramidal neuron. The parameters were obtained by automatically fitting the models to experimental data using a multi objective evolutionary search strategy. Details on the algorithm can be found at http://www.g-node.org/emoo and in Bahl et al. (2012).
30.	A simplified cerebellar Purkinje neuron (the PPR model) (Brown et al. 2011)
		These models were implemented in NEURON by Sherry-Ann Brown in the laboratory of Leslie M. Loew. The files reproduce Figures 2c-f from Brown et al, 2011 "Virtual NEURON: a Strategy For Merged Biochemical and Electrophysiological Modeling".
31.	A single column thalamocortical network model (Traub et al 2005)
		To better understand population phenomena in thalamocortical neuronal ensembles, we have constructed a preliminary network model with 3,560 multicompartment neurons (containing soma, branching dendrites, and a portion of axon). Types of neurons included superficial pyramids (with regular spiking [RS] and fast rhythmic bursting [FRB] firing behaviors); RS spiny stellates; fast spiking (FS) interneurons, with basket-type and axoaxonic types of connectivity, and located in superficial and deep cortical layers; low threshold spiking (LTS) interneurons, that contacted principal cell dendrites; deep pyramids, that could have RS or intrinsic bursting (IB) firing behaviors, and endowed either with non-tufted apical dendrites or with long tufted apical dendrites; thalamocortical relay (TCR) cells; and nucleus reticularis (nRT) cells. To the extent possible, both electrophysiology and synaptic connectivity were based on published data, although many arbitrary choices were necessary.
32.	A single kinetic model for all human voltage-gated sodium channels (Balbi et al, 2017)
		Code for simulating macroscopic currents of sodium channels (Nav1.1. to Nav1.9), by means of a single kinetic model. Intensity-voltage curves, normalized conductance-voltage relationship, steady-state availability and recovery from inactivation are simulated.
33.	A two networks model of connectivity-dependent oscillatory activity (Avella OJ et al. 2014)
		Activity in a cortical network may express a single oscillation frequency, alternate between two or more distinct frequencies, or continually express multiple frequencies. In addition, oscillation amplitude may fluctuate over time. Interactions between oscillatory networks may contribute, but their effects are poorly known. Here, we created a two model networks, one generating on its own a relatively slow frequency (slow network) and one generating a fast frequency (fast network). We chose the slow or the fast network as source network projecting feed-forward connections to the other, or target network, and systematically investigated how type and strength of inter-network connections affected target network activity. Our results strongly depended on three factors: the type of the relevant (main) connection, its strength and the amount of source synapses. For high inter-network connection strengths, we found that the source network could completely impose its rhythm on the target network. Interestingly, the slow network was more effective at imposing its rhythm on the fast network than the other way around. The strongest entrainment occurred when excitatory cells of the slow network projected to excitatory or inhibitory cells of the fast network. Just as observed in rat activity at the prefrontal cortex satisfies the behavior described above, such that together, our results suggest that input from other oscillating networks may markedly alter a network’s frequency spectrum and may partly be responsible for the rich repertoire of temporal oscillation patterns observed in the brain.
34.	A two-layer biophysical olfactory bulb model of cholinergic neuromodulation (Li and Cleland 2013)
		This is a two-layer biophysical olfactory bulb (OB) network model to study cholinergic neuromodulation. Simulations show that nicotinic receptor activation sharpens mitral cell receptive field, while muscarinic receptor activation enhances network synchrony and gamma oscillations. This general model suggests that the roles of nicotinic and muscarinic receptors in OB are both distinct and complementary to one another, together regulating the effects of ascending cholinergic inputs on olfactory bulb transformations.
35.	Accurate and fast simulation of channel noise in conductance-based model neurons (Linaro et al 2011)
		We introduce and operatively present a general method to simulate channel noise in conductance-based model neurons, with modest computational overheads. Our approach may be considered as an accurate generalization of previous proposal methods, to the case of voltage-, ion-, and ligand-gated channels with arbitrary complexity. We focus on the discrete Markov process descriptions, routinely employed in experimental identification of voltage-gated channels and synaptic receptors.
36.	Acetylcholine Boosts Dendritic NMDA Spikes in a CA3 Pyramidal Neuron Model (Humphries et al., 2021)
		This model was used to compare the nonlinearity of NMDA inputs between dendritic sections in a CA3 pyramidal neuron as well as investigate the effect of cholinergic modulation/potassium channel inhibition on this dendritic NMDA-mediated nonlinearity.
37.	Action Potential initiation and backpropagation in Neocortical L5 Pyramidal Neuron (Hu et al. 2009)
		"...Previous computational studies have yielded conflicting conclusions about the role of Na+ channel density and biophysical properties in action potential initiation as a result of inconsistent estimates of channel density. Our modeling studies integrated the immunostaining and electrophysiological results and showed that the lowest threshold for action potential initiation at the distal AIS was largely determined by the density of low-threshold Nav1.6 channels ... Distinct from the function of Nav1.6 channel, the Nav1.2 channel may control action potential backpropagation because of its high density at the proximal AIS and high threshold. ... In conclusion, distal AIS accumulation of Nav1.6 channels determines the low threshold for action potential initiation; whereas proximal AIS accumulation of Nav1.2 channels sets the threshold for the generation of somatodendritic potentials and ensures action potential backpropagation to the soma and dendrites. Thus, Nav1.6 and Nav1.2 channels serve distinct functions in action potential initiation and backpropagation."
38.	Action potential initiation in the olfactory mitral cell (Shen et al 1999)
		Mitral cell model with standard parameters for the paper: Shen, G.Y., Chen, W. R., Midtgaard, J., Shepherd, G.M., and Hines, M.L. (1999) Computational Analysis of Action Potential Initiation in Mitral Cell Soma and Dendrites Based on Dual Patch Recordings. Journal of Neurophysiology 82:3006. Contact Michael.Hines@yale.edu if you have any questions about the implementation of the model.
39.	Action potential of mouse urinary bladder smooth muscle (Mahapatra et al 2018)
		Urinary incontinence is associated with enhanced spontaneous phasic contractions of the detrusor smooth muscle (DSM). Although a complete understanding of the etiology of these spontaneous contractions is not yet established, it is suggested that the spontaneously evoked action potentials (sAPs) in DSM cells initiate and modulate the contractions. In order to further our understanding of the ionic mechanisms underlying sAP generation, we present here a biophysically detailed computational model of a single DSM cell. First, we constructed mathematical models for nine ion channels found in DSM cells based on published experimental data: two voltage-gated Ca2+ ion channels, an hyperpolarization-activated ion channel, two voltage-gated K+ ion channels, three Ca2+-activated K+ ion channels and a non-specific background leak ion channel. Incorporating these channels, our DSM model is capable of reproducing experimentally recorded spike-type sAPs of varying configurations, ranging from sAPs displaying after-hyperpolarizations to sAPs displaying after-depolarizations. Our model, constrained heavily by physiological data, provides a powerful tool to investigate the ionic mechanisms underlying the genesis of DSM electrical activity, which can further shed light on certain aspects of urinary bladder function and dysfunction.
40.	Action potential reconstitution from measured current waveforms (Alle et al. 2009)
		This NEURON code reconstitutes action potentials in a model of a hippocampal mossy fiber from experimentally measured sodium, potassium and calcium current waveforms as described in Alle et al. (2009).
41.	Action potential-evoked Na+ influx are similar in axon and soma (Fleidervish et al. 2010)
		"In cortical pyramidal neurons, the axon initial segment (AIS) is pivotal in synaptic integration. It has been asserted that this is because there is a high density of Na+ channels in the AIS. However, we found that action potential-associated Na+ flux, as measured by high-speed fluorescence Na+ imaging, was about threefold larger in the rat AIS than in the soma. Spike-evoked Na+ flux in the AIS and the first node of Ranvier was similar and was eightfold lower in basal dendrites. ... In computer simulations, these data were consistent with the known features of action potential generation in these neurons."
42.	Action potential-evoked Na+ influx similar in axon and soma (Fleidervish et al. 2010) (Python)
		"In cortical pyramidal neurons, the axon initial segment (AIS) is pivotal in synaptic integration. It has been asserted that this is because there is a high density of Na+ channels in the AIS. However, we found that action potential-associated Na+ flux, as measured by high-speed fluorescence Na+ imaging, was about threefold larger in the rat AIS than in the soma. Spike-evoked Na+ flux in the AIS and the first node of Ranvier was similar and was eightfold lower in basal dendrites. ... In computer simulations, these data were consistent with the known features of action potential generation in these neurons."
43.	Active dendrites and spike propagation in a hippocampal interneuron (Saraga et al 2003)
		We create multi-compartment models of an Oriens-Lacunosum/Moleculare (O-LM) hippocampal interneuron using passive properties, channel kinetics, densities and distributions specific to this cell type, and explore its signaling characteristics. We find that spike initiation depends on both location and amount of input, as well as the intrinsic properties of the interneuron. Distal synaptic input always produces strong back-propagating spikes whereas proximal input could produce both forward and back-propagating spikes depending on the input strength. Please see paper for more details.
44.	Active dendrites shape signaling microdomains in hippocampal neurons (Basak & Narayanan 2018)
		The spatiotemporal spread of biochemical signals in neurons and other cells regulate signaling specificity, tuning of signal propagation, along with specificity and clustering of adaptive plasticity. Theoretical and experimental studies have demonstrated a critical role for cellular morphology and the topology of signaling networks in regulating this spread. In this study, we add a significantly complex dimension to this narrative by demonstrating that voltage-gated ion channels (A-type Potassium channels and T-type Calcium channels) on the plasma membrane could actively amplify or suppress the strength and spread of downstream signaling components. We employed a multiscale, multicompartmental, morphologically realistic, conductance-based model that accounted for the biophysics of electrical signaling and the biochemistry of calcium handling and downstream enzymatic signaling in a hippocampal pyramidal neuron. We chose the calcium – calmodulin – calcium/calmodulin-dependent protein kinase II (CaMKII) – protein phosphatase 1 (PP1) signaling pathway owing to its critical importance to several forms of neuronal plasticity, and employed physiologically relevant theta-burst stimulation (TBS) or theta-burst pairing (TBP) protocol to initiate a calcium microdomain through NMDAR activation at a synapse.
45.	Active dendritic action potential propagation (Casale & McCormick 2011)
		This model explores the dendritic sodium and potassium conductances needed to recapitulate voltage-sensitive dye optical recordings of thalamic interneuron dendrites in the dorsal lateral geniculate nucleus. Model ion channels were selected based on pharmacological data.
46.	Activity dependent conductances in a neuron model (Liu et al. 1998)
		"... We present a model of a stomatogastric ganglion (STG) neuron in which several Ca2+-dependent pathways are used to regulate the maximal conductances of membrane currents in an activity-dependent manner. Unlike previous models of this type, the regulation and modification of maximal conductances by electrical activity is unconstrained. The model has seven voltage-dependent membrane currents and uses three Ca2+ sensors acting on different time scales. ... The model suggests that neurons may regulate their conductances to maintain fixed patterns of electrical activity, rather than fixed maximal conductances, and that the regulation process requires feedback systems capable of reacting to changes of electrical activity on a number of different time scales."
47.	Activity dependent regulation of pacemaker channels by cAMP (Wang et al 2002)
		Demonstration of the physiological consequences of the cyclic allosteric gating scheme for Ih mediated by HCN2 in thalamocortical relay cells.
48.	Activity patterns in a subthalamopallidal network of the basal ganglia model (Terman et al 2002)
		"Based on recent experimental data, we have developed a conductance-based computational network model of the subthalamic nucleus and the external segment of the globus pallidus in the indirect pathway of the basal ganglia. Computer simulations and analysis of this model illuminate the roles of the coupling architecture of the network, and associated synaptic conductances, in modulating the activity patterns displayed by this network. Depending on the relationships of these coupling parameters, the network can support three general classes of sustained firing patterns: clustering, propagating waves, and repetitive spiking that may show little regularity or correlation. ...". Terman's XPP code and a partial implementation by Taylor Malone in NEURON and python are included.
49.	Afferent Integration in the NAcb MSP Cell (Wolf et al. 2005)
		"We describe a computational model of the principal cell in the nucleus accumbens (NAcb), the medium spiny projection (MSP) neuron. The model neuron, constructed in NEURON, includes all of the known ionic currents in these cells and receives synaptic input from simulated spike trains via NMDA, AMPA, and GABAA receptors. ... results suggest that afferent information integration by the NAcb MSP cell may be compromised by pathology in which the NMDA current is altered or modulated, as has been proposed in both schizophrenia and addiction."
50.	Age-dependent excitability of CA1 pyramidal neurons in APPPS1 Alzheimer's model (Vitale et al 2021)
		Age-dependent accumulation of amyloid-b, provoking increasing brain amyloidopathy, triggers abnormal patterns of neuron activity and circuit synchronization in Alzheimer’s disease (AD) as observed in human AD patients and AD mouse models. Recent studies on AD mouse models, mimicking this age-dependent amyloidopathy, identified alterations in CA1 neuron excitability. However, these models generally also overexpress mutated amyloid precursor protein (APP) and presenilin 1 (PS1) and there is a lack of a clear correlation of neuronal excitability alterations with progressive amyloidopathy. The active development of computational models of AD points out the need of collecting such experimental data to build a reliable disease model exhibiting AD-like disease progression. We therefore used the feature extraction tool of the Human Brain Project (HBP) Brain Simulation Platform to systematically analyze the excitability profile of CA1 pyramidal neuron in the APPPS1 mouse model. We identified specific features of neuron excitability that best correlate either with over-expression of mutated APP and PS1 or increasing Ab amyloidopathy. Notably, we report strong alterations in membrane time constant and action potential width and weak alterations in firing behavior. Also, using a CA1 pyramidal neuron model, we evidence amyloidopathy-dependent alterations in Ih. Finally, cluster analysis of these recordings showed that we could reliably assign a trace to its correct group, opening the door to a more refined, less variable analysis of AD-affected neurons. This inter-disciplinary analysis, bringing together experimentalists and modelers, helps to further unravel the neuronal mechanisms most affected by AD and to build a biologically plausible computational model of the AD brain. Reference: Paola Vitale, Ana Rita Salgueiro-Pereira, Carmen Alina Lupascu, Rosanna Migliore, Michele Migliore, Hélène Marie. "Analysis of age-dependent alterations in excitability properties of CA1 pyramidal neurons in an APPPS1 model of Alzheimer's disease". Frontiers in Aging Neuroscience (2021) DOI: 10.3389/fnagi.2021.668948
51.	Alcohol action in a detailed Purkinje neuron model and an efficient simplified model (Forrest 2015)
		" ... we employ a novel reduction algorithm to produce a 2 compartment model of the cerebellar Purkinje neuron from a previously published, 1089 compartment model. It runs more than 400 times faster and retains the electrical behavior of the full model. So, it is more suitable for inclusion in large network models, where computational power is a limiting issue. We show the utility of this reduced model by demonstrating that it can replicate the full model’s response to alcohol, which can in turn reproduce experimental recordings from Purkinje neurons following alcohol application. ..."
52.	Alcohol excites Cerebellar Golgi Cells by inhibiting the Na+/K+ ATPase (Botta et al.2010)
		Patch-clamp in cerebellar slices and computer modeling show that ethanol excites Golgi cells by inhibiting the Na+/K+ ATPase. In particular, voltage-clamp recordings of Na+/K+ ATPase currents indicated that ethanol partially inhibits this pump and this effect could be mimicked by low concentrations of the Na+/K+ ATPase blocker ouabain. The partial inhibition of Na+/K+ ATPase in a computer model of the Golgi cell reproduced these experimental findings that established a novel mechanism of action of ethanol on neural excitability.
53.	Allen Institute: Gad2-IRES-Cre VISp layer 5 472447460
		This is an Allen Cell Types Database model of a Gad2-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
54.	Allen Institute: Gad2-IRES-Cre VISp layer 5 473561729
		This is an Allen Cell Types Database model of a Gad2-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
55.	Allen Institute: Htr3a-Cre VISp layer 2/3 472352327
		This is an Allen Cell Types Database model of a Htr3a-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
56.	Allen Institute: Htr3a-Cre VISp layer 2/3 472421285
		This is an Allen Cell Types Database model of a Htr3a-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
57.	Allen Institute: Nr5a1-Cre VISp layer 2/3 473862496
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
58.	Allen Institute: Nr5a1-Cre VISp layer 4 329322394
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
59.	Allen Institute: Nr5a1-Cre VISp layer 4 472306544
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
60.	Allen Institute: Nr5a1-Cre VISp layer 4 472442377
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
61.	Allen Institute: Nr5a1-Cre VISp layer 4 472451419
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
62.	Allen Institute: Nr5a1-Cre VISp layer 4 472915634
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
63.	Allen Institute: Nr5a1-Cre VISp layer 4 473834758
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
64.	Allen Institute: Nr5a1-Cre VISp layer 4 473863035
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
65.	Allen Institute: Nr5a1-Cre VISp layer 4 473871429
		This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
66.	Allen Institute: Ntsr1-Cre VISp layer 4 472430904
		This is an Allen Cell Types Database model of a Ntsr1-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
67.	Allen Institute: Pvalb-IRES-Cre VISp layer 2/3 472306616
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
68.	Allen Institute: Pvalb-IRES-Cre VISp layer 5 471085845
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
69.	Allen Institute: Pvalb-IRES-Cre VISp layer 5 472349114
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
70.	Allen Institute: Pvalb-IRES-Cre VISp layer 5 472912177
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
71.	Allen Institute: Pvalb-IRES-Cre VISp layer 5 473465774
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
72.	Allen Institute: Pvalb-IRES-Cre VISp layer 5 473862421
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
73.	Allen Institute: Pvalb-IRES-Cre VISp layer 6a 471081668
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
74.	Allen Institute: Pvalb-IRES-Cre VISp layer 6a 472301074
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
75.	Allen Institute: Pvalb-IRES-Cre VISp layer 6a 473860269
		This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
76.	Allen Institute: Rbp4-Cre VISp layer 5 472424854
		This is an Allen Cell Types Database model of a Rbp4-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
77.	Allen Institute: Rbp4-Cre VISp layer 6a 473871592
		This is an Allen Cell Types Database model of a Rbp4-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
78.	Allen Institute: Rorb-IRES2-Cre-D VISp layer 2/3 472299294
		This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
79.	Allen Institute: Rorb-IRES2-Cre-D VISp layer 2/3 472434498
		This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
80.	Allen Institute: Rorb-IRES2-Cre-D VISp layer 4 473863510
		This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
81.	Allen Institute: Rorb-IRES2-Cre-D VISp layer 5 471087975
		This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
82.	Allen Institute: Rorb-IRES2-Cre-D VISp layer 5 473561660
		This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
83.	Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 472300877
		This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
84.	Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 472427533
		This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
85.	Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 472912107
		This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
86.	Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 473465456
		This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
87.	Allen Institute: Scnn1a-Tg2-Cre VISp layer 5 472306460
		This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
88.	Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 329321704
		This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
89.	Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 472363762
		This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
90.	Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 473862845
		This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
91.	Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 473872986
		This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
92.	Allen Institute: Scnn1a-Tg3-Cre VISp layer 5 472455509
		This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
93.	Allen Institute: Scnn1a-Tg3-Cre VISp layer 5 473863578
		This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
94.	Allen Institute: Scnn1a-Tg3-Cre VISp layer 5 473871773
		This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
95.	Allen Institute: Sst-IRES-Cre VISp layer 2/3 471086533
		This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
96.	Allen Institute: Sst-IRES-Cre VISp layer 2/3 472304676
		This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
97.	Allen Institute: Sst-IRES-Cre VISp layer 4 472304539
		This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
98.	Allen Institute: Sst-IRES-Cre VISp layer 5 472299363
		This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
99.	Allen Institute: Sst-IRES-Cre VISp layer 5 472450023
		This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
100.	Allen Institute: Sst-IRES-Cre VISp layer 5 473835796
		This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
101.	Allen Institute: Sst-IRES-Cre VISp layer 6a 472440759
		This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
102.	Altered complexity in layer 2/3 pyramidal neurons (Luuk van der Velden et al. 2012)
		" ... Our experimental results show that hypercomplexity of the apical dendritic tuft of layer 2/3 pyramidal neurons affects neuronal excitability by reducing the amount of spike frequency adaptation. This difference in firing pattern, related to a higher dendritic complexity, was accompanied by an altered development of the afterhyperpolarization slope with successive action potentials. Our abstract and realistic neuronal models, which allowed manipulation of the dendritic complexity, showed similar effects on neuronal excitability and confirmed the impact of apical dendritic complexity. Alterations of dendritic complexity, as observed in several pathological conditions such as neurodegenerative diseases or neurodevelopmental disorders, may thus not only affect the input to layer 2/3 pyramidal neurons but also shape their firing pattern and consequently alter the information processing in the cortex."
103.	Ambient glutamate shapes AMPA receptor responses to simulated transients (Balmer et al. 2021)
		To explore how ambient glutamate contributes to the generation of ultra-slow signaling through AMPARs at the cerebellar unipolar brush cell synapse, we created this 13-state kinetic model in NEURON. A tool was also created to produce trains of glutamate concentration transients using 2D or 3D diffusion equations, a sum of up to 3 exponentials, or an alpha function that can be applied to the AMPA receptor model. After compiling the model using mkrndll, run 'mosinit_fast-flow.hoc' to simulate fast application of glutamate to the AMPA receptor model. 'mosinit_GluTransTrainTool_demo.hoc' opens a session where trains of synaptic glutamate transients can be created using various equations. The top panel shows the glutamate concentration transients (in mM) and the bottom panel shows the AMPA receptor mediated currents (in nA).
104.	Amyloid beta (IA block) effects on a model CA1 pyramidal cell (Morse et al. 2010)
		The model simulations provide evidence oblique dendrites in CA1 pyramidal neurons are susceptible to hyper-excitability by amyloid beta block of the transient K+ channel, IA. See paper for details.
105.	Amyloid-beta effects on release probability and integration at CA3-CA1 synapses (Romani et al. 2013)
		The role of amyloid beta (Aß) in brain function and in the pathogenesis of Alzheimer’s disease remains elusive. Recent publications reported that an increase in Aß concentration perturbs presynaptic release in hippocampal neurons, in particular by increasing release probability of CA3-CA1 synapses. The model predics how this alteration can affect synaptic plasticity and signal integration. The results suggest that the perturbation of release probability induced by increased Aß can significantly alter the spike probability of CA1 pyramidal neurons and thus contribute to abnormal hippocampal function during Alzheimer’s disease.
106.	AOB mitral cell: persistent activity without feedback (Zylbertal et al., 2015)
		Persistent activity has been reported in many brain areas and is hypothesized to mediate working memory and emotional brain states and to rely upon network or biophysical feedback. Here we demonstrate a novel mechanism by which persistent neuronal activity can be generated without feedback, relying instead on the slow removal of Na+ from neurons following bursts of activity. This is a realistic conductance-based model that was constructed using the detailed morphology of a single typical accessory olfactory bulb (AOB) mitral cell for which the electrophysiological properties were characterized.
107.	AP back-prop. explains threshold variability and rapid rise (McCormick et al. 2007, Yu et al. 2008)
		This simple axon-soma model explained how the rapid rising phase in the somatic spike is derived from the propagated axon initiated spike, and how the somatic spike threshold variance is affected by spike propagation.
108.	AP initiation and propagation in type II cochlear ganglion cell (Hossain et al 2005)
		The model of type II cochlear ganglion cell was based on the immunostaining of the mouse auditory pathway. Specific antibodies were used to map the distribution of voltage-dependent sodium channels along the two unmyelinated axon-like processes of the bipolar ganglion cells. Three distinct hot spots were detected. A high density of sodium channels was present over the entire trajectory of sensory endings beneath the outer hair cells (the most distal portion of the peripheral axon). The other two hot spots were localized in the initial segments of both of the axons that flank the unmyelinated bipolar ganglion cell bodies. A biophysical model indicates that all three hot spots might play important roles in action potential initiation and propagation. For instance, the hot spot in the receptor segment is important for transforming the receptor potentials into a full blown action potential (Supplemental Fig. 1). The hot spots in the two paraganglionic axon initial segments are there to ensure the successful propagation of action potentials from the peripheral to the central axon through the cell body. The Readme.txt file provides step by step instructions on how to recreate Figures 6 and 7 of Hossain et al., 2005 paper.
109.	AP initiation, propagation, and cortical invasion in a Layer 5 pyramidal cell (Anderson et 2018)
		" ... High frequency (~130 Hz) deep brain stimulation (DBS) of the subthalamic region is an established clinical therapy for the treatment of late stage Parkinson's disease (PD). Direct modulation of the hyperdirect pathway, defined as cortical layer V pyramidal neurons that send an axon collateral to the subthalamic nucleus (STN), has emerged as a possible component of the therapeutic mechanisms. ...We found robust AP propagation throughout the complex axonal arbor of the hyperdirect neuron. Even at therapeutic DBS frequencies, stimulation induced APs could reach all of the intracortical axon terminals with ~100% fidelity. The functional result of this high frequency axonal driving of the thousands of synaptic connections made by each directly stimulated hyperdirect neuron is a profound synaptic suppression that would effectively disconnect the neuron from the cortical circuitry. ..."
110.	AP shape and parameter constraints in optimization of compartment models (Weaver and Wearne 2006)
		"... We construct an objective function that includes both time-aligned action potential shape error and errors in firing rate and firing regularity. We then implement a variant of simulated annealing that introduces a recentering algorithm to handle infeasible points outside the boundary constraints. We show how our objective function captures essential features of neuronal firing patterns, and why our boundary management technique is superior to previous approaches."
111.	Application of a common kinetic formalism for synaptic models (Destexhe et al 1994)
		Application to AMPA, NMDA, GABAA, and GABAB receptors is given in a book chapter. The reference paper synthesizes a comprehensive general description of synaptic transmission with Markov kinetic models. This framework is applicable to modeling ion channels, synaptic release, and all receptors. Please see the references for more details. A simple introduction to this method is given in a seperate paper Destexhe et al Neural Comput 6:14-18 , 1994). More information and papers at http://cns.iaf.cnrs-gif.fr/Main.html and through email: Destexhe@iaf.cnrs-gif.fr
112.	Arteriolar networks: Spread of potential (Crane et al 2001)
		Crane, G.J., Hines, M.L., and Neild, T.O. (2001) Simulating the spread of membrane potential changes in arteriolar networks. Microcirculation 8:33-43. This model uses a gap junction density mechanism to couple arteriolar smooth muscle and endothelium in microvascular trees.
113.	Artificial neuron model (Izhikevich 2003, 2004, 2007)
		A set of models is presented based on 2 related parameterizations to reproduce spiking and bursting behavior of multiple types of cortical neurons and thalamic neurons. These models combine the biologically plausibility of Hodgkin Huxley-type dynamics and the computational efficiency of integrate-and-fire neurons. Using these model, one can simulate tens of thousands of spiking cortical neurons in real time (1 ms resolution) using a desktop PC.
114.	Availability of low-threshold Ca2+ current in retinal ganglion cells (Lee SC et al. 2003)
		"... we measured T-type current of isolated goldfish retinal ganglion cells with perforated-patch voltageclamp methods in solutions containing a normal extracellular Ca2+ concentration. The voltage sensitivities and rates of current activation, inactivation, deactivation, and recovery from inactivation were similar to those of expressed +1G (CaV3.1) Ca2+ channel clones, except that the rate of deactivation was significantly faster. We reproduced the amplitude and kinetics of measured T currents with a numerical simulation based on a kinetic model developed for an +1G Ca2+ channel. Finally, we show that this model predicts the increase of T-type current made available between resting potential and spike threshold by repetitive hyperpolarizations presented at rates that are within the bandwidth of signals processed in situ by these neurons."
115.	Axon-somatic back-propagation in a detailed model of cat spinal motoneuron (Balbi et al, 2015)
		Morphologically detailed conductance-based models of cat spinal alpha motoneurons have been developed, with the aim to reproduce and clarify some aspects of the electrophysiological behavior of the antidromic axon-somatic spike propagation. Fourteen 3D morphologically detailed somata and dendrites of cat spinal alpha motoneurons have been imported from an open-access web-based database of neuronal morphologies, NeuroMorpho.org, and instantiated in neurocomputational models.
116.	Axonal NaV1.6 Sodium Channels in AP Initiation of CA1 Pyramidal Neurons (Royeck et al. 2008)
		"... We show that the Na+ channel NaV1.6 displays a striking aggregation at the AIS of cortical neurons. ... In combination with simulations using a realistic computer model of a CA1 pyramidal cell, our results imply that a hyperpolarized voltage-dependence of activation of AIS NaV1.6 channels is important both in determining spike threshold and localizing spike initiation to the AIS. ... These results suggest that NaV1.6 subunits at the AIS contribute significantly to its role as spike trigger zone and shape repetitive discharge properties of CA1 neurons."
117.	Axonal spheroids and conduction defects in Alzheimer’s disease (Yuan, Zhang, Tong, et al 2022)
		PAAS (plaque-associated axonal spheroid(s)) are dystrophic structures that sprout from axons that pass through amyloid beta plaques. If small enough they do not interfere with action potential (AP) propagation. Medium sized ones delay APs, and large, or many spheroids can block single APs and block or delay trains of APs.
118.	Axonal subthreshold voltage signaling along hippocampal mossy fiber (Kamiya 2022)
		Subthreshold depolarization of soma passively propagates into the axons for a substantial distance and thereby caused enhancement of the transmitter release from the axon terminals of hippocampal mossy fibers. Here we developed the granule cell-mossy fiber model implemented with axonal sodium potassium and calcium channels and explored the mechanisms underlying analog modulation of the action potential-evoked transmitter release by subthreshold voltage signaling along the axons. Action potential-induced calcium entry to the terminals was reduced, while subthreshold depolarization itself caused small calcium entry.
119.	Balance of excitation and inhibition (Carvalho and Buonomano 2009)
		" ... Here, theoretical analyses reveal that excitatory synaptic strength controls the threshold of the neuronal input-output function, while inhibitory plasticity alters the threshold and gain. Experimentally, changes in the balance of excitation and inhibition in CA1 pyramidal neurons also altered their input-output function as predicted by the model. These results support the existence of two functional modes of plasticity that can be used to optimize information processing: threshold and gain plasticity."
120.	Basal ganglia network model of subthalamic deep brain stimulation (Hahn and McIntyre 2010)
		Basal ganglia network model of parkinsonian activity and subthalamic deep brain stimulation in non-human primates from the article Instructions are provided in the README.txt file. Contact hahnp@ccf.org if you have any questions about the implementation of the model. Please include "ModelDB - BGnet" in the subject heading.
121.	Basket cell extrasynaptic inhibition modulates network oscillations (Proddutur et al., 2013)
		Among the rhythmic firing patterns observed in brain, gamma oscillations, which are involved in memory formation and retrieval, are generated by networks of fast-spiking basket cells (FS-BCs) with robust interconnectivity through fast GABA synapses. Recently, we identified presence of extrasynaptic tonic GABA currents in FS-BCs and showed that experimentally-induced seizures enhance extrasynaptic tonic GABA currents and render GABA reversal potential (EGABA) depolarizing (Yu et al., 2013). Extrasynaptic GABA currents are mediated by extra- and peri-synaptically located GABAARs and can contribute to synaptic decay kinetics. Additionally, shunting rather than hyperpolarizing EGABA has been shown to increase the frequency and reduce coherence of network oscillations. Using homogeneous networks of biophysically-based, multi-compartmental model FS-BCs, we examined how the presence of extrasynaptic GABA currents and the experimentally identified seizure-induced alterations in GABA currents and EGABA modify the frequency and coherence of network firing.
122.	BCM-like synaptic plasticity with conductance-based models (Narayanan Johnston, 2010)
		" ... Although the BCM-like plasticity framework has been a useful formulation to understand synaptic plasticity and metaplasticity, a mechanism for the activity-dependent regulation of this modification threshold has remained an open question. In this simulation study based on CA1 pyramidal cells, we use a modification of the calcium-dependent hypothesis proposed elsewhere and show that a change in the hyperpolarization-activated, nonspecific-cation h current is capable of shifting the modification threshold. ..."
123.	Biochemically detailed model of LTP and LTD in a cortical spine (Maki-Marttunen et al 2020)
		"Signalling pathways leading to post-synaptic plasticity have been examined in many types of experimental studies, but a unified picture on how multiple biochemical pathways collectively shape neocortical plasticity is missing. We built a biochemically detailed model of post-synaptic plasticity describing CaMKII, PKA, and PKC pathways and their contribution to synaptic potentiation or depression. We developed a statistical AMPA-receptor-tetramer model, which permits the estimation of the AMPA-receptor-mediated maximal synaptic conductance based on numbers of GluR1s and GluR2s predicted by the biochemical signalling model. We show that our model reproduces neuromodulator-gated spike-timing-dependent plasticity as observed in the visual cortex and can be fit to data from many cortical areas, uncovering the biochemical contributions of the pathways pinpointed by the underlying experimental studies. Our model explains the dependence of different forms of plasticity on the availability of different proteins and can be used for the study of mental disorder-associated impairments of cortical plasticity."
124.	Biophysical and phenomenological models of spike-timing dependent plasticity (Badoual et al. 2006)
		"Spike-timing dependent plasticity (STDP) is a form of associative synaptic modification which depends on the respective timing of pre- and post-synaptic spikes. The biophysical mechanisms underlying this form of plasticity are currently not known. We present here a biophysical model which captures the characteristics of STDP, such as its frequency dependency, and the effects of spike pair or spike triplet interactions. ... A simplified phenomenological model is also derived..."
125.	Biophysically detailed model of somatosensory thalamocortical circuit
		Large-scale biophysically detailed model of somatosensory thalamocortical circuits in NetPyNE
126.	Biophysically Realistic Network Model of the Wild-Type and Degenerate Retina (Ly et al 2022)
		Please read the readme.txt file before running any code. Objective: A major reason for poor visual outcomes provided by existing retinal prostheses is the limited knowledge of the impact of photoreceptor loss on retinal remodelling and its subsequent impact on neural responses to electrical stimulation. Computational network models of the neural retina assist in the understanding of normal retinal function but can be also useful for investigating diseased retinal responses to electrical stimulation. Approach: We developed and validated a biophysically detailed discrete neuronal network model of the retina in the software package NEURON. The model includes rod and cone photoreceptors, ON and OFF bipolar cell pathways, amacrine and horizontal cells and finally, ON and OFF retinal ganglion cells with detailed network connectivity and neural intrinsic properties. By accurately controlling the network parameters, we simulated the impact of varying levels of degeneration on retinal electrical function. Main results: Our model was able to reproduce characteristic monophasic and biphasic oscillatory patterns seen in ON and OFF neurons during retinal degeneration. Oscillatory activity occurred at 3 Hz with partial photoreceptor loss and at 6 Hz when all photoreceptor input to the retina was removed. Oscillations were found to gradually weaken, then disappear when synapses and gap junctions were destroyed in the inner retina. Without requiring any changes to intrinsic cellular properties of individual inner retinal neurons, our results suggest that changes in connectivity alone were sufficient to give rise to neural oscillations during photoreceptor degeneration, and significant network connectivity destruction in the inner retina terminated the oscillations. Significance: Our results provide a platform for further understanding physiological retinal changes with progressive photoreceptor and inner retinal degeneration. Furthermore, our model can be used to guide future stimulation strategies for retinal prostheses to benefit patients at different stages of disease progression, particularly in the early and mid-stages of retinal degeneration.
127.	Biophysically realistic neural modeling of the MEG mu rhythm (Jones et al. 2009)
		"Variations in cortical oscillations in the alpha (7–14 Hz) and beta (15–29 Hz) range have been correlated with attention, working memory, and stimulus detection. The mu rhythm recorded with magnetoencephalography (MEG) is a prominent oscillation generated by Rolandic cortex containing alpha and beta bands. Despite its prominence, the neural mechanisms regulating mu are unknown. We characterized the ongoing MEG mu rhythm from a localized source in the finger representation of primary somatosensory (SI) cortex. Subjects showed variation in the relative expression of mu-alpha or mu-beta, which were nonoverlapping for roughly 50% of their respective durations on single trials. To delineate the origins of this rhythm, a biophysically principled computational neural model of SI was developed, with distinct laminae, inhibitory and excitatory neurons, and feedforward (FF, representative of lemniscal thalamic drive) and feedback (FB, representative of higher-order cortical drive or input from nonlemniscal thalamic nuclei) inputs defined by the laminar location of their postsynaptic effects. ..."
128.	Biophysically realistic neuron models for simulation of cortical stimulation (Aberra et al. 2018)
		This archive instantiates the single-cell cortical models used in (Aberra et al. 2018) and sets up extracellular stimulation with either a point-current source, to simulate intracortical microstimulation (ICMS), or a uniform E-field distribution, with a monophasic, rectangular pulse waveform in both cases.
129.	Boolean network-based analysis of the apoptosis network (Mai and Liu 2009)
		"To understand the design principles of the molecular interaction network associated with the irreversibility of cell apoptosis and the stability of cell surviving, we constructed a Boolean network integrating both the intrinsic and extrinsic pro-apoptotic pathways with pro-survival signal transduction pathways. We performed statistical analyses of the dependences of cell fate on initial states and on input signals. The analyses reproduced the well-known pro- and anti-apoptotic effects of key external signals and network components. We found that the external GF signal by itself did not change the apoptotic ratio from randomly chosen initial states when there is no external TNF signal, but can significantly offset apoptosis induced by the TNF signal. ..."
130.	Brain networks simulators - a comparative study (Tikidji-Hamburyan et al 2017)
		" ... In this article, we select the three most popular simulators, as determined by the number of models in the ModelDB database, such as NEURON, GENESIS, and BRIAN, and perform an independent evaluation of these simulators. In addition, we study NEST, one of the lead simulators of the Human Brain Project. First, we study them based on one of the most important characteristics, the range of supported models. Our investigation reveals that brain network simulators may be biased toward supporting a specific set of models. ... we carry out an evaluation using two case studies: a large network with simplified neural and synaptic models and a small network with detailed models. These two case studies allow us to avoid any bias toward a particular software package ..."
131.	Broadening of activity with flow across neural structures (Lytton et al. 2008)
		"Synfire chains have long been suggested as a substrate for perception and information processing in the nervous system. However, embedding activation chains in a densely connected nervous matrix risks spread of signal that will obscure or obliterate the message. We used computer modeling and physiological measurements in rat hippocampus to assess this problem of activity broadening. We simulated a series of neural modules with feedforward propagation and random connectivity within each module and from one module to the next. ..."
132.	Bursting and resonance in cerebellar granule cells (D'Angelo et al. 2001)
		In this study we report theta-frequency (3-12 Hz) bursting and resonance in rat cerebellar granule cells and show that these neurons express a previously unidentified slow repolarizing K1 current (IK-slow ). Our experimental and modeling results indicate that IK-slow was necessary for both bursting and resonance. See paper for more.
133.	Bursting respiratory net: clustered architecture gives large phase diff`s (Fietkiewicz et al 2011)
		Using a previous model of respiratory rhythm generation, we modified the network architecture such that cells can be segregated into two clusters. Cells within a given cluster burst with smaller phase differences than do cells from different clusters. This may explain the large phase differences seen experimentally, as reported in the paper.
134.	Ca+/HCN channel-dependent persistent activity in multiscale model of neocortex (Neymotin et al 2016)
		"Neuronal persistent activity has been primarily assessed in terms of electrical mechanisms, without attention to the complex array of molecular events that also control cell excitability. We developed a multiscale neocortical model proceeding from the molecular to the network level to assess the contributions of calcium regulation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in providing additional and complementary support of continuing activation in the network. ..."
135.	Ca-dependent K Channel: kinetics from rat muscle (Moczydlowski, Latorre 1983) NEURON
		Macroscopic channel model based on Moczydlowski, E. and Latorre, R. (1983). Gating kinetics of Ca++ activated K+ channels from rat muscle incorporated into planar lipid bilayers. J. Gen. Physiol. 82: 511-542 See README file for more information.
136.	CA1 interneuron: K currents (Lien et al 2002)
		NEURON mod files for slow and fast K-DR, and K-A potassium currents in inhibitory interneurones of stratum oriens-alveus of the hippocampal CA1 region.
137.	CA1 network model for place cell dynamics (Turi et al 2019)
		Biophysical model of CA1 hippocampal region. The model simulates place cells/fields and explores the place cell dynamics as function of VIP+ interneurons.
138.	CA1 network model: interneuron contributions to epileptic deficits (Shuman et al 2020)
		Temporal lobe epilepsy causes significant cognitive deficits in both humans and rodents, yet the specific circuit mechanisms underlying these deficits remain unknown. There are profound and selective interneuron death and axonal reorganization within the hippocampus of both humans and animal models of temporal lobe epilepsy. To assess the specific contribution of these mechanisms on spatial coding, we developed a biophysically constrained network model of the CA1 region that consists of different subtypes of interneurons. More specifically, our network consists of 150 cells, 130 excitatory pyramidal cells and 20 interneurons (Fig. 1A). To simulate place cell formation in the network model, we generated grid cell and place cell inputs from the Entorhinal Cortex (ECLIII) and CA3 regions, respectively, activated in a realistic manner as observed when an animal transverses a linear track. Realistic place fields emerged in a subpopulation of pyramidal cells (40-50%), in which similar EC and CA3 grid cell inputs converged onto distal/proximal apical and basal dendrites. The tuning properties of these cells are very similar to the ones observed experimentally in awake, behaving animals To examine the role of interneuron death and axonal reorganization in the formation and/or tuning properties of place fields we selectively varied the contribution of each interneuron type and desynchronized the two excitatory inputs. We found that desynchronized inputs were critical in reproducing the experimental data, namely the profound reduction in place cell numbers, stability and information content. These results demonstrate that the desynchronized firing of hippocampal neuronal populations contributes to poor spatial processing in epileptic mice, during behavior. Given the lack of experimental data on the selective contributions of interneuron death and axonal reorganization in spatial memory, our model findings predict the mechanistic effects of these alterations at the cellular and network levels.
139.	CA1 oriens alveus interneurons: signaling properties (Minneci et al. 2007)
		The model supports the experimental findings showing that the dynamic interaction between cells with various firing patterns could differently affect GABAergic signaling, leading to a wide range of interneuronal communication within the hippocampal network.
140.	CA1 pyr cell: Inhibitory modulation of spatial selectivity+phase precession (Grienberger et al 2017)
		Spatially uniform synaptic inhibition enhances spatial selectivity and temporal coding in CA1 place cells by suppressing broad out-of-field excitation.
141.	CA1 pyramidal cell: reconstructed axonal arbor and failures at weak gap junctions (Vladimirov 2011)
		Model of pyramidal CA1 cells connected by gap junctions in their axons. Cell geometry is based on anatomical reconstruction of rat CA1 cell (NeuroMorpho.Org ID: NMO_00927) with long axonal arbor. Model init_2cells.hoc shows failures of second spike propagation in a spike doublet, depending on conductance of an axonal gap junction. Model init_ring.hoc shows that spike failure result in reentrant oscillations of a spike in a loop of axons connected by gap junctions, where one gap junction is weak. The paper shows that in random networks of axons connected by gap junctions, oscillations are driven by single pacemaker loop of axons. The shortest loop, around which a spike can travel, is the most likely pacemaker. This principle allows us to predict the frequency of oscillations from network connectivity and visa versa. We propose that this type of oscillations corresponds to so-called fast ripples in epileptic hippocampus.
142.	CA1 pyramidal neuron (Combe et al 2018)
		"Gamma oscillations are thought to play a role in learning and memory. Two distinct bands, slow (25-50 Hz) and fast (65-100 Hz) gamma, have been identified in area CA1 of the rodent hippocampus. Slow gamma is phase-locked to activity in area CA3 and presumably driven by the Schaffer collaterals. We used a combination of computational modeling and in vitro electrophysiology in hippocampal slices of male rats to test whether CA1 neurons responded to Schaffer collateral stimulation selectively at slow gamma frequencies, and to identify the mechanisms involved. Both approaches demonstrated that in response to temporally precise input at Schaffer collaterals, CA1 pyramidal neurons fire preferentially in the slow gamma range regardless of whether the input is at fast or slow gamma frequencies, suggesting frequency selectivity in CA1 output with respect to CA3 input. In addition, phase-locking, assessed by the vector strength, was more precise for slow gamma than fast gamma input. ..."
143.	CA1 pyramidal neuron (Migliore et al 1999)
		Hippocampal CA1 pyramidal neuron model from the paper M.Migliore, D.A Hoffman, J.C. Magee and D. Johnston (1999) Role of an A-type K+ conductance in the back-propagation of action potentials in the dendrites of hippocampal pyramidal neurons, J. Comput. Neurosci. 7, 5-15. Instructions are provided in the below README file.Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model.
144.	CA1 pyramidal neuron synaptic integration (Bloss et al. 2016)
		"... We examined synaptic connectivity between molecularly defined inhibitory interneurons and CA1 pyramidal cell dendrites using correlative light-electron microscopy and large-volume array tomography. We show that interneurons can be highly selective in their connectivity to specific dendritic branch types and, furthermore, exhibit precisely targeted connectivity to the origin or end of individual branches. Computational simulations indicate that the observed subcellular targeting enables control over the nonlinear integration of synaptic input or the initiation and backpropagation of action potentials in a branchselective manner. Our results demonstrate that connectivity between interneurons and pyramidal cell dendrites is more precise and spatially segregated than previously appreciated, which may be a critical determinant of how inhibition shapes dendritic computation."
145.	CA1 pyramidal neuron synaptic integration (Li and Ascoli 2006, 2008)
		The model shows how different input patterns (irregular & asynchronous, irregular & synchronous, regular & asynchronous, regular & synchronous) affect the neuron's output rate when 1000 synapses are distributed in the proximal apical dendritic tree of a hippocampus CA1 pyramidal neuron.
146.	CA1 pyramidal neuron to study INaP properties and repetitive firing (Uebachs et al. 2010)
		A model of a CA1 pyramidal neuron containing a biophysically realistic morphology and 15 distributed voltage and Ca2+-dependent conductances. Repetitive firing is modulated by maximal conductance and the voltage dependence of the persistent Na+ current (INaP).
147.	CA1 pyramidal neuron: as a 2-layer NN and subthreshold synaptic summation (Poirazi et al 2003)
		We developed a CA1 pyramidal cell model calibrated with a broad spectrum of in vitro data. Using simultaneous dendritic and somatic recordings, and combining results for two different response measures (peak vs. mean EPSP), two different stimulus formats (single shock vs. 50 Hz trains), and two different spatial integration conditions (within vs. between-branch summation), we found the cell's subthreshold responses to paired inputs are best described as a sum of nonlinear subunit responses, where the subunits correspond to different dendritic branches. In addition to suggesting a new type of experiment and providing testable predictions, our model shows how conclusions regarding synaptic arithmetic can be influenced by an array of seemingly innocuous experimental design choices.
148.	CA1 pyramidal neuron: action potential backpropagation (Gasparini & Migliore 2015)
		" ... the investigation of AP backpropagation and its functional roles has greatly benefitted from computational models that use biophysically and morphologically accurate implementations. ..." This model entry recreates figures 2 and 4 from the paper illustrating how conductance densities of voltage gated channels (fig 2) and the timing of synaptic input with backpropagating action potentials (fig 4) affects membrane voltage trajectories.
149.	CA1 pyramidal neuron: calculation of MRI signals (Cassara et al. 2008)
		NEURON mod files from the paper: Cassarà AM, Hagberg GE, Bianciardi M, Migliore M, Maraviglia B. Realistic simulations of neuronal activity: A contribution to the debate on direct detection of neuronal currents by MRI. Neuroimage. 39:87-106 (2008). In this paper, we use a detailed calculation of the magnetic field produced by the neuronal currents propagating over a hippocampal CA1 pyramidal neuron placed inside a cubic MR voxel of length 1.2 mm to estimate the Magnetic Resonance signal.
150.	CA1 pyramidal neuron: conditional boosting of dendritic APs (Watanabe et al 2002)
		Model files from the paper Watanabe S, Hoffman DA, Migliore M, Johnston D (2002). The experimental and modeling results support the hypothesis that dendritic K-A channels and the boosting of back-propagating action potentials contribute to the induction of LTP in CA1 neurons. See the paper for details. Questions about the model may be addressed to Michele Migliore: michele.migliore@pa.ibf.cnr.it
151.	CA1 pyramidal neuron: dendritic Ca2+ inhibition (Muellner et al. 2015)
		In our experimental study, we combined paired patch-clamp recordings and two-photon Ca2+ imaging to quantify inhibition exerted by individual GABAergic contacts on hippocampal pyramidal cell dendrites. We observed that Ca2+ transients from back-propagating action potentials were significantly reduced during simultaneous activation of individual nearby GABAergic synapses. To simulate dendritic Ca2+ inhibition by individual GABAergic synapses, we employed a multi-compartmental CA1 pyramidal cell model with detailed morphology, voltage-gated channel distributions, and calcium dynamics, based with modifications on the model of Poirazi et al., 2003, modelDB accession # 20212.
152.	CA1 pyramidal neuron: Dendritic Na+ spikes are required for LTP at distal synapses (Kim et al 2015)
		This model simulates the effects of dendritic sodium spikes initiated in distal apical dendrites on the voltage and the calcium dynamics revealed by calcium imaging. It shows that dendritic sodium spike promotes large and transient calcium influxes via NMDA receptor and L-type voltage-gated calcium channels, which contribute to the induction of LTP at distal synapses.
153.	CA1 pyramidal neuron: dendritic spike initiation (Gasparini et al 2004)
		NEURON mod files from the paper: Sonia Gasparini, Michele Migliore, and Jeffrey C. Magee On the initiation and propagation of dendritic spikes in CA1 pyramidal neurons, J. Neurosci., J. Neurosci. 24:11046-11056 (2004).
154.	CA1 pyramidal neuron: depolarization block (Bianchi et al. 2012)
		NEURON files from the paper: On the mechanisms underlying the depolarization block in the spiking dynamics of CA1 pyramidal neurons by D.Bianchi, A. Marasco, A.Limongiello, C.Marchetti, H.Marie,B.Tirozzi, M.Migliore (2012). J Comput. Neurosci. In press. DOI: 10.1007/s10827-012-0383-y. Experimental findings shown that under sustained input current of increasing strength neurons eventually stop firing, entering a depolarization block. We analyze the spiking dynamics of CA1 pyramidal neuron models using the same set of ionic currents on both an accurate morphological reconstruction and on its reduction to a single-compartment. The results show the specic ion channel properties and kinetics that are needed to reproduce the experimental findings, and how their interplay can drastically modulate the neuronal dynamics and the input current range leading to depolarization block.
155.	CA1 pyramidal neuron: effects of Ih on distal inputs (Migliore et al 2004)
		NEURON mod files from the paper: M. Migliore, L. Messineo, M. Ferrante Dendritic Ih selectively blocks temporal summation of unsynchronized distal inputs in CA1 pyramidal neurons, J.Comput. Neurosci. 16:5-13 (2004). The model demonstrates how the dendritic Ih in pyramidal neurons could selectively suppress AP generation for a volley of excitatory afferents when they are asynchronously and distally activated.
156.	CA1 pyramidal neuron: effects of Lamotrigine on dendritic excitability (Poolos et al 2002)
		NEURON mod files from N. Poolos, M. Migliore, and D. Johnston, Nature Neuroscience (2002). The experimental and modeling results in this paper demonstrate for the first time that neuronal excitability can be altered by pharmaceuticals acting selectively on dendrites, and suggest an important role for Ih in controlling dendritic excitability and epileptogenesis.
157.	CA1 pyramidal neuron: effects of R213Q and R312W Kv7.2 mutations (Miceli et al. 2013)
		NEURON mod files from the paper: Miceli et al, Genotype–phenotype correlations in neonatal epilepsies caused by mutations in the voltage sensor of Kv7.2 potassium channel subunits, PNAS 2013 Feb 25. [Epub ahead of print] In this paper, functional studies revealed that in homomeric or heteromeric configuration with KV7.2 and/or KV7.3 subunits, R213W and R213Q mutations markedly destabilized the open state, causing a dramatic decrease in channel voltage sensitivity. Modeling these channels in CA1 hippocampal pyramidal cells revealed that both mutations increased cell firing frequency, with the R213Q mutation prompting more dramatic functional changes compared with the R213W mutation.
158.	CA1 pyramidal neuron: functional significance of axonal Kv7 channels (Shah et al. 2008)
		The model used in this paper confirmed the experimental findings suggesting that axonal Kv7 channels are critically and uniquely required for determining the inherent spontaneous firing of hippocampal CA1 pyramids, independently of alterations in synaptic activity. The model predicts that the axonal Kv7 density could be 3-5 times that at the soma.
159.	CA1 pyramidal neuron: h channel-dependent deficit of theta oscill. resonance (Marcelin et al. 2008)
		This model was used to confirm and support experimental data suggesting that the neuronal/circuitry changes associated with temporal lobe epilepsy, including Ih-dependent inductive mechanisms, can disrupt hippocampal theta function.
160.	CA1 pyramidal neuron: Ih current (Migliore et al. 2012)
		NEURON files from the paper: Migliore M, Migliore R (2012) Know Your Current Ih: Interaction with a Shunting Current Explains the Puzzling Effects of Its Pharmacological or Pathological Modulations. PLoS ONE 7(5): e36867. doi:10.1371/journal.pone.0036867. Experimental findings on the effects of Ih current modulation, which is particularly involved in epilepsy, appear to be inconsistent. In the paper, using a realistic model we show how and why a shunting current, such as that carried by TASK-like channels, dependent on the Ih peak conductance is able to explain virtually all experimental findings on Ih up- or down-regulation by modulators or pathological conditions.
161.	CA1 pyramidal neuron: integration of subthreshold inputs from PP and SC (Migliore 2003)
		The model shows how the experimentally observed increase in the dendritic density of Ih and IA could have a major role in constraining the temporal integration window for the main CA1 synaptic inputs.
162.	CA1 pyramidal neuron: nonlinear a5-GABAAR controls synaptic NMDAR activation (Schulz et al 2018)
		The study shows that IPSCs mediated by a5-subunit containing GABAA receptors are strongly outward-rectifying generating 4-fold larger conductances above -50?mV than at rest. Experiments and modeling show that synaptic activation of these receptors can very effectively control voltage-dependent NMDA-receptor activation in a spatiotemporally controlled manner in fine dendrites of CA1 pyramidal cells. The files contain the NEURON code for Fig.8, Fig.S8 and Fig.S9 of the paper. The model is based on the model published by Bloss et al., 2017. Physiological properties of GABA synapses were modified as determined by optogenetic activation of inputs during voltage-clamp recordings in Schulz et al. 2018. Other changes include stochastic synaptic release and short-term synaptic plasticity. All changes of mechanisms and parameters are detailed in the Methods of the paper. Simulation can be run by starting start_simulation.hoc after running mknrndll. The files that model the individual figures have to be uncommented in start_simulation.hoc beforehand.
163.	CA1 pyramidal neuron: Persistent Na current mediates steep synaptic amplification (Hsu et al 2018)
		This paper shows that persistent sodium current critically contributes to the subthreshold nonlinear dynamics of CA1 pyramidal neurons and promotes rapidly reversible conversion between place-cell and silent-cell in the hippocampus. A simple model built with realistic axo-somatic voltage-gated sodium channels in CA1 (Carter et al., 2012; Neuron 75, 1081–1093) demonstrates that the biophysics of persistent sodium current is sufficient to explain the synaptic amplification effects. A full model built previously (Grienberger et al., 2017; Nature Neuroscience, 20(3): 417–426) with detailed morphology, ion channel types and biophysical properties of CA1 place cells naturally reproduces the steep voltage dependence of synaptic responses.
164.	CA1 pyramidal neuron: rebound spiking (Ascoli et al.2010)
		The model demonstrates that CA1 pyramidal neurons support rebound spikes mediated by hyperpolarization-activated inward current (Ih), and normally masked by A-type potassium channels (KA). Partial KA reduction confined to one or few branches of the apical tuft may be sufficient to elicit a local spike following a train of synaptic inhibition. These data suggest that the plastic regulation of KA can provide a dynamic switch to unmask post-inhibitory spiking in CA1 pyramidal neurons, further increasing the signal processing power of the CA1 synaptic microcircuitry.
165.	Ca1 pyramidal neuron: reduction model (Marasco et al. 2012)
		"... Here we introduce a new, automatic and fast method to map realistic neurons into equivalent reduced models running up to >40 times faster while maintaining a very high accuracy of the membrane potential dynamics during synaptic inputs, and a direct link with experimental observables. The mapping of arbitrary sets of synaptic inputs, without additional fine tuning, would also allow the convenient and efficient implementation of a new generation of large-scale simulations of brain regions reproducing the biological variability observed in real neurons, with unprecedented advances to understand higher brain functions."
166.	CA1 pyramidal neuron: schizophrenic behavior (Migliore et al. 2011)
		NEURON files from the paper: A modeling study suggesting how a reduction in the context-dependent input on CA1 pyramidal neurons could generate schizophrenic behavior. by M. Migliore, I. De Blasi, D. Tegolo, R. Migliore, Neural Networks,(2011), doi:10.1016/j.neunet.2011.01.001. Starting from the experimentally supported assumption on hippocampal neurons we explore an experimentally testable prediction at the single neuron level. The model shows how and to what extent a pathological hypofunction of a contextdependent distal input on a CA1 neuron can generate hallucinations by altering the normal recall of objects on which the neuron has been previously tuned. The results suggest that a change in the context during the recall phase may cause an occasional but very significant change in the set of active dendrites used for features recognition, leading to a distorted perception of objects.
167.	CA1 pyramidal neuron: signal propagation in oblique dendrites (Migliore et al 2005)
		NEURON mod files from the paper: M. Migliore, M. Ferrante, GA Ascoli (2005). The model shows how the back- and forward propagation of action potentials in the oblique dendrites of CA1 neurons could be modulated by local properties such as morphology or active conductances.
168.	CA1 Pyramidal Neuron: slow Na+ inactivation (Migliore 1996)
		Model files from the paper: M. Migliore, Modeling the attenuation and failure of action potentials in the dendrites of hippocampal neurons, Biophys. J. 71:2394-403 (1996). Please see the below readme file for installation and use instructions. Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model.
169.	CA1 pyramidal neuron: synaptic plasticity during theta cycles (Saudargiene et al. 2015)
		This NEURON code implements a microcircuit of CA1 pyramidal neuron and consists of a detailed model of CA1 pyramidal cell and four types of inhibitory interneurons (basket, bistratified, axoaxonic and oriens lacunosum-moleculare cells). Synaptic plasticity during theta cycles at a synapse in a single spine on the stratum radiatum dendrite of the CA1 pyramidal cell is modeled using a phenomenological model of synaptic plasticity (Graupner and Brunel, PNAS 109(20):3991-3996, 2012). The code is adapted from the Poirazi CA1 pyramidal cell (ModelDB accession number 20212) and the Cutsuridis microcircuit model (ModelDB accession number 123815)
170.	CA1 pyramidal neuron: Synaptic Scaling (Magee, Cook 2000)
		Jeffrey Magee and Erik Cook found evidence in experiments and modeling that support the hypothesis that an increase in synaptic conductance for synapses at larger distances from the soma is responsible for reducing the location dependence (relative to the soma) of synapses.
171.	CA1 pyramidal neuron: synaptically-induced bAP predicts synapse location (Sterratt et al. 2012)
		This is an adaptation of Poirazi et al.'s (2003) CA1 model that is used to measure BAP-induced voltage and calcium signals in spines after simulated Schaffer collateral synapse stimulation. In the model, the peak calcium concentration is highly correlated with soma-synapse distance under a number of physiologically-realistic suprathreshold stimulation regimes and for a range of dendritic morphologies. There are also simulations demonstrating that peak calcium can be used to set up a synaptic democracy in a homeostatic manner, whereby synapses regulate their synaptic strength on the basis of the difference between peak calcium and a uniform target value.
172.	CA1 pyramidal neurons: binding properties and the magical number 7 (Migliore et al. 2008)
		NEURON files from the paper: Single neuron binding properties and the magical number 7, by M. Migliore, G. Novara, D. Tegolo, Hippocampus, in press (2008). In an extensive series of simulations with realistic morphologies and active properties, we demonstrate how n radial (oblique) dendrites of these neurons may be used to bind n inputs to generate an output signal. The results suggest a possible neural code as the most effective n-ple of dendrites that can be used for short-term memory recollection of persons, objects, or places. Our analysis predicts a straightforward physiological explanation for the observed puzzling limit of about 7 short-term memory items that can be stored by humans.
173.	CA1 pyramidal neurons: effect of external electric field from power lines (Cavarretta et al. 2014)
		The paper discusses the effects induced by an electric field at power lines frequency.
174.	CA1 pyramidal neurons: effects of a Kv7.2 mutation (Miceli et al. 2009)
		NEURON mod files from the paper: Miceli et al, Neutralization of a unique, negatively-charged residue in the voltage sensor of K(V)7.2 subunits in a sporadic case of benign familial neonatal seizures, Neurobiol Dis., in press (2009). In this paper, the model revealed that the gating changes introduced by a mutation in K(v)7.2 genes encoding for the neuronal KM current in a case of benign familial neonatal seizures, increased cell firing frequency, thereby triggering the neuronal hyperexcitability which underlies the observed neonatal epileptic condition.
175.	CA1 pyramidal neurons: effects of Alzheimer (Culmone and Migliore 2012)
		The model predicts possible therapeutic treatments of Alzheimers's Disease in terms of pharmacological manipulations of channels' kinetic and activation properties. The results suggest how and which mechanism can be targeted by a drug to restore the original firing conditions. The simulations reproduce somatic membrane potential in control conditions, when 90% of membrane is affected by AD (Fig.4A of the paper), and after treatment (Fig.4B of the paper).
176.	CA1 pyramidal neurons: effects of Kv7 (M-) channels on synaptic integration (Shah et al. 2011)
		NEURON mod files from the paper: Shah et al., 2011. In this study, using a combination of electrophysiology and computational modelling, we show that these channels selectively influence peri-somatic but not dendritic post-synaptic excitatory synaptic potential (EPSP) integration in CA1 pyramidal cells. This may be important for their relative contributions to physiological processes such as synaptic plasticity as well as patho-physiological conditions such as epilepsy.
177.	CA1 stratum radiatum interneuron multicompartmental model (Katona et al. 2011)
		The model examines dendritic NMDA-spike generation and propagation in the dendrites of CA1 stratum radiatum interneurons. It contains NMDA-channels in a clustered pattern on a dendrite and K-channels. The simulation shows the whole NMDA spike and the rising phase of the traces in separate windows.
178.	CA3 hippocampal pyramidal neuron with voltage-clamp intrinsic conductance data (Traub et al 1991)
		This is a third-party implementation of the model from Traub et al 1991; as of 2021, Google Scholar reports about 780 citation articles. This model was one of the first biophysical models of a hippocampal pyramidal neuron with realistic conductances and the conductance equations have been used as a starting point for many models since, particularly those examining calcium dynamics and bursting.
179.	CA3 Network Model of Epileptic Activity (Sanjay et. al, 2015)
		This computational study investigates how a CA3 neuronal network consisting of pyramidal cells, basket cells and OLM interneurons becomes epileptic when dendritic inhibition to pyramidal cells is impaired due to the dysfunction of OLM interneurons. After standardizing the baseline activity (theta-modulated gamma oscillations), systematic changes are made in the connectivities between the neurons, as a result of step-wise impairment of dendritic inhibition.
180.	CA3 pyramidal cell: rhythmogenesis in a reduced Traub model (Pinsky, Rinzel 1994)
		Fig. 2A and 3 are reproduced in this simulation of Pinsky PF, Rinzel J (1994).
181.	CA3 pyramidal neuron (Lazarewicz et al 2002)
		The model shows how using a CA1-like distribution of active dendritic conductances in a CA3 morphology results in dendritic initiation of spikes during a burst.
182.	CA3 Pyramidal Neuron (Migliore et al 1995)
		Model files from the paper: M. Migliore, E. Cook, D.B. Jaffe, D.A. Turner and D. Johnston, Computer simulations of morphologically reconstructed CA3 hippocampal neurons, J. Neurophysiol. 73, 1157-1168 (1995). Demonstrates how the same cell could be bursting or non bursting according to the Ca-independent conductance densities. Includes calculation of intracellular Calcium. Instructions are provided in the below README file. Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model.
183.	CA3 pyramidal neuron (Safiulina et al. 2010)
		In this review some of the recent work carried out in our laboratory concerning the functional role of GABAergic signalling at immature mossy fibres (MF)-CA3 principal cell synapses has been highlighted. To compare the relative strength of CA3 pyramidal cell output in relation to their MF glutamatergic or GABAergic inputs in postnatal development, a realistic model was constructed taking into account the different biophysical properties of these synapses.
184.	CA3 pyramidal neuron: firing properties (Hemond et al. 2008)
		In the paper, this model was used to identify how relative differences in K+ conductances, specifically KC, KM, & KD, between cells contribute to the different characteristics of the three types of firing patterns observed experimentally.
185.	Ca3 pyramidal neuron: membrane response near rest (Hemond et al. 2009)
		In this paper, the model was used to show how the temporal summation of excitatory inputs in CA3 pyramidal neurons was affected by the presence of Ih in the dendrites in a frequency- and distance-dependent fashion.
186.	CA3 pyramidal neurons: Kv1.2 mediates modulation of cortical inputs (Hyun et al., 2015)
		This model simulates the contribution of dendritic Na+ and D-type K+ channels to EPSPs at three different locations of apical dendrites, which mimicking innervation sites of mossy fibers (MF), recurrent fibers (AC), and perforant pathway (PP).
187.	Calcium and potassium currents of olfactory bulb juxtaglomerular cells (Masurkar and Chen 2011)
		Inward and outward currents of the olfactory bulb juxtaglomerular cells are characterized in the experiments and modeling in these two Masurkar and Chen 2011 papers.
188.	Calcium dynamics depend on dendritic diameters (Anwar et al. 2014)
		"... in dendrites there is a strong contribution of morphology because the peak calcium levels are strongly determined by the surface to volume ratio (SVR) of each branch, which is inversely related to branch diameter. In this study we explore the predicted variance of dendritic calcium concentrations due to local changes in dendrite diameter and how this is affected by the modeling approach used. We investigate this in a model of dendritic calcium spiking in different reconstructions of cerebellar Purkinje cells and in morphological analysis of neocortical and hippocampal pyramidal neurons. ..."
189.	Calcium response prediction in the striatal spines depending on input timing (Nakano et al. 2013)
		We construct an electric compartment model of the striatal medium spiny neuron with a realistic morphology and predict the calcium responses in the synaptic spines with variable timings of the glutamatergic and dopaminergic inputs and the postsynaptic action potentials. The model was validated by reproducing the responses to current inputs and could predict the electric and calcium responses to glutamatergic inputs and back-propagating action potential in the proximal and distal synaptic spines during up and down states.
190.	Calcium spikes in basal dendrites (Kampa and Stuart 2006)
		This model was published in Kampa & Stuart (2006) J Neurosci 26(28):7424-32. The simulation creates two plots showing voltage and calcium changes in basal dendrites of layer 5 pyramidal neurons during action potential backpropagation. created by B. Kampa (2006)
191.	Calcium waves and mGluR-dependent synaptic plasticity in CA1 pyr. neurons (Ashhad & Narayanan 2013)
		A morphologically realistic, conductance-based model equipped with kinetic schemes that govern several calcium signalling modules and pathways in CA1 pyramidal neurons
192.	Calcium waves in neuroblastoma cells (Fink et al. 2000)
		Uses a model of IP3-mediated release of Ca from endoplasmic reticulum (ER) to study how initiation and propagation of Ca waves are affected by cell geometry, spatial distributions of ER and IP3 generation, and diffusion of Ca and mobile buffer.
193.	Calculating the consequences of left-shifted Nav channel activity in sick cells (Joos et al 2018)
		"Two features common to diverse sick excitable cells are “leaky” Nav channels and bleb damage-damaged membranes. The bleb damage, we have argued, causes a channel kinetics based “leakiness.” Recombinant (node of Ranvier type) Nav1.6 channels voltage-clamped in mechanically-blebbed cell-attached patches undergo a damage intensity dependent kinetic change. Specifically, they experience a coupled hyperpolarizing (left) shift of the activation and inactivation processes. The biophysical observations on Nav1.6 currents formed the basis of Nav-Coupled Left Shift (Nav-CLS) theory. Node of Ranvier excitability can be modeled with Nav-CLS imposed at varying LS intensities and with varying fractions of total nodal membrane affected. Mild damage from which sick excitable cells might recover is of most interest pathologically. Accordingly, Na+/K+ ATPase (pump) activity was included in the modeling. As we described more fully in our other recent reviews, Nav-CLS in nodes with pumps proves sufficient to predict many of the pathological excitability phenomena reported for sick excitable cells. ..."
194.	Carbon nanotubes as electrical interfaces to neurons (Giugliano et al. 2008)
		In the present NEURON model, we explore simple phenomenological models of the extracellular coupling, occurring at the neuron-metal microelectrode junction and (possibly) at the neuron-carbon nanotube junction.
195.	Cardiac action potentials and pacemaker activity of sinoatrial node (DiFrancesco & Noble 1985)
		"Equations have been developed to describe cardiac action potentials and pacemaker activity. The model takes account of extensive developments in experimental work ..."
196.	Cardiac Atrial Cell (Courtemanche et al 1998)
		Marc Courtemanche, Rafael J. Ramirez, and Stanley Nattel. Ionic mechanisms underlying human atrial action potential properties insights from a mathematical model Am J Physiol Heart Circ Physiol 1998 275: H301-H321. The implementation of this model in NEURON was contributed by Ingemar Jacobson.
197.	Cardiac sarcomere dynamics (Negroni and Lascano 1996)
		"A muscle model establishing the link between cross-bridge dynamics and intracellular Ca2+ kinetics was assessed by simulation of experiments performed in isolated cardiac muscle. The model is composed by the series arrangement of muscle units formed by inextensible thick and thin filaments in parallel with an elastic element. Attached cross-bridges act as independent force generators whose force is linearly related to the elongation of their elastic structure. Ca2+ kinetics is described by a four-state system of sites on the thin filament associated with troponin C: sites with free troponin C (T), sites with Ca2+ bound to troponin C (TCa); sites with Ca2+ bound to troponin C and attached cross-bridges (TCa*); and sites with troponin C not associated with Ca2+ and attached cross-bridges (T*). The intracellular Ca2+ concentration ([Ca2+]) is controlled solely by the sarcoplasmic reticulum through an inflow function and a saturated outflow pump function. ..."
198.	Cell splitting in neural networks extends strong scaling (Hines et al. 2008)
		Neuron tree topology equations can be split into two subtrees and solved on different processors with no change in accuracy, stability, or computational effort; communication costs involve only sending and receiving two double precision values by each subtree at each time step. Application of the cell splitting method to two published network models exhibits good runtime scaling on twice as many processors as could be effectively used with whole-cell balancing.
199.	Cell-type specific integration of feedforward and feedback synaptic inputs (Ridner et al, 2022)
		Simple compartmental model is used to explore and predict channel mechanisms that underlie differences in non-integration of synaptic inputs to posterior parietal cortex pyramidal subtypes, namely regular spiking cell and intrinsically bursting cell.
200.	Cellular and Synaptic Mechanisms Differentiate Mitral & Superficial Tufted Cells (Jones et al 2020)
		"To evaluate how... different electrophysiological aspects contributed to spiking of the output MCs and sTCs, we used computational modeling. By exchanging the different cell properties in our modeled MCs and sTCs, we could evaluate each property's contribution to spiking differences between these cell types. This analysis suggested that the higher sensitivity of spiking in sTCs vs. MCs reflected both their larger monosynaptic OSN signal as well as their higher input resistance, while their smaller prolonged currents had a modest opposing effect. Taken together, our results indicate that both synaptic and intrinsic cellular features contribute to the production of parallel output channels in the olfactory bulb."
201.	Central Nervous System tadpole model in Matlab and NEURON-Python (Ferrario et al, 2021)
		This is the source code for three compuational models used for generating connectivity and swimming dynamics of spinal cord and hindbrain neurons in the Xenopus tadpoles using biological data. The model reproduces the initiation, continuation, termination and accelaration of forward swimming.
202.	Cerebellar cortex oscil. robustness from Golgi cell gap jncs (Simoes de Souza and De Schutter 2011)
		" ... Previous one-dimensional network modeling of the cerebellar granular layer has been successfully linked with a range of cerebellar cortex oscillations observed in vivo. However, the recent discovery of gap junctions between Golgi cells (GoCs), which may cause oscillations by themselves, has raised the question of how gap-junction coupling affects GoC and granular-layer oscillations. To investigate this question, we developed a novel two-dimensional computational model of the GoC-granule cell (GC) circuit with and without gap junctions between GoCs. ..."
203.	Cerebellar Golgi cell (Solinas et al. 2007a, 2007b)
		"... Our results suggest that a complex complement of ionic mechanisms is needed to fine-tune separate aspects of the neuronal response dynamics. Simulations also suggest that the Golgi cell may exploit these mechanisms to obtain a fine regulation of timing of incoming mossy fiber responses and granular layer circuit oscillation and bursting."
204.	Cerebellar Golgi cells, dendritic processing, and synaptic plasticity (Masoli et al 2020)
		The Golgi cells are the main inhibitory interneurons of the cerebellar granular layer. To study the mechanisms through which these neurons integrate complex input patterns, a new set of models were developed using the latest experimental information and a genetic algorithm approach to fit the maximum ionic channel conductances. The models faithfully reproduced a rich pattern of electrophysiological and pharmacological properties and predicted the operating mechanisms of these neurons.
205.	Cerebellar granule cell (Masoli et al 2020)
		"The cerebellar granule cells (GrCs) are classically described as a homogeneous neuronal population discharging regularly without adaptation. We show that GrCs in fact generate diverse response patterns to current injection and synaptic activation, ranging from adaptation to acceleration of firing. Adaptation was predicted by parameter optimization in detailed computational models based on available knowledge on GrC ionic channels. The models also predicted that acceleration required additional mechanisms. We found that yet unrecognized TRPM4 currents specifically accounted for firing acceleration and that adapting GrCs outperformed accelerating GrCs in transmitting high-frequency mossy fiber (MF) bursts over a background discharge. This implied that GrC subtypes identified by their electroresponsiveness corresponded to specific neurotransmitter release probability values. Simulations showed that fine-tuning of pre- and post-synaptic parameters generated effective MF-GrC transmission channels, which could enrich the processing of input spike patterns and enhance spatio-temporal recoding at the cerebellar input stage."
206.	Cerebellar nuclear neuron (Sudhakar et al., 2015)
		"... In this modeling study, we investigate different forms of Purkinje neuron simple spike pause synchrony and its influence on candidate coding strategies in the cerebellar nuclei. That is, we investigate how different alignments of synchronous pauses in synthetic Purkinje neuron spike trains affect either time-locking or rate-changes in the downstream nuclei. We find that Purkinje neuron synchrony is mainly represented by changes in the firing rate of cerebellar nuclei neurons. ..."
207.	Cerebellar purkinje cell: interacting Kv3 and Na currents influence firing (Akemann, Knopfel 2006)
		Purkinje neurons spontaneously generate action potentials in the absence of synaptic drive and thereby exert a tonic, yet plastic, input to their target cells in the deep cerebellar nuclei. Purkinje neurons express two ionic currents with biophysical properties that are specialized for high-frequency firing: resurgent sodium currents and potassium currents mediated by Kv3.3. Numerical simulations indicated that Kv3.3 increases the spontaneous firing rate via cooperation with resurgent sodium currents. We conclude that the rate of spontaneous action potential firing of Purkinje neurons is controlled by the interaction of Kv3.3 potassium currents and resurgent sodium currents. See paper for more and details.
208.	Cerebellar purkinje cell: K and Ca channels regulate APs (Miyasho et al 2001)
		We adopted De Schutter and Bower's model as the starting point, then modified the descriptions of several ion channels, such as the P-type Ca channel and the delayed rectifier K channel, and added class-E Ca channels and D-type K channels to the model. Our new model reproduces most of our experimental results and supports the conclusions of our experimental study that class-E Ca channels and D-type K channels are present and functioning in the dendrites of Purkinje neurons.
209.	Cerebellar Purkinje Cell: resurgent Na current and high frequency firing (Khaliq et al 2003)
		These mod files supplied by Dr Raman are for the below two references. ... we modeled action potential firing by simulating eight currents directly recorded from Purkinje cells in both wild-type and (mutant) med mice. Regular, high-frequency firing was slowed in med Purkinje neurons. In addition to disrupted sodium currents, med neurons had small but significant changes in potassium and leak currents. Simulations indicated that these modified non-sodium currents could not account for the reduced excitability of med cells but instead slightly facilitated spiking. The loss of NaV1.6-specific kinetics, however, slowed simulated spontaneous activity. Together, the data suggest that across a range of conditions, sodium currents with a resurgent component promote and accelerate firing. See papers for more and details.
210.	Cerebellum granule cell FHF (Dover et al. 2016)
		"Neurons in vertebrate central nervous systems initiate and conduct sodium action potentials in distinct subcellular compartments that differ architecturally and electrically. Here, we report several unanticipated passive and active properties of the cerebellar granule cell's unmyelinated axon. Whereas spike initiation at the axon initial segment relies on sodium channel (Nav)-associated fibroblast growth factor homologous factor (FHF) proteins to delay Nav inactivation, distal axonal Navs show little FHF association or FHF requirement for high-frequency transmission, velocity and waveforms of conducting action potentials. ...'
211.	Cerebellum Purkinje cell: dendritic ion channels activated by climbing fibre (Ait Ouares et al 2019)
		"In cerebellar Purkinje neuron (PN) dendrites, the transient depolarisation associated with a climbing fibre (CF) EPSP activates voltage-gated Ca2+ channels (VGCCs), voltage-gated K+ channels (VGKCs) and Ca2+ activated SK and BK K+ channels. The resulting membrane potential (Vm) and Ca2+ transients play a fundamental role in dendritic integration and synaptic plasticity of parallel fibre inputs. Here we report a detailed investigation of the kinetics of dendritic Ca2+ and K+ channels activated by CF-EPSPs, based on optical measurements of Vm and Ca2+ transients and on a single-compartment NEURON model reproducing experimental data. ... "
212.	Changes of ionic concentrations during seizure transitions (Gentiletti et al. 2016)
		"... In order to investigate the respective roles of synaptic interactions and nonsynaptic mechanisms in seizure transitions, we developed a computational model of hippocampal cells, involving the extracellular space, realistic dynamics of Na+, K+, Ca2+ and Cl - ions, glial uptake and extracellular diffusion mechanisms. We show that the network behavior with fixed ionic concentrations may be quite different from the neurons’ behavior when more detailed modeling of ionic dynamics is included. In particular, we show that in the extended model strong discharge of inhibitory interneurons may result in long lasting accumulation of extracellular K+, which sustains the depolarization of the principal cells and causes their pathological discharges. ..."
213.	Channel density variability among CA1 neurons (Migliore et al. 2018)
		The peak conductance of many ion channel types measured in any given animal is highly variable across neurons, both within and between neuronal populations. The current view is that this occurs because a neuron needs to adapt its intrinsic electrophysiological properties either to maintain the same operative range in the presence of abnormal inputs or to compensate for the effects of pathological conditions. Limited experimental and modeling evidence suggests this might be implemented via the correlation and/or degeneracy in the function of multiple types of conductances. To study this mechanism in hippocampal CA1 neurons and interneurons, we systematically generated a set of morphologically and biophysically accurate models. We then analyzed the ensembles of peak conductance obtained for each model neuron. The results suggest that the set of conductances expressed in the various neuron types may be divided into two groups: one group is responsible for the major characteristics of the firing behavior in each population and the other more involved with degeneracy. These models provide experimentally testable predictions on the combination and relative proportion of the different conductance types that should be present in hippocampal CA1 pyramidal cells and interneurons.
214.	Chirp stimulus responses in a morphologically realistic model (Narayanan and Johnston, 2007)
		...we built a multicompartmental model with a morphologically realistic three-dimensional reconstruction of a CA1 pyramidal neuron. The only active conductance we added to the model was the h conductance. ... We conclude that experimentally observed gradient in density of h channels could theoretically account for experimentally observed gradient in resonance properties (Narayanan and Johnston, 2007).
215.	Circadian rhythmicity shapes astrocyte morphology and neuronal function in CA1 (McCauley et al 2020)
		Most animal species operate according to a 24-hour period set by the suprachiasmatic nucleus (SCN) of the hypothalamus. The rhythmic activity of the SCN modulates hippocampal-dependent memory, but the molecular and cellular mechanisms that account for this effect remain largely unknown. In McCauley et al. 2020 [1], we identify cell-type specific structural and functional changes that occur with circadian rhythmicity in neurons and astrocytes in hippocampal area CA1. Pyramidal neurons change the surface expression of NMDA receptors. Astrocytes change their proximity clustered excitatory synaptic inputs, ultimately shaping hippocampal-dependent learning in vivo. We identify to synapses. Together, these phenomena alter glutamate clearance, receptor activation and integration of temporally corticosterone as a key contributor to changes in synaptic strength. These findings highlight important mechanisms through which neurons and astrocytes modify the molecular composition and structure of the synaptic environment, contribute to the local storage of information in the hippocampus and alter the temporal dynamics of cognitive processing. [1] "Circadian modulation of neurons and astrocytes controls synaptic plasticity in hippocampal area CA1" by J.P. McCauley, M.A. Petroccione, L.Y. D’Brant, G.C. Todd, N. Affinnih, J.J. Wisnoski, S. Zahid, S. Shree, A.A. Sousa, R.M. De Guzman, R. Migliore, A. Brazhe, R.D. Leapman, A. Khmaladze, A. Semyanov, D.G. Zuloaga, M. Migliore and A. Scimemi. Cell Reports (2020), https://doi.org/10.1016/j.celrep.2020.108255
216.	Cl- homeostasis in immature hippocampal CA3 neurons (Kolbaev et al 2020)
		Model used for the revision of the manuscript. Insertion of a passive Cl- flux and an active Cl-accumulation. Parameters adapted to match the properties of [Cl-]i determined in immature rat CA3 neurons in-vitro.
217.	Classic model of the Tritonia Swim CPG (Getting, 1989)
		Classic model developed by Petter Getting of the 3-cell core CPG (DSI, C2, and VSI-B) mediating escape swimming in Tritonia diomedea. Cells use a hybrid integrate-and-fire scheme pioneered by Peter Getting. Each model cell is reconstructed from extensive physiological measurements to precisely mimic I-F curves, synaptic waveforms, and functional connectivity. **However, continued physiological measurements show that Getting may have inadvertently incorporated modulatory and or polysynaptic effects -- the properties of this model do *not* match physiological measurements in rested preparations.** This simulation reconstructs the Getting model as reported in: Getting (1989) 'Reconstruction of small neural networks' In Methods in Neural Modeling, 1st ed, p. 171-196. See also, an earlier version of this model reported in Getting (1983). Every attempt has been made to replicate the 1989 model as precisely as possible.
218.	CN bushy, stellate neurons (Rothman, Manis 2003)
		Using kinetic data from three different K+ currents in acutely isolated neurons, a single electrical compartment model representing the soma of a ventral cochlear nucleus (VCN) neuron was created. The K+ currents include a fast transient current (IA), a slow-inactivating low-threshold current (ILT), and a noninactivating high-threshold current (IHT). The model also includes a fast-inactivating Na+ current, a hyperpolarization-activated cation current (Ih), and 1-50 auditory nerve synapses. With this model, the role IA, ILT, and IHT play in shaping the discharge patterns of VCN cells is explored. Simulation results indicate these currents have specific roles in shaping the firing patterns of stellate and bushy CN cells. (see readme.txt and the papers, esp 2003c, for details). Any questions regarding these implementations should be directed to: pmanis@med.unc.edu 2 April 2004 Paul B Manis, Ph.D.
219.	CN Octopus Cell: Ih current (Bal, Oertel 2000)
		NEURON mod files for the Ih current from the paper R. Bal and D. Oertel Hyperpolarization-Activated, Mixed-Cation Current (Ih) in Octopus Cells of the Mammalian Cochlear Nucleus, J. Neurophysiol. 84, 806-817 (2000). Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model.
220.	CN pyramidal fusiform cell (Kanold, Manis 2001)
		Pyramidal cells in the dorsal cochlear nucleus (DCN) show three characteristic discharge patterns in response tones: pauser, buildup, and regular firing. Experimental evidence suggests that a rapidly inactivating K+ current (I(KIF)) plays a critical role in generating these discharge patterns. To explore the role of I(KIF), we used a computational model based on the biophysical data. The model replicated the dependence of the discharge pattern on the magnitude and duration of hyperpolarizing prepulses, and I(KIF) was necessary to convey this dependence. Experimentally, half-inactivation voltage and kinetics of I(KIF) show wide variability. Varying these parameters in the model ... suggests that pyramidal cells can adjust their sensitivity to different temporal patterns of inhibition and excitation by modulating the kinetics of I(KIF). Overall, I(KIF) is a critical conductance controlling the excitability of DCN pyramidal cells. (See readme.txt and paper for details). Any questions regarding these implementations should be directed to: pmanis@med.unc.edu 2 April 2004 Paul B Manis, Ph.D.
221.	Coincidence detection in avian brainstem (Simon et al 1999)
		A detailed biophysical model of coincidence detector neurons in the nucleus laminaris (auditory brainstem) which are purported to detect interaural time differences (ITDs) from Simon et al 1999.
222.	Coincident glutamatergic depolarization effects on Cl- dynamics (Lombardi et al, 2021)
		"... we used compartmental biophysical models of Cl- dynamics simulating either a simple ball-and-stick topology or a reconstructed CA3 neuron. These computational experiments demonstrated that glutamatergic co-stimulation enhances GABA receptor-mediated Cl- influx at low and attenuates or reverses the Cl- efflux at high initial [Cl-]i. The size of glutamatergic influence on GABAergic Cl--fluxes depends on the conductance, decay kinetics, and localization of glutamatergic inputs. Surprisingly, the glutamatergic shift in GABAergic Cl--fluxes is invariant to latencies between GABAergic and glutamatergic inputs over a substantial interval..."
223.	Coincident signals in Olfactory Bulb Granule Cell spines (Aghvami et al 2019)
		"In the mammalian olfactory bulb, the inhibitory axonless granule cells (GCs) feature reciprocal synapses that interconnect them with the principal neurons of the bulb, mitral, and tufted cells. These synapses are located within large excitable spines that can generate local action potentials (APs) upon synaptic input (“spine spike”). Moreover, GCs can fire global APs that propagate throughout the dendrite. Strikingly, local postsynaptic Ca2+ entry summates mostly linearly with Ca2+ entry due to coincident global APs generated by glomerular stimulation, although some underlying conductances should be inactivated. We investigated this phenomenon by constructing a compartmental GC model to simulate the pairing of local and global signals as a function of their temporal separation ?t. These simulations yield strongly sublinear summation of spine Ca2+ entry for the case of perfect coincidence ?t = 0 ms. ..."
224.	Comparison of DA-based Stochastic Algorithms (Pezo et al. 2014)
		" ... Here we review and test a set of the most recently published DA (Langevin-based Diffusion Approximation) implementations (Goldwyn et al., 2011; Linaro et al., 2011; Dangerfield et al., 2012; Orio and Soudry, 2012; Schmandt and Galán, 2012; Güler, 2013; Huang et al., 2013a), comparing all of them in a set of numerical simulations that asses numerical accuracy and computational efficiency on three different models: the original Hodgkin and Huxley model, a model with faster sodium channels, and a multi-compartmental model inspired in granular cells. ..."
225.	Compartmental model of a mitral cell (Popovic et al. 2005)
		Usage of a morphologically realistic compartmental model of a mitral cell and data obtained from whole-cell patch-clamp and voltage-imaging experiments in order to explore passive parameter space in which reported low EPSP attenuation is observed.
226.	Compartmentalization of GABAergic inhibition by dendritic spines (Chiu et al. 2013)
		A spiny dendrite model supports the hypothesis that only inhibitory inputs on spine heads, not shafts, compartmentalizes inhibition of calcium signals to spine heads as seen in paired inhibition with back-propagating action potential experiments on prefrontal cortex layer 2/3 pyramidal neurons in mouse (Chiu et al. 2013).
227.	Competition for AP initiation sites in a circuit controlling simple learning (Cruz et al. 2007)
		"The spatial and temporal patterns of action potential initiations were studied in a behaving leech preparation to determine the basis of increased firing that accompanies sensitization, a form of non-associative learning requiring the S-interneurons. ... The S-interneurons, one in each ganglion and linked by electrical synapses with both neighbors to form a chain, are interposed between sensory and motor neurons. ... the single site with the largest initiation rate, the S-cell in the stimulated segment, suppressed initiations in adjacent ganglia. Experiments showed this was both because (1) it received the earliest, greatest input and (2) the delayed synaptic input to the adjacent S-cells coincided with the action potential refractory period. A compartmental model of the S-cell and its inputs showed that a simple, intrinsic mechanism of inexcitability after each action potential may account for suppression of impulse initiations. Thus, a non-synaptic competition between neurons alters synaptic integration in the chain. In one mode, inputs to different sites sum independently, whereas in another, synaptic input to a single site precisely specifies the overall pattern of activity."
228.	Complex CA1-neuron to study AP initiation (Wimmer et al. 2010)
		Complex model of a pyramidal CA1-neuron, adapted from Royeck, M., et al. Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons. Journal of neurophysiology 100, 2361-2380 (2008). It contains a biophysically realistic morphology comprising 265 compartments (829 segments) and 15 different distributed Ca2+- and/or voltage-dependent conductances.
229.	Computational analysis of NN activity and spatial reach of sharp wave-ripples (Canakci et al 2017)
		Network oscillations of different frequencies, durations and amplitudes are hypothesized to coordinate information processing and transfer across brain areas. Among these oscillations, hippocampal sharp wave-ripple complexes (SPW-Rs) are one of the most prominent. SPW-Rs occurring in the hippocampus are suggested to play essential roles in memory consolidation as well as information transfer to the neocortex. To-date, most of the knowledge about SPW-Rs comes from experimental studies averaging responses from neuronal populations monitored by conventional microelectrodes. In this work, we investigate spatiotemporal characteristics of SPW-Rs and how microelectrode size and distance influence SPW-R recordings using a biophysical model of hippocampus. We also explore contributions from neuronal spikes and synaptic potentials to SPW-Rs based on two different types of network activity. Our study suggests that neuronal spikes from pyramidal cells contribute significantly to ripples while high amplitude sharp waves mainly arise from synaptic activity. Our simulations on spatial reach of SPW-Rs show that the amplitudes of sharp waves and ripples exhibit a steep decrease with distance from the network and this effect is more prominent for smaller area electrodes. Furthermore, the amplitude of the signal decreases strongly with increasing electrode surface area as a result of averaging. The relative decrease is more pronounced when the recording electrode is closer to the source of the activity. Through simulations of field potentials across a high-density microelectrode array, we demonstrate the importance of finding the ideal spatial resolution for capturing SPW-Rs with great sensitivity. Our work provides insights on contributions from spikes and synaptic potentials to SPW-Rs and describes the effect of measurement configuration on LFPs to guide experimental studies towards improved SPW-R recordings.
230.	Computational model of bladder small DRG neuron soma (Mandge & Manchanda 2018)
		Bladder small DRG neurons, which are putative nociceptors pivotal to urinary bladder function, express more than a dozen different ionic membrane mechanisms: ion channels, pumps and exchangers. Small-conductance Ca2+-activated K+ (SKCa) channels which were earlier thought to be gated solely by intracellular Ca2+ concentration ([Ca]i ) have recently been shown to exhibit inward rectification with respect to membrane potential. The effect of SKCa inward rectification on the excitability of these neurons is unknown. Furthermore, studies on the role of KCa channels in repetitive firing and their contributions to different types of afterhyperpolarization (AHP) in these neurons are lacking. In order to study these phenomena, we first constructed and validated a biophysically detailed single compartment model of bladder small DRG soma constrained by physiological data. The model includes twenty-two major known membrane mechanisms along with intracellular Ca2+ dynamics comprising Ca2+ diffusion, cytoplasmic buffering, and endoplasmic reticulum (ER) and mitochondrial mechanisms. Using modelling studies, we show that inward rectification of SKCa is an important parameter regulating neuronal repetitive firing and that its absence reduces action potential (AP) firing frequency. We also show that SKCa is more potent in reducing AP spiking than the large-conductance KCa channel (BKCa) in these neurons. Moreover, BKCa was found to contribute to the fast AHP (fAHP) and SKCa to the medium-duration (mAHP) and slow AHP (sAHP). We also report that the slow inactivating A-type K+ channel (slow KA) current in these neurons is composed of 2 components: an initial fast inactivating (time constant ~ 25-100 ms) and a slow inactivating (time constant ~ 200-800 ms) current. We discuss the implications of our findings, and how our detailed model can help further our understanding of the role of C-fibre afferents in the physiology of urinary bladder as well as in certain disorders.
231.	Computational model of cerebellar tDCS (Zhang et al., 2021)
		This archive contains models used in (Zhang et al. 2021) and simulates Purkinje cell, granule cell, and deep cerebellar neuron activities under cerebellar tDCS (transcranial direct current stimulation).
232.	Computational modeling of gephyrin-dependent inhibitory transsynaptic signaling (Lupascu et al 2020)
233.	Computational neuropharmacology of CA1 pyramidal neuron (Ferrante et al. 2008)
		In this paper, the model was used to show how neuroactive drugs targeting different neuronal mechanisms affect the signal integration in CA1 pyramidal neuron. Ferrante M, Blackwell KT, Migliore M, Ascoli GA (2008)
234.	Computational Surgery (Lytton et al. 2011)
		Figure 2 in Neocortical simulation for epilepsy surgery guidance: Localization and intervention, by William W. Lytton, Samuel A. Neymotin, Jason C. Wester, and Diego Contreras in Computational Surgery and Dual Training, Springer, 2011
235.	Computer model of clonazepam's effect in thalamic slice (Lytton 1997)
		Demonstration of the effect of a minor pharmacological synaptic change at the network level. Clonazepam, a benzodiazepine, enhances inhibition but is paradoxically useful for certain types of seizures. This simulation shows how inhibition of inhibitory cells (the RE cells) produces this counter-intuitive effect.
236.	Computer models of corticospinal neurons replicate in vitro dynamics (Neymotin et al. 2017)
		"Corticospinal neurons (SPI), thick-tufted pyramidal neurons in motor cortex layer 5B that project caudally via the medullary pyramids, display distinct class-specific electrophysiological properties in vitro: strong sag with hyperpolarization, lack of adaptation, and a nearly linear frequency-current (FI) relationship. We used our electrophysiological data to produce a pair of large archives of SPI neuron computer models in two model classes: 1. Detailed models with full reconstruction; 2. Simplified models with 6 compartments. We used a PRAXIS and an evolutionary multiobjective optimization (EMO) in sequence to determine ion channel conductances. ..."
237.	Computer simulations of neuron-glia interactions mediated by ion flux (Somjen et al. 2008)
		"... To examine the effect of glial K+ uptake, we used a model neuron equipped with Na+, K+, Ca2+ and Cl− conductances, ion pumps and ion exchangers, surrounded by interstitial space and glia. The glial membrane was either “passive”, incorporating only leak channels and an ion exchange pump, or it had rectifying K+ channels. We computed ion fluxes, concentration changes and osmotic volume changes. ... We conclude that voltage gated K+ currents can boost the effectiveness of the glial “potassium buffer” and that this buffer function is important even at moderate or low levels of excitation, but especially so in pathological states."
238.	Concentration dependent nonlinear K+ and Cl- leak current (Huang et al. 2015)
		"In their seminal works on squid giant axons, Hodgkin, and Huxley approximated the membrane leak current as Ohmic, i.e., linear, since in their preparation, sub-threshold current rectification due to the influence of ionic concentration is negligible. Most studies on mammalian neurons have made the same, largely untested, assumption. Here we show that the membrane time constant and input resistance of mammalian neurons (when other major voltage-sensitive and ligand-gated ionic currents are discounted) varies non-linearly with membrane voltage, following the prediction of a Goldman-Hodgkin-Katz-based passive membrane model. ..." (see paper for details and more).
239.	Conditions for synaptic specificity in maintenance phase of synaptic plasticity (Huertas et al, '22)
		Long-lasting effects on synaptic efficacies are associated with the sustained increase in concentration of specific proteins like PKM?. Assuming that the long-term maintenance of synaptic plasticity is accomplished by a molecular switch we perform simulations using the reaction-diffusion package in NEURON and analytical calculations to determine the limits of synapse specificity during maintenance.
240.	Conditions of dominant effectiveness of distal dendrites (Korogod, Kulagina 1998)
		The model illustrates and explains bistable spatial patterns of the current transfer effectiveness in the active dendrite with distributed (multiple) tonic excitatory, NMDA type, synaptic input.
241.	Conductance based model for short term plasticity at CA3-CA1 synapses (Mukunda & Narayanan 2017)
		We develop a new biophysically rooted, physiologically constrained conductance-based synaptic model to mechanistically account for short-term facilitation and depression, respectively through residual calcium and transmitter depletion kinetics. The model exhibits different synaptic filtering profiles upon changing certain parameters in the base model. We show degenercy in achieving similar plasticity profiles with different presynaptic parameters. Finally, by virtually knocking out certain conductances, we show the differential contribution of conductances.
242.	Conduction in uniform myelinated axons (Moore et al 1978)
		Examines the relative sensitivity of the velocity of impulse propagation to changes in nodal and internodal parameters.
243.	Constructed Tessellated Neuronal Geometries (CTNG) (McDougal et al. 2013)
		We present an algorithm to form watertight 3D surfaces consistent with the point-and-diameter based neuronal morphology descriptions widely used with spatial electrophysiology simulators. ... This (point-and-diameter) representation is well-suited for electrophysiology simulations, where the space constants are larger than geometric ambiguities. However, the simple interpretations used for pure electrophysiological simulation produce geometries unsuitable for multi-scale models that also involve three-dimensional reaction–diffusion, as such models have smaller space constants. ... Although one cannot exactly reproduce an original neuron's full shape from point-and-diameter data, our new constructive tessellated neuronal geometry (CTNG) algorithm uses constructive solid geometry to define a plausible reconstruction without gaps or cul-de-sacs. CTNG then uses “constructive cubes” to produce a watertight triangular mesh of the neuron surface, suitable for use in reaction–diffusion simulations. ..."
244.	Contrast invariance by LGN synaptic depression (Banitt et al. 2007)
		"Simple cells in layer 4 of the primary visual cortex of the cat show contrast-invariant orientation tuning, in which the amplitude of the peak response is proportional to the stimulus contrast but the width of the tuning curve hardly changes with contrast. This study uses a detailed model of spiny stellate cells (SSCs) from cat area 17 to explain this property. The model integrates our experimental data, including morphological and intrinsic membrane properties and the number and spatial distribution of four major synaptic input sources of the SSC: the dorsal lateral geniculate nucleus (dLGN) and three cortical sources. ... The model response is in close agreement with experimental results, in terms of both output spikes and membrane voltage (amplitude and fluctuations), with reasonable exceptions given that recurrent connections were not incorporated."
245.	Control of oscillations and spontaneous firing in dopamine neurons (Rumbell & Kozloski 2019)
		Model of Substantia Nigra pars Compacta Dopamine Neuron. 'Toy' morphology with 4 dendrites, one of which is the axon-bearing dendrite, with an axon branching from it. The axon is a short 'axon initial segment' compartment, followed by a longer 'axon'. 727 parameter sets for ion channel conductance and kinetic parameters were found using evolutionary optimization, all of which are viable candidates representing a plausible model of a SNc DA.
246.	Controlling KCa channels with different Ca2+ buffering models in Purkinje cell (Anwar et al. 2012)
		In this work, we compare the dynamics of different buffering models during generation of a dendritic Ca2+ spike in a single compartment model of a Purkinje cell dendrite. The Ca2+ buffering models used are 1) a single Ca2+ pool, 2) two Ca2+ pools respectively for the fast and slow transients, 3) a detailed calcium model with buffers, pump (Schmidt et al., 2003), and diffusion and 4) a calcium model with buffers, pump and diffusion compensation. The parameters of single pool and double pool are tuned, using Neurofitter (Van Geit et al., 2007), to approximate the behavior of detailed calcium dynamics over range of 0.5 µM to 8 µM of intracellular calcium. The diffusion compensation is modeled using a buffer-like mechanism called DCM. To use DCM robustly for different diameter compartments, its parameters are estimated, using Neurofitter (Van Geit et al., 2007), as a function of compartment diameter (0.8 µm-20 µm).
247.	Convergence regulates synchronization-dependent AP transfer in feedforward NNs (Sailamul et al 2017)
		We study how synchronization-dependent spike transfer can be affected by the structure of convergent feedforward wiring. We implemented computer simulations of model neural networks: a source and a target layer connected with different types of convergent wiring rules. In the Gaussian-Gaussian (GG) model, both the connection probability and the strength are given as Gaussian distribution as a function of spatial distance. In the Uniform-Constant (UC) and Uniform-Exponential (UE) models, the connection probability density is a uniform constant within a certain range, but the connection strength is set as a constant value or an exponentially decaying function, respectively. Then we examined how the spike transfer function is modulated under these conditions, while static or synchronized input patterns were introduced to simulate different levels of feedforward spike synchronization. We observed that the synchronization-dependent modulation of the transfer function appeared noticeably different for each convergence condition. The modulation of the spike transfer function was largest in the UC model, and smallest in the UE model. Our analysis showed that this difference was induced by the different spike weight distributions that was generated from convergent synapses in each model. Our results suggest that the structure of the feedforward convergence is a crucial factor for correlation-dependent spike control, thus must be considered important to understand the mechanism of information transfer in the brain.
248.	Cooling reverses pathological spontaneous firing caused by mild traumatic injury (Barlow et al 2018)
		"Mild traumatic injury can modify the key sodium (Na+) current underlying the excitability of neurons. It causes the activation and inactivation properties of this current to become shifted to more negative trans-membrane voltages. This so-called coupled left shift (CLS) leads to a chronic influx of Na+ into the cell that eventually causes spontaneous or “ectopic” firing along the axon, even in the absence of stimuli. The bifurcations underlying this enhanced excitability have been worked out in full ionic models of this effect. Here, we present computational evidence that increased temperature T can exacerbate this pathological state. Conversely, and perhaps of clinical relevance, mild cooling is shown to move the naturally quiescent cell further away from the threshold of ectopic behavior. ..."
249.	Correcting space clamp in dendrites (Schaefer et al. 2003 and 2007)
		In voltage-clamp experiments, incomplete space clamp distorts the recorded currents, rendering accurate analysis impossible. Here, we present a simple numerical algorithm that corrects such distortions. The method enabled accurate retrieval of the local densities, kinetics, and density gradients of somatic and dendritic channels. The correction method was applied to two-electrode voltage-clamp recordings of K currents from the apical dendrite of layer 5 neocortical pyramidal neurons. The generality and robustness of the algorithm make it a useful tool for voltage-clamp analysis of voltage-gated currents in structures of any morphology that is amenable to the voltage-clamp technique.
250.	Cortical Basal Ganglia Network Model during Closed-loop DBS (Fleming et al 2020)
		We developed a computational model of the cortical basal ganglia network to investigate closed-loop control of deep brain stimulation (DBS) for Parkinson’s disease (PD). The cortical basal ganglia network model incorporates the (i) the extracellular DBS electric field, (ii) antidromic and orthodromic activation of STN afferent fibers, (iii) the LFP detected at non-stimulating contacts on the DBS electrode and (iv) temporal variation of network beta-band activity within the thalamo-cortico-basal ganglia loop. The model facilitates investigation of clinically-viable closed-loop DBS control approaches, modulating either DBS amplitude or frequency, using an LFP derived measure of network beta-activity.
251.	Cortical feedback alters visual response properties of dLGN relay cells (Martínez-Cañada et al 2018)
		Network model that includes biophysically detailed, single-compartment and multicompartment neuron models of relay-cells and interneurons in the dLGN and a population of orientation-selective layer 6 simple cells, consisting of pyramidal cells (PY). We have considered two different arrangements of synaptic feedback from the ON and OFF zones in the visual cortex to the dLGN: phase-reversed (‘push-pull’) and phase-matched (‘push-push’), as well as different spatial extents of the corticothalamic projection pattern. This project is the result of a research work and its associated publication is: (Martínez-Cañada et al 2018). Installation instructions as well as the latest version can be found in the Github repository: https://github.com/CINPLA/biophysical_thalamocortical_system
252.	Cortical Layer 5b pyr. cell with [Na+]i mechanisms, from Hay et al 2011 (Zylbertal et al 2017)
		" ... Based on a large body of experimental recordings from both the soma and dendrites of L5b pyramidal cells in adult rats, we characterized key features of the somatic and dendritic firing and quantified their statistics. We used these features to constrain the density of a set of ion channels over the soma and dendritic surface via multi-objective optimization with an evolutionary algorithm, thus generating a set of detailed conductance-based models that faithfully replicate the back-propagating action potential activated Ca(2+) spike firing and the perisomatic firing response to current steps, as well as the experimental variability of the properties. Furthermore, we show a useful way to analyze model parameters with our sets of models, which enabled us to identify some of the mechanisms responsible for the dynamic properties of L5b pyramidal cells as well as mechanisms that are sensitive to morphological changes. ..."
253.	Cortical model with reinforcement learning drives realistic virtual arm (Dura-Bernal et al 2015)
		We developed a 3-layer sensorimotor cortical network of consisting of 704 spiking model-neurons, including excitatory, fast-spiking and low-threshold spiking interneurons. Neurons were interconnected with AMPA/NMDA, and GABAA synapses. We trained our model using spike-timing-dependent reinforcement learning to control a virtual musculoskeletal human arm, with realistic anatomical and biomechanical properties, to reach a target. Virtual arm position was used to simultaneously control a robot arm via a network interface.
254.	Cortical network model of posttraumatic epileptogenesis (Bush et al 1999)
		This simulation from Bush, Prince, and Miller 1999 shows the epileptiform response (Fig. 6C) to a brief single stimulation in a 500 cell network of multicompartment models, some of which have active dendrites. The results which I obtained under Redhat Linux is shown in result.gif. Original 1997 code from Paul Bush modified slightly by Bill Lytton to make it work with current version of NEURON (5.7.139). Thanks to Paul Bush and Ken Miller for making the code available.
255.	Cortical pyramidal neuron, phase response curve (Stiefel et al 2009)
		Three models of increasing complexity all showing a switch from type II (biphasic) to type I (monophasic) phase response curves with a cholinergic down-modulation of K+ conductances.
256.	Current Dipole in Laminar Neocortex (Lee et al. 2013)
		Laminar neocortical model in NEURON/Python, adapted from Jones et al 2009. https://bitbucket.org/jonescompneurolab/corticaldipole
257.	Current flow during PAP in squid axon at diameter change (Joyner et al 1980)
		From the paper abstract: An impulse ... sees an increased electrical load at regions of increasing diameter or at branch points with certain morphologies. We present here theoretical and experimental studies on the changes in membrane current and axial current associated with diameter changes. The theoretical studies were done with numerical solutions for cable equations that were generalized to include a varying diameter; the Hodgkin-Huxley equations were used to represent the membrane properties. ... As an action potential approaches a region of increased electrical load, the action potential amplitude and rate of rise decrease, but there is a marked increase in the magnitude of the inward sodium current. ... (See paper for more details.)
258.	Cycle skipping in ING Type 1 / Type 2 networks (Tikidji-Hamburyan & Canavier 2020)
		"All-to-all homogeneous networks of inhibitory neurons synchronize completely under the right conditions; however, many modeling studies have shown that biological levels of heterogeneity disrupt synchrony. Our fundamental scientific question is “how can neurons maintain partial synchrony in the presence of heterogeneity and noise?” A particular subset of strongly interconnected interneurons, the PV+ fast spiking basket neurons, are strongly implicated in gamma oscillations and in phase locking of nested gamma oscillations to theta. Their excitability type apparently varies between brain regions: in CA1 and the dentate gyrus they have type 1 excitability, meaning that they can fire arbitrarily slowly, whereas in the striatum and cortex they have type 2 excitability, meaning that there is a frequency threshold below which they cannot sustain repetitive firing. We constrained the models to study the effect of excitability type (more precisely bifurcation type) in isolation from all other factors. We use sparsely connected, heterogeneous, noisy networks with synaptic delays to show that synchronization properties, namely the resistance to suppression and the strength of theta phase to gamma amplitude coupling, are strongly dependent on the pairing of excitability type with the type of inhibition. ..."
259.	D2 dopamine receptor modulation of interneuronal activity (Maurice et al. 2004)
		"... Using a combination of electrophysiological, molecular, and computational approaches, the studies reported here show that D2 dopamine receptor modulation of Na+ currents underlying autonomous spiking contributes to a slowing of discharge rate, such as that seen in vivo. Four lines of evidence support this conclusion. ... Fourth, simulation of cholinergic interneuron pacemaking revealed that a modest increase in the entry of Na+ channels into the slow-inactivated state was sufficient to account for the slowing of pacemaker discharge. These studies establish a cellular mechanism linking dopamine and the reduction in striatal cholinergic interneuron activity seen in the initial stages of associative learning." See paper for more and details.
260.	DBS of a multi-compartment model of subthalamic nucleus projection neurons (Miocinovic et al. 2006)
		We built a comprehensive computational model of subthalamic nucleus (STN) deep brain stimulation (DBS) in parkinsonian macaques to study the effects of stimulation in a controlled environment. The model consisted of three fundamental components: 1) a three-dimensional (3D) anatomical model of the macaque basal ganglia, 2) a finite element model of the DBS electrode and electric field transmitted to the tissue medium, and 3) multicompartment biophysical models of STN projection neurons, GPi fibers of passage, and internal capsule fibers of passage. Populations of neurons were positioned within the 3D anatomical model. Neurons were stimulated with electrode positions and stimulation parameters defined as clinically effective in two parkinsonian monkeys. The model predicted axonal activation of STN neurons and GPi fibers during STN DBS. Model predictions regarding the degree of GPi fiber activation matched well with experimental recordings in both monkeys.
261.	DCN fusiform cell (Ceballos et al. 2016)
		Dorsal cochlear nucleus principal neurons, fusiform neurons, display heterogeneous spontaneous action potential activity and thus represent an appropriate model to study the role of different conductances in establishing firing heterogeneity. Particularly, fusiform neurons are divided into quiet, with no spontaneous firing, or active neurons, presenting spontaneous, regular firing. These modes are determined by the expression levels of an intrinsic membrane conductance, an inwardly rectifying potassium current (IKir). We used a computational model to test whether other subthreshold conductances vary homeostatically to maintain membrane excitability constant across the two subtypes. We found that Ih expression covaries specifically with IKir in order to maintain membrane resistance constant. The impact of Ih on membrane resistance is dependent on the level of IKir expression, being much smaller in quiet neurons with bigger IKir, but Ih variations are not relevant for creating the quiet and active phenotypes. We conclude that in fusiform neurons the variations of their different subthreshold conductances are limited to specific conductances in order to create firing heterogeneity and maintain membrane homeostasis.
262.	Deconstruction of cortical evoked potentials generated by subthalamic DBS (Kumaravelu et al 2018)
		"... High frequency deep brain stimulation (DBS) of the subthalamic nucleus (STN) suppresses parkinsonian motor symptoms and modulates cortical activity. ... Cortical evoked potentials (cEP) generated by STN DBS reflect the response of cortex to subcortical stimulation, and the goal was to determine the neural origin of cEP using a two-step approach. First, we recorded cEP over ipsilateral primary motor cortex during different frequencies of STN DBS in awake healthy and unilateral 6-OHDA lesioned parkinsonian rats. Second, we used a biophysically-based model of the thalamocortical network to deconstruct the neural origin of the cEP. The in vivo cEP included short (R1), intermediate (R2) and long-latency (R3) responses. Model-based cortical responses to simulated STN DBS matched remarkably well the in vivo responses. R1 was generated by antidromic activation of layer 5 pyramidal neurons, while recurrent activation of layer 5 pyramidal neurons via excitatory axon collaterals reproduced R2. R3 was generated by polysynaptic activation of layer 2/3 pyramidal neurons via the cortico-thalamic-cortical pathway. Antidromic activation of the hyperdirect pathway and subsequent intracortical and cortico-thalamo-cortical synaptic interactions were sufficient to generate cEP by STN DBS, and orthodromic activation through basal ganglia-thalamus-cortex pathways was not required. These results demonstrate the utility of cEP to determine the neural elements activated by STN DBS that might modulate cortical activity and contribute to the suppression of parkinsonian symptoms."
263.	Demyelinated and remyelinating axon conductances (Hines, Shrager 1991)
		Hines, Michael and Peter Shrager (1991). A computational test of the requirements for conduction in demyelinated axons. J. Restorative Neurology and Neuroscience. 3 81--93.
264.	Dendritic action potentials and computation in human layer 2/3 cortical neurons (Gidon et al 2020)
		Code for supplemental figure 12 in the paper.
265.	Dendritic action potentials and computation in human layer 2/3 cortical neurons (Gidon et al 2020)
		This code reproduces figs 3 and S9 in Dendritic action potentials in layer 2/3 pyramidal neurons of the human neocortex.
266.	Dendritic Discrimination of Temporal Input Sequences (Branco et al. 2010)
		Compartmental model of a layer 2/3 pyramidal cell in the rat somatosensory cortex, exploring NMDA-dependent sensitivity to the temporal sequence of synaptic activation.
267.	Dendritic Impedance in Neocortical L5 PT neurons (Kelley et al. 2021)
		We simulated chirp current stimulation in the apical dendrites of 5 biophysically-detailed multi-compartment models of neocortical pyramidal tract neurons and found that a combination of HCN channels and TASK-like channels produced the best fit to experimental measurements of dendritic impedance. We then explored how HCN and TASK-like channels can shape the dendritic impedance as well as the voltage response to synaptic currents.
268.	Dendritic L-type Ca currents in motoneurons (Carlin et al 2000)
		A component of recorded currents demonstrated kinetics consistent with a current originating at a site spatially segregated from the soma. In response to step commands this component was seen as a late-onset, low amplitude persistent current whilst in response to depolarizing-repolarizing ramp commands a low voltage clockwise current hysteresis was recorded. Simulations using a neuromorphic motoneuron model could reproduce these currents only if a noninactivating calcium conductance was placed in the dendritic compartments.
269.	Dendritic Na+ spike initiation and backpropagation of APs in active dendrites (Nevian et al. 2007)
		NEURON model used to create simulations shown in figure 6 of the paper. The model includes two point processes; one for dendritic spike initiation and the other for somatic action potential generation. The effect of filtering by imperfect recording electrode can be examined in somatic and dendritic locations.
270.	Dendritic signals command firing dynamics in a Cerebellar Purkinje Cell model (Genet et al. 2010)
		This model endows the dendrites of a reconstructed Purkinje cells (PC) with the mechanism of Ca-dependent plateau potentials and spikes described in Genet, S., and B. Delord. 2002. A biophysical model of nonlinear dynamics underlying plateau potentials and calcium spikes in Purkinje cell dendrites. J. Neurophysiol. 88:2430–2444). It is a part of a comprehensive mathematical study suggesting that active electric signals in the dendrites of PC command epochs of firing and silencing of the PC soma.
271.	Dendritic tip geometry effects electrical properties (Tsutsui, Oka 2001)
		In their teleost thalamic neuron models the authors demonstrate a dramatic increase in the passive propagation of synaptic inputs through the dendritic stalk to the soma in cells with larger tips.
272.	Dendritica (Vetter et al 2001)
		Dendritica is a collection of programs for relating dendritic geometry and signal propagation. The programs are based on those used for the simulations described in: Vetter, P., Roth, A. & Hausser, M. (2001) For reprint requests and additional information please contact Dr. M. Hausser, email address: m.hausser@ucl.ac.uk
273.	Dendro-dendritic synaptic circuit (Shepherd Brayton 1979)
		A NEURON simulation has been created to model the passive spread of an EPSP from a mitral cell synapse on a granule cell spine. The EPSP was shown to propagate subthreshold through the dendritic shaft into an adjacent spine with significant amplitude (figure 2B).
274.	Dentate Basket Cell: spatial summation of inhibitory synaptic inputs (Bartos et al 2001)
		Spatial summation of inhibitory synaptic input in a passive model of a basket cell from the dentate gyrus of rat hippocampus. Reproduces Figs. 5Ac and d in Bartos, M., Vida, I., Frotscher, M., Geiger, J.R.P, and Jonas, P.. Rapid signaling at inhibitory synapses in a dentate gyrus interneuron network. Journal of Neuroscience 21:2687-2698, 2001.
275.	Dentate granule cell: mAHP & sAHP; SK & Kv7/M channels (Mateos-Aparicio et al., 2014)
		The model is based on that of Aradi & Holmes (1999; Journal of Computational Neuroscience 6, 215-235). It was used to help understand the contribution of M and SK channels to the medium afterhyperpolarization (mAHP) following one or seven spikes, as well as the contribution of M channels to the slow afterhyperpolarization (sAHP). We found that SK channels are the main determinants of the mAHP, in contrast to CA1 pyramidal cells where the mAHP is primarily caused by the opening of M channels. The model reproduced these experimental results, but we were unable to reproduce the effects of the M-channel blocker XE991 on the sAHP. It is suggested that either the XE991-sensitive component of the sAHP is not due to M channels, or that when contributing to the sAHP, these channels operate in a mode different from that associated with the mAHP.
276.	Dentate gyrus (Morgan et al. 2007, 2008, Santhakumar et al. 2005, Dyhrfjeld-Johnsen et al. 2007)
		This model was implemented by Rob Morgan in the Soltesz lab at UC Irvine. It is a scaleable model of the rat dentate gyrus including four cell types. This model runs in serial (on a single processor) and has been published at the size of 50,000 granule cells (with proportional numbers of the other cells).
277.	Dentate Gyrus Feed-forward inhibition (Ferrante et al. 2009)
		In this paper, the model was used to show how that FFI can change a steeply sigmoidal input-output (I/O) curve into a double-sigmoid typical of buffer systems.
278.	Dentate gyrus granule cell: calcium and calcium-dependent conductances (Aradi and Holmes 1999)
		We have constructed a detailed model of a hippocampal dentate granule (DG) cell that includes nine different channel types. Channel densities and distributions were chosen to reproduce reported physiological responses observed in normal solution and when blockers were applied. The model was used to explore the contribution of each channel type to spiking behavior with particular emphasis on the mechanisms underlying postspike events. ... The model was used to predict changes in channel densities that could lead to epileptogenic burst discharges and to predict the effect of altered buffering capacity on firing behavior. We conclude that the clustered spatial distributions of calcium related channels, the presence of slow delayed rectifier potassium currents in dendrites, and calcium buffering properties, together, might explain the resistance of DG cells to the development of epileptogenic burst discharges.
279.	Dentate gyrus granule cell: subthreshold signal processing (Schmidt-Hieber et al. 2007)
		Detailed compartmental cable models of 8 hippocampal granule cells of adult mice were obtained from dual patch-clamp whole-cell recordings and subsequent 3D reconstructions. This code allows to reproduce figures 6-8 from the paper.
280.	Dentate gyrus network model (Santhakumar et al 2005)
		Mossy cell loss and mossy fiber sprouting are two characteristic consequences of repeated seizures and head trauma. However, their precise contributions to the hyperexcitable state are not well understood. Because it is difficult, and frequently impossible, to independently examine using experimental techniques whether it is the loss of mossy cells or the sprouting of mossy fibers that leads to dentate hyperexcitability, we built a biophysically realistic and anatomically representative computational model of the dentate gyrus to examine this question. The 527-cell model, containing granule, mossy, basket, and hilar cells with axonal projections to the perforant-path termination zone, showed that even weak mossy fiber sprouting (10-15% of the strong sprouting observed in the pilocarpine model of epilepsy) resulted in the spread of seizure-like activity to the adjacent model hippocampal laminae after focal stimulation of the perforant path. See reference for more and details.
281.	Dentate gyrus network model (Tejada et al 2014)
		" ... Here we adapted an existing computational model of the dentate gyrus (J Neurophysiol 93: 437-453, 2005) by replacing the reduced granule cell models with morphologically detailed models coming from (3D) reconstructions of mature cells. ... Different fractions of the mature granule cell models were replaced by morphologically reconstructed models of newborn dentate granule cells from animals with PILO-induced Status Epilepticus, which have apical dendritic alterations and spine loss, and control animals, which do not have these alterations. This complex arrangement of cells and processes allowed us to study the combined effect of mossy fiber sprouting, altered apical dendritic tree and dendritic spine loss in newborn granule cells on the excitability of the dentate gyrus model. Our simulations suggest that alterations in the apical dendritic tree and dendritic spine loss in newborn granule cells have opposing effects on the excitability of the dentate gyrus after Status Epilepticus. Apical dendritic alterations potentiate the increase of excitability provoked by mossy fiber sprouting while spine loss curtails this increase. "
282.	Dentate gyrus network model pattern separation and granule cell scaling in epilepsy (Yim et al 2015)
		The dentate gyrus (DG) is thought to enable efficient hippocampal memory acquisition via pattern separation. With patterns defined as spatiotemporally distributed action potential sequences, the principal DG output neurons (granule cells, GCs), presumably sparsen and separate similar input patterns from the perforant path (PP). In electrophysiological experiments, we have demonstrated that during temporal lobe epilepsy (TLE), GCs downscale their excitability by transcriptional upregulation of ‘leak’ channels. Here we studied whether this cell type-specific intrinsic plasticity is in a position to homeostatically adjust DG network function. We modified an established conductance-based computer model of the DG network such that it realizes a spatiotemporal pattern separation task, and quantified its performance with and without the experimentally constrained leaky GC phenotype. ...
283.	Depolarization Enhacement of Dendritic Spike Propagation (Bock et al 2022)
		This model shows that small subthreshold depolarization of the soma powerfully enhances the propagation of dendritic spikes, through inactivation of dendritic A-type potassium channels.
284.	Detailed passive cable model of Dentate Gyrus Basket Cells (Norenberg et al. 2010)
		Fast-spiking, parvalbumin-expressing basket cells (BCs) play a key role in feedforward and feedback inhibition in the hippocampus. ... To quantitatively address this question, we developed detailed passive cable models of BCs in the dentate gyrus based on dual somatic or somatodendritic recordings and complete morphologic reconstructions. Both specific membrane capacitance and axial resistivity were comparable to those of pyramidal neurons, but the average somatodendritic specific membrane resistance (R(m)) was substantially lower in BCs. Furthermore, R(m) was markedly nonuniform, being lowest in soma and proximal dendrites, intermediate in distal dendrites, and highest in the axon. ... Further computational analysis revealed that these unique cable properties accelerate the time course of synaptic potentials at the soma in response to fast inputs, while boosting the efficacy of slow distal inputs. These properties will facilitate both rapid phasic and efficient tonic activation of BCs in hippocampal microcircuits.
285.	Determinants of the intracellular and extracellular waveforms in DA neurons (Lopez-Jury et al 2018)
		To systematically address the contribution of AIS, dendritic and somatic compartments to shaping the two-component action potentials (APs), we modeled APs of male mouse and rat dopaminergic neurons. A parsimonious two-domain model, with high (AIS) and lower (dendro-somatic) Na+ conductance, reproduced the notch in the temporal derivatives, but not in the extracellular APs, regardless of morphology. The notch was only revealed when somatic active currents were reduced, constraining the model to three domains. Thus, an initial AIS spike is followed by an actively generated spike by the axon-bearing dendrite (ABD), in turn followed mostly passively by the soma. Larger AISs and thinner ABD (but not soma-to-AIS distance) accentuate the AIS component.
286.	DG adult-born granule cell: nonlinear a5-GABAARs control AP firing (Lodge et al, 2021)
		GABA can depolarize immature neurons close to the action potential (AP) threshold in development and adult neurogenesis. Nevertheless, GABAergic synapses effectively inhibit AP firing in newborn granule cells of the adult hippocampus as early as 2 weeks post mitosis. Parvalbumin and dendrite-targeting somatostatin interneurons activate a5-subunit containing GABAA receptors (a5-GABAARs) in young neurons, which show a voltage dependent conductance profile with increasing conductance around the AP threshold. The present computational models show that the depolarized GABA reversal potential promotes NMDA receptor activation. However, the voltage-dependent conductance of a5-GABAARs in young neurons is crucial for inhibition of AP firing to generate balanced and sparse firing activity.
287.	DG granule cell: I-A model (Beck et al 1992)
		NEURON mod files for the I-A current from the paper: Beck H, Ficker E, Heinemann U. Properties of two voltage-activated potassium currents in acutely isolated juvenile rat dentate gyrus granule cells. J. Neurophysiol. 68, 2086-2099 (1992) Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model.
288.	Diameter, Myelination and Na/K pump interactions affect axonal resilience to high frequency spiking
289.	Differential modulation of pattern and rate in a dopamine neuron model (Canavier and Landry 2006)
		"A stylized, symmetric, compartmental model of a dopamine neuron in vivo shows how rate and pattern can be modulated either concurrently or differentially. If two or more parameters in the model are varied concurrently, the baseline firing rate and the extent of bursting become decorrelated, which provides an explanation for the lack of a tight correlation in vivo and is consistent with some independence of the mechanisms that generate baseline firing rates versus bursting. ..." See paper for more and details.
290.	Direct recruitment of S1 pyramidal cells and interneurons via ICMS (Overstreet et al., 2013)
		Study of the pyramidal cells and interneurons recruited by intracortical microstimulation in primary somatosensory cortex. Code includes morphological models for seven types of pyramidal cells and eight types of interneurons, NEURON code to simulate ICMS, and an artificial reconstruction of a 3D slab of cortex implemented in MATLAB.
291.	Discharge hysteresis in motoneurons (Powers & Heckman 2015)
		"Motoneuron activity is strongly influenced by the activation of persistent inward currents (PICs) mediated by voltage-gated sodium and calcium channels. ... It has recently been suggested that a number of factors other than PIC can contribute to delta F (firing rate differences between motoneurons) values, including mechanisms underlying spike frequency adaptation and spike threshold accommodation. In the present study, we used a set of compartmental models representing a sample of 20 motoneurons with a range of thresholds to investigate how several different intrinsic motoneuron properties can potentially contribute to variations in F values. ... Our results indicate that, although other factors can contribute, variations in discharge hysteresis and delta F values primarily reflect the contribution of dendritic PICs to motoneuron activation.
292.	Discrete event simulation in the NEURON environment (Hines and Carnevale 2004)
		A short introduction to how "integrate and fire" cells are implemented in NEURON. Network simulations that use only artificial spiking cells are extremely efficient, with runtimes proportional to the total number of synaptic inputs received and independent of the number of cells or problem time.
293.	Disentangling astroglial physiology with a realistic cell model in silico (Savtchenko et al 2018)
		"Electrically non-excitable astroglia take up neurotransmitters, buffer extracellular K+ and generate Ca2+ signals that release molecular regulators of neural circuitry. The underlying machinery remains enigmatic, mainly because the sponge-like astrocyte morphology has been difficult to access experimentally or explore theoretically. Here, we systematically incorporate multi-scale, tri-dimensional astroglial architecture into a realistic multi-compartmental cell model, which we constrain by empirical tests and integrate into the NEURON computational biophysical environment. This approach is implemented as a flexible astrocyte-model builder ASTRO. As a proof-of-concept, we explore an in silico astrocyte to evaluate basic cell physiology features inaccessible experimentally. ..."
294.	Distal inhibitory control of sensory-evoked excitation (Egger, Schmitt et al. 2015)
		Model of a cortical layer (L) 2 pyramidal neuron embedded in an anatomically realistic network of two barrel columns in rat vibrissal cortex. This model is used to investigate the effects of spatially and temporally specific inhibition from L1 inhibitory interneurons on the sensory-evoked subthreshold responses of the L2 pyramidal neuron, and can be used to create simulation results underlying Figures 3D, 4B, 4C and 4E from (Egger, Schmitt et al. 2015).
295.	Distance-dependent inhibition in the hippocampus (Strüber et al. 2017)
		Network model of a hippocampal circuit including interneurons and principal cells. Amplitude and decay time course of inhibitory synapses can be systematically changed for different distances between connected cells. Various forms of excitatory drives can be administered to the network including spatially structured input.
296.	Distance-dependent synaptic strength in CA1 pyramidal neurons (Menon et al. 2013)
		Menon et al. (2013) describes the experimentally-observed variation in synaptic AMPA and NMDA conductance as a function of distance from the soma. This model explores the effect of this variation on somatic EPSPs and dendritic spike initiation, as compared to the case of uniform AMPA and NMDA conductance.
297.	Distinct current modules shape cellular dynamics in model neurons (Alturki et al 2016)
		" ... We hypothesized that currents are grouped into distinct modules that shape specific neuronal characteristics or signatures, such as resting potential, sub-threshold oscillations, and spiking waveforms, for several classes of neurons. For such a grouping to occur, the currents within one module should have minimal functional interference with currents belonging to other modules. This condition is satisfied if the gating functions of currents in the same module are grouped together on the voltage axis; in contrast, such functions are segregated along the voltage axis for currents belonging to different modules. We tested this hypothesis using four published example case models and found it to be valid for these classes of neurons. ..."
298.	Distinct integration properties of noisy inputs in active dendritic subunits (Poleg-Polsky 2019)
		The brain operates surprisingly well despite the noisy nature of individual neurons. The central mechanism for noise mitigation in the nervous system is thought to involve averaging over multiple noise-corrupted inputs. Subsequently, there has been considerable interest recently to identify noise structures that can be integrated linearly in a way that preserves reliable signal encoding. By analyzing realistic synaptic integration in biophysically accurate neuronal models, I report a complementary de-noising approach that is mediated by focal dendritic spikes. Dendritic spikes might seem to be unlikely candidates for noise reduction due to their miniscule integration compartments and poor averaging abilities. Nonetheless, the extra thresholding step introduced by dendritic spike generation increases neuronal tolerance for a broad category of noise structures, some of which cannot be resolved well with averaging. This property of active dendrites compensates for compartment size constraints and expands the repertoire of conditions that can be processed by neuronal populations.
299.	Dopamine neuron of the vent. periaqu. gray and dors. raphe nucleus (vlPAG/DRN) (Dougalis et al 2017)
		The following computer model describes the electrophysiological properties of dopamine (DA) neurons of the ventrolateral periaquaductal gray and dorsal raphe nucleus (vlPAG/DRN). the model and how to replicate Figures 7-10 of the manuscript (Dougalis et al., 2017 J Comput Neurosci). SUMMARY: We have conducted a voltage-clamp study to provide a kinetic description of major sodium, potassium and calcium ionic currents operant on adult DA vlPAG/DRN neurons in brain slices obtained from pitx3-GFP mice. Based on experimentally derived voltage-clamp data, we then constructed a simplified, conductance-based, Hodgkin and Huxley-type, computer model and validated its behaviour against in vitro neurophysiological data. Using simulations in the computational DA model, we explored the contribution of individual ionic currents in vlPAG/DRN DA neuron’s spontaneous firing, pacemaker frequency and threshold for spike frequency adaptation in silico. The data presented here extend our previous physiological characterization (Dougalis et al. 2012) and argue that DA neurons of the vlPAG/DRN express autorhythmicity in the absence of synaptic transmission via the interplay of potassium and sodium currents without the absolute need of calcium currents. The properties of the ionic currents recorded here (IH current, IA current), the lack of small oscillating potentials in the presence of sodium channel blockers taken together with the mechanisms for autorhythmicity (reliance more on sodium rather than calcium currents) also support further the idea that vlPAG/DRN DA neurons are operationally similar to VTA, rather than SNc, DA neurons. In particular, the properties of a slowly inactivating IA current in conjunction with the small and slowly activating IH current described herein pinpoint that vlPAG/DRN DA neurons are most similar to prefrontal cortex or medial shell of nucleus accumbens projecting DA neurons (see Lammel et al. 2008, 2011).
300.	Dopaminergic subtantia nigra neuron (Moubarak et al 2019)
		Axon initial segment (AIS) geometry critically influences neuronal excitability. Interestingly, the axon of substantia nigra pars compacta (SNc) dopaminergic (DA) neurons displays a highly variable location and most often arises from an axon-bearing dendrite (ABD). We combined current-clamp somatic and dendritic recordings, outside-out recordings of dendritic sodium and potassium currents, morphological reconstructions and multi-compartment modelling to determine cell-to-cell variations in AIS and ABD geometry and their influence on neuronal output (spontaneous pacemaking frequency, AP shape). Both AIS and ABD geometries are highly variable between SNc DA neurons. Surprisingly, we found that AP shape and pacemaking frequency were independent of AIS geometry. Modelling realistic morphological and biophysical variations clarify this result: in SNc DA neurons, the complexity of the ABD combined with its excitability predominantly define pacemaking frequency and AP shape, such that large variations in AIS geometry negligibly affect neuronal output, and are tolerated.
301.	Dorsal root ganglion (DRG) neuronal model (Amir, Devor 2003)
		The model shows that an electrically excitable soma is not necessary for spike through-conduction in the t-shaped geometry of a dorsal root ganglion neuron axon. Electrical excitability of the soma is required, however, for soma spike invasion. See papers for details and more.
302.	Dorsal root ganglion (DRG) neuronal model (Kovalsky et al. 2009)
		This model, diverged from oscillatory parameters seen in live cells and failed to produce characteristic ectopic discharge patterns. Here we show that use of a more complete set of Na+ conductances--which includes several delayed components--enables simulation of the entire repertoire of oscillation-triggered electrogenic phenomena seen in live dorsal root ganglion (DRG) neurons. This includes a physiological window of induction and natural patterns of spike discharge. An INa+ component at 2-20 ms was particularly important, even though it represented only a tiny fraction of overall INa+ amplitude. With the addition of a delayed rectifier IK+ the singlet firing seen in some DRG neurons can also be simulated. The model reveals the key conductances that underlie afferent ectopia, conductances that are potentially attractive targets in the search for more effective treatments of neuropathic pain.
303.	Double cable myelinated axon (Layer 5 pyramidal neuron; Cohen et al 2020)
		The periaxonal space in myelinated axons is conductive (~50 ohm cm). Together with a rapidly charging myelin sheath and relatively sealed paranodes, periaxonal conduction shapes the saltating voltage profiles of transaxonal (Vm), transmyelin (Vmy) and transfibre (Vmym) potentials. This model exemplifies double cable saltatory conduction across both time and space, and is the same cell (#6) as seen in Movie S4 of Cohen et al. 2020. This model version allows one to visualize and manipulate the controlling parameters of a propagating action potential. Further notes: The corresponding potentials in NEURON to those named above are v, vext (or vext[0]) and v+vext, respectively. The loaded biophysical parameters were those optimized for this cell (Cohen et al. 2020).
304.	DRG neuron models investigate how ion channel levels regulate firing properties (Zheng et al 2019)
		We present computational models for an Abeta-LTMR (low-threshold mechanoreceptor) and a C-LTMR expressing four Na channels and four K channels to investigate how the expression level of Kv1 and Kv4 regulate number of spikes (repetitive firing) and onset latency to action potentials in Abeta-LTMRs and C-LTMRs, respectively.
305.	Drosophila 3rd instar larval aCC motoneuron (Gunay et al. 2015)
		Single compartmental, ball-and-stick models implemented in XPP and full morphological model in Neuron. Paper has been submitted and correlates anatomical properties with electrophysiological recordings from these hard-to-access neurons. For instance we make predictions about location of the spike initiation zone, channel distributions, and synaptic input parameters.
306.	Drosophila projection neuron electrotonic structure (Gouwens and Wilson 2009)
		We address the issue of how electrical signals propagate in Drosophila neurons by modeling the electrotonic structure of the antennal lobe projection neurons innervating glomerulus DM1. The readme file contains instructions for running the model.
307.	Drosophila T4 neuron (Gruntman et al 2018)
		Passive, multi-compartment conductance-based model of a T4 cell. The model reproduces the neuron's response to moving stimuli via integration of spatially offset fast excitatory and slow inhibitory inputs.
308.	DRt neuron model (Sousa et al., 2014)
		Despite the importance and significant clinical impact of understanding information processing in the nociceptive system, the functional properties of neurons in many parts of this system are still unknown. In this work we performed whole-cell patch-clamp recording in rat brainstem blocks to characterize the electrophysiological properties of neurons in the dorsal reticular nucleus (DRt), a region known to be involved in pronociceptive modulation. We also compared properties of DRt neurons with those in the adjacent parvicellular reticular nucleus (PCRt) and in neighboring regions outside the reticular formation. We found that neurons in the DRt and PCRt had similar electrophysiological properties and exhibited mostly tonic-like firing patterns, whereas neurons outside the reticular formation showed a larger diversity of firing-patterns. The dominance of tonic neurons in the DRt supports previous conclusions that these neurons encode stimulus intensity through their firing frequency.
309.	Duration-tuned neurons from the inferior colliculus of vertebrates (Aubie et al. 2012)
		These models reproduce the responses of duration-tuned neurons in the auditory midbrain of the big brown bat, the rat, the mouse and the frog (Aubie et al. 2012). They are written in the Python interface to NEURON and a subset of the figures from Aubie et al. (2012) are pre-set in run.py (raw data is generated and a separate graphing program must be used to visualize the results).
310.	Dynamical model of olfactory bulb mitral cell (Rubin, Cleland 2006)
		This four-compartment mitral cell exhibits endogenous subthreshold oscillations, phase resetting, and evoked spike phasing properties as described in electrophysiological studies of mitral cells. It is derived from the prior work of Davison et al (2000) and Bhalla and Bower (1993). See readme.txt for details.
311.	Early-onset epileptic encephalopathy (Miceli et al. 2015)
		Model files from the paper "Early-Onset Epileptic Encephalopathy Caused by Gain-of-Function Mutations in the Voltage Sensor of Kv7.2 and Kv7.3 Potassium Channel Subunits" by Francesco Miceli, Maria Virginia Soldovieri, Paolo Ambrosino, Michela De Maria, Michele Migliore, Rosanna Migliore, and Maurizio Taglialatela J Neurosci. 2015 Mar 4;35(9):3782-93. The file fig7C.hoc reproduces the simulations shown in Fig.7C of the paper.
312.	Effect of ionic diffusion on extracellular potentials (Halnes et al 2016)
		"Recorded potentials in the extracellular space (ECS) of the brain is a standard measure of population activity in neural tissue. Computational models that simulate the relationship between the ECS potential and its underlying neurophysiological processes are commonly used in the interpretation of such measurements. Standard methods, such as volume-conductor theory and current-source density theory, assume that diffusion has a negligible effect on the ECS potential, at least in the range of frequencies picked up by most recording systems. This assumption remains to be verified. We here present a hybrid simulation framework that accounts for diffusive effects on the ECS potential. ..."
313.	Effect of the initial synaptic state on the probability to induce LTP and LTD (Migliore et al. 2015)
		NEURON mod files from the paper: M. Migliore, et al. (2015). In this paper, we investigate the possibility that the experimental protocols on synaptic plasticity may result in different consequences (e.g., LTD instead of LTP), according to the initial conditions of the stimulated synapses, and can generate confusing results. Using biophysical models of synaptic plasticity and hippocampal CA1 pyramidal neurons, we study how, why, and to what extent EPSPs observed at the soma after induction of LTP/LTD reflects the actual (local) synaptic state. The model and the results suggest a physiologically plausible explanation of why LTD induction is experimentally difficult, and they offer experimentally testable predictions on the stimulation protocols that may be more effective.
314.	Effect of voltage sensitive fluorescent proteins on neuronal excitability (Akemann et al. 2009)
		"Fluorescent protein voltage sensors are recombinant proteins that are designed as genetically encoded cellular probes of membrane potential using mechanisms of voltage-dependent modulation of fluorescence. Several such proteins, including VSFP2.3 and VSFP3.1, were recently reported with reliable function in mammalian cells. ... Expression of these proteins in cell membranes is accompanied by additional dynamic membrane capacitance, ... We used recordings of sensing currents and fluorescence responses of VSFP2.3 and of VSFP3.1 to derive kinetic models of the voltage-dependent signaling of these proteins. Using computational neuron simulations, we quantitatively investigated the perturbing effects of sensing capacitance on the input/output relationship in two central neuron models, a cerebellar Purkinje and a layer 5 pyramidal neuron. ... ". The Purkinje cell model is included in ModelDB.
315.	Effects of Chloride accumulation and diffusion on GABAergic transmission (Jedlicka et al 2011)
		"In the CNS, prolonged activation of GABA(A) receptors (GABA(A)Rs) has been shown to evoke biphasic postsynaptic responses, consisting of an initial hyperpolarization followed by a depolarization. A potential mechanism underlying the depolarization is an acute chloride (Cl(-)) accumulation resulting in a shift of the GABA(A) reversal potential (E(GABA)). The amount of GABA-evoked Cl(-) accumulation and accompanying depolarization depends on presynaptic and postsynaptic properties of GABAergic transmission, as well as on cellular morphology and regulation of Cl(-) intracellular concentration ([Cl(-)](i)). To analyze the influence of these factors on the Cl(-) and voltage behavior, we studied spatiotemporal dynamics of activity-dependent [Cl(-)](i) changes in multicompartmental models of hippocampal cells based on realistic morphological data. ..."
316.	Effects of Dopamine Modulation and KIR Inactivation in NAc Medium Spiny Neurons (Steephen 2011)
		Due to the involvement of nucleus accumbens (NAc) medium spiny neurons (MSNs) in diverse behaviors, their excitability changes can have broad functional significance. Dopamine modulates the biophysical behavior of MSNs. In ~40% of MSNs, inward rectifying potassium (KIR) currents inactivate significantly, imparting greater excitability. Employing a 189-compartment computational model of the MSN and using spatiotemporally distributed synaptic inputs, the regulation of excitability by KIR inactivation and dopaminergic modulation was investigated and quantitatively characterized. It was shown that by forming different combinations, these regulating agents could fine tune MSN excitability across a wide range. With existing evidence indicating MSNs with and without KIR inactivation to be the likely targets for D2- and D1-receptor mediated modulations, respectively, the present findings suggest that dopaminergic channel modulation may intensify the existing excitability difference between them by suppressing the excitability of MSNs without KIR inactivation while further enhancing the excitability of the more excitable MSNs with KIR inactivation. On the other hand, the combined modulation of channels and synapses by dopamine may reverse the relative excitability of one cell type with respect to the other. This model contains a complete biophysical model of MSN cell. The application allows the user to vary the cell properties by choosing the type of KIR channels included (inKIR or non-inKIR), the type of Dopamine receptors (D1R or D2R) and the modulation mechanism (Intrinsic modulation , Intrinsic-synaptic modulation, or No modulation). The user can also choose between the single pulse current clamp stimulation or a physiologically realistic synaptic stimulation scheme. More details are available in the Help provided with the application.
317.	Effects of electric fields on cognitive functions (Migliore et al 2016)
		The paper discusses the effects induced by an electric field at power lines frequency on neuronal activity during cognitive processes.
318.	Effects of increasing CREB on storage and recall processes in a CA1 network (Bianchi et al. 2014)
		Several recent results suggest that boosting the CREB pathway improves hippocampal-dependent memory in healthy rodents and restores this type of memory in an AD mouse model. However, not much is known about how CREB-dependent neuronal alterations in synaptic strength, excitability and LTP can boost memory formation in the complex architecture of a neuronal network. Using a model of a CA1 microcircuit, we investigate whether hippocampal CA1 pyramidal neuron properties altered by increasing CREB activity may contribute to improve memory storage and recall. With a set of patterns presented to a network, we find that the pattern recall quality under AD-like conditions is significantly better when boosting CREB function with respect to control. The results are robust and consistent upon increasing the synaptic damage expected by AD progression, supporting the idea that the use of CREB-based therapies could provide a new approach to treat AD.
319.	Effects of KIR current inactivation in NAc Medium Spiny Neurons (Steephen and Manchanda 2009)
		"Inward rectifying potassium (KIR) currents in medium spiny (MS) neurons of nucleus accumbens inactivate significantly in ~40% of the neurons but not in the rest, which may lead to differences in input processing by these two groups. Using a 189-compartment computational model of the MS neuron, we investigate the influence of this property using injected current as well as spatiotemporally distributed synaptic inputs. Our study demonstrates that KIR current inactivation facilitates depolarization, firing frequency and firing onset in these neurons. ..."
320.	Effects of neural morphology on global and focal NMDA-spikes (Poleg-Polsky 2015)
		This entry contains the NEURON files required to recreate figures 4-8 of the paper "Effects of Neural Morphology and Input Distribution on Synaptic Processing by Global and Focal NMDA-spikes" by Alon Poleg-Polsky
321.	Effects of spinal cord stimulation on WDR dorsal horn network (Zhang et al 2014)
		" ... To study the mechanisms underlying SCS (Spinal cord stimulation), we constructed a biophysically-based network model of the dorsal horn circuit consisting of interconnected dorsal horn interneurons and a wide dynamic range (WDR) projection neuron and representations of both local and surround receptive field inhibition. We validated the network model by reproducing cellular and network responses relevant to pain processing including wind-up, A-fiber mediated inhibition, and surround receptive field inhibition. ..." See paper for more.
322.	Effects of synaptic location and timing on synaptic integration (Rall 1964)
		Reproduces figures 5 - 8 from Rall, W. Theoretical significance of dendritic trees for neuronal input-output relations. In: Neural Theory and Modeling, ed. Reiss, R.F., Palo Alto: Stanford University Press (1964).
323.	Effects of the membrane AHP on the Lateral Superior Olive (LSO) (Zhou & Colburn 2010)
		This simulation study investigated how membrane afterhyperpolarization (AHP) influences spiking activity of neurons in the Lateral Superior Olive (LSO). The model incorporates a general integrate-and-fire spiking mechanism with a first-order adaptation channel. Simulations focus on differentiating the effects of GAHP, tauAHP, and input strength on (1) spike interval statistics, such as negative serial correlation and chopper onset, and (2) neural sensitivity to interaural level difference (ILD) of LSO neurons. The model simulated electrophysiological data collected in cat LSO (Tsuchitani and Johnson, 1985).
324.	Efficient Method for Computing Synaptic Conductance (Destexhe et al 1994)
		A simple model of transmitter release is used to solve first order kinetic equations of neurotransmiter/receptor binding. This method is applied to a glutamate and gabaa receptor. See reference for more details. The method is extended to more complex kinetic schemes in a seperate paper (Destexhe et al J Comp Neuro 1:195-231, 1994). Application to AMPA, NMDA, GABAA, and GABAB receptors is given in a book chapter (Destexhe et al In: The Neurobiology of Computation, Edited by Bower, J., Kluwer Academic Press, Norwell MA, 1995, pp. 9-14.) More information and papers at http://cns.iaf.cnrs-gif.fr/Main.html and through email: Destexhe@iaf.cnrs-gif.fr
325.	Efficient simulation of 3D reaction-diffusion in models of neurons (McDougal et al, 2022)
		Validation, visualization, and analysis scripts for NEURON's 3D reaction-diffusion support.
326.	Electrically-coupled Retzius neurons (Vazquez et al. 2009)
		"Dendritic electrical coupling increases the number of effective synaptic inputs onto neurons by allowing the direct spread of synaptic potentials from one neuron to another. Here we studied the summation of excitatory postsynaptic potentials (EPSPs) produced locally and arriving from the coupled neuron (transjunctional) in pairs of electrically-coupled Retzius neurons of the leech. We combined paired recordings of EPSPs, the production of artificial EPSPs (APSPs) in neuron pairs with different coupling coefficients and simulations of EPSPs produced in the coupled dendrites. ..."
327.	Electrostimulation to reduce synaptic scaling driven progression of Alzheimers (Rowan et al. 2014)
		"... As cells die and synapses lose their drive, remaining cells suffer an initial decrease in activity. Neuronal homeostatic synaptic scaling then provides a feedback mechanism to restore activity. ... The scaling mechanism increases the firing rates of remaining cells in the network to compensate for decreases in network activity. However, this effect can itself become a pathology, ... Here, we present a mechanistic explanation of how directed brain stimulation might be expected to slow AD progression based on computational simulations in a 470-neuron biomimetic model of a neocortical column. ... "
328.	Electrotonic transform and EPSCs for WT and Q175+/- spiny projection neurons (Goodliffe et al 2018)
		This model achieves electrotonic transform and computes mean inward and outward attenuation from 0 to 500 Hz input; and randomly activates synapses along dendrites to simulate AMPAR mediated EPSCs. For electrotonic analysis, in Elec folder, the entry file is MSNelec_transform.hoc. For EPSC simulation, in Syn folder, the entry file is randomepsc.hoc. Run read_EPSCsims_mdb_alone.m next with the simulated parameter values specified to compute the mean EPSC.
329.	eLIF and mAdExp: energy-based integrate-and-fire neurons (Fardet and Levina 2020)
		The eLIF and mAdExp neurons respectively extend the leaky integrate-and-fire and adaptive exponential (AdExp) neuron models. They include a new variable modelling the availability of energy substrate and model constraints that energy availability may have on the subthreshold and spiking dynamics. In the paper, we show how these models can reproduce complex dynamics and prove especially useful to model metabolic disruption, for instance in large-scale models of epilepsy or other diseases with metabolic components, such as Alzheimer, or Parkinson. Git repository: https://git.sr.ht/~tfardet/elif-madexp
330.	ELL Medium Ganglion cell (Muller et al 2019)
		"Distributing learning across multiple layers has proven extremely powerful in artificial neural networks. However, little is known about how multi-layer learning is implemented in the brain. Here, we provide an account of learning across multiple processing layers in the electrosensory lobe (ELL) of mormyrid fish and report how it solves problems well known from machine learning. Because the ELL operates and learns continuously, it must reconcile learning and signaling functions without switching its mode of operation. We show that this is accomplished through a functional compartmentalization within intermediate layer neurons in which inputs driving learning differentially affect dendritic and axonal spikes. We also find that connectivity based on learning rather than sensory response selectivity assures that plasticity at synapses onto intermediate-layer neurons is matched to the requirements of output neurons. The mechanisms we uncover have relevance to learning in the cerebellum, hippocampus, and cerebral cortex, as well as in artificial systems."
331.	Emergence of physiological oscillation frequencies in neocortex simulations (Neymotin et al. 2011)
		"Coordination of neocortical oscillations has been hypothesized to underlie the "binding" essential to cognitive function. However, the mechanisms that generate neocortical oscillations in physiological frequency bands remain unknown. We hypothesized that interlaminar relations in neocortex would provide multiple intermediate loops that would play particular roles in generating oscillations, adding different dynamics to the network. We simulated networks from sensory neocortex using 9 columns of event-driven rule-based neurons wired according to anatomical data and driven with random white-noise synaptic inputs. ..."
332.	Encoding and retrieval in a model of the hippocampal CA1 microcircuit (Cutsuridis et al. 2009)
		This NEURON code implements a small network model (100 pyramidal cells and 4 types of inhibitory interneuron) of storage and recall of patterns in the CA1 region of the mammalian hippocampus. Patterns of PC activity are stored either by a predefined weight matrix generated by Hebbian learning, or by STDP at CA3 Schaffer collateral AMPA synapses.
333.	Energy-efficient information transfer at thalamocortical synapses (Harris et al 2019)
		" ... Using both multicompartment Hodgkin-Huxley-type simulations and electrophysiological recordings in rodent brain slices, we find that increasing or decreasing the postsynaptic conductance of the set of thalamocortical inputs to one L4SS (Layer 4 Spiny Stellate) cell decreases the energy efficiency of information transmission from a single thalamocortical input. ..."
334.	Engaging distinct oscillatory neocortical circuits (Vierling-Claassen et al. 2010)
		"Selective optogenetic drive of fast-spiking (FS) interneurons (INs) leads to enhanced local field potential (LFP) power across the traditional “gamma” frequency band (20–80 Hz; Cardin et al., 2009). In contrast, drive to regular-spiking (RS) pyramidal cells enhances power at lower frequencies, with a peak at 8 Hz. The first result is consistent with previous computational studies emphasizing the role of FS and the time constant of GABAA synaptic inhibition in gamma rhythmicity. However, the same theoretical models do not typically predict low-frequency LFP enhancement with RS drive. To develop hypotheses as to how the same network can support these contrasting behaviors, we constructed a biophysically principled network model of primary somatosensory neocortex containing FS, RS, and low-threshold spiking (LTS) INs. ..."
335.	Enhancing the HH eqs: simulations based on the first publication in Biophys J (Moore 2015)
		"The experiments in the Cole and Moore article in the first issue of the Biophysical Journal provided the first independent experimental confirmation of the Hodgkin-Huxley (HH) equations. A log-log plot of the K current versus time showed that raising the HH variable n to the sixth power provided the best fit to the data. Subsequent simulations using n6 and setting the resting potential at the in vivo value simplifies the HH equations by eliminating the leakage term. ..."
336.	Ephaptic interactions in olfactory nerve (Bokil et al 2001)
		Bokil, H., Laaris, N., Blinder, K., Ennis, M., and Keller, A. (2001) Ephaptic interactions in the mammalian olfactory system. J. Neurosci. 21:RC173(1-5)
337.	Escape response latency in the Giant Fiber System of Drosophila melanogastor (Augustin et al 2019)
		"The Giant Fiber System (GFS) is a multi-component neuronal pathway mediating rapid escape response in the adult fruit-fly Drosophila melanogaster, usually in the face of a threatening visual stimulus. Two branches of the circuit promote the response by stimulating an escape jump followed by flight initiation. Our recent work demonstrated an age-associated decline in the speed of signal propagation through the circuit, measured as the stimulus-to-muscle depolarization response latency. The decline is likely due to the diminishing number of inter-neuronal gap junctions in the GFS of ageing flies. In this work, we presented a realistic conductance-based, computational model of the GFS that recapitulates our experimental results and identifies some of the critical anatomical and physiological components governing the circuit's response latency. According to our model, anatomical properties of the GFS neurons have a stronger impact on the transmission than neuronal membrane conductance densities. The model provides testable predictions for the effect of experimental interventions on the circuit's performance in young and ageing flies."
338.	Estimation and Production of Time Intervals (Migliore et al 2001)
		NEURON model files from the paper M. Migliore, L. Messineo, M. Cardaci, G.F. Ayala, Quantitative modeling of perception and production of time intervals, J.Neurophysiol. 86, 2754-2760 (2001). Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model.
339.	Evaluation of passive component of propagating AP in mossy fiber axons (Ohura & Kamiya 2018)
		"Action potentials propagating along axons are often followed by prolonged afterdepolarization (ADP) lasting for several tens of milliseconds. Axonal ADP is thought to be an important factor in modulating the fidelity of spike propagation during repetitive firings. However, the mechanism as well as the functional significance of axonal ADP remain unclear, partly due to inaccessibility to small structures of axon for direct electrophysiological recordings. Here, we examined the ionic and electrical mechanisms underlying axonal ADP using whole-bouton recording from mossy fiber terminals in mice hippocampal slices. ADP following axonal action potentials was strongly enhanced by focal application of veratridine, an inhibitor of Na+ channel inactivation. In contrast, tetrodotoxin (TTX) partly suppressed ADP, suggesting that a Na+ channel–dependent component is involved in axonal ADP. The remaining TTX-resistant Na+ channel–independent component represents slow capacitive discharge reflecting the shape and electrical properties of the axonal membrane. We also addressed the functional impact of axonal ADP on presynaptic function. In paired-pulse stimuli, we found that axonal ADP minimally affected the peak height of subsequent action potentials, although the rising phase of action potentials was slightly slowed, possibly due to steady-state inactivation of Na+ channels by prolonged depolarization. Voltage clamp analysis of Ca2+ current elicited by action potential waveform commands revealed that axonal ADP assists short-term facilitation of Ca2+ entry into the presynaptic terminals. Taken together, these data show that axonal ADP maintains reliable firing during repetitive stimuli and plays important roles in the fine-tuning of short-term plasticity of transmitter release by modulating Ca2+ entry into presynaptic terminals."
340.	Excitability of PFC Basal Dendrites (Acker and Antic 2009)
		".. We carried out multi-site voltage-sensitive dye imaging of membrane potential transients from thin basal branches of prefrontal cortical pyramidal neurons before and after application of channel blockers. We found that backpropagating action potentials (bAPs) are predominantly controlled by voltage-gated sodium and A-type potassium channels. In contrast, pharmacologically blocking the delayed rectifier potassium, voltage-gated calcium or Ih, conductance had little effect on dendritic action potential propagation. Optically recorded bAP waveforms were quantified and multicompartmental modeling (NEURON) was used to link the observed behavior with the underlying biophysical properties. The best-fit model included a non-uniform sodium channel distribution with decreasing conductance with distance from the soma, together with a non-uniform (increasing) A-type potassium conductance. AP amplitudes decline with distance in this model, but to a lesser extent than previously thought. We used this model to explore the mechanisms underlying two sets of published data involving high frequency trains of action potentials, and the local generation of sodium spikelets. ..."
341.	Excitability of the soma in central nervous system neurons (Safronov et al 2000)
		The ability of the soma of a spinal dorsal horn neuron, a spinal ventral horn neuron, and a hippocampal pyramidal neuron to generate action potentials was studied using experiments and computer simulations. By comparing recordings ... of a dorsal horn neuron with simulated responses, it was shown that computer models can be adequate for the study of somatic excitability. The modeled somata of both spinal neurons were unable to generate action potentials, showing only passive and local responses to current injections. ... In contrast to spinal neurons, the modeled soma of the hippocampal pyramidal neuron generated spikes with an overshoot of +9 mV. It is concluded that the somata of spinal neurons cannot generate action potentials and seem to resist their propagation from the axon to dendrites. ... See paper for more and details.
342.	Excitation Properties of Computational Models of Unmyelinated Peripheral Axons (Pelot et al., 2021)
		We implemented the single-compartment model of vagal afferents from Schild et al. 1994 and extended the model into a multi-compartment axon, presenting the first C-fiber cable model of a C-fiber vagal afferent. We also implemented the updated parameters from Schild and Kunze 1997. We compared the responses of these novel models to three published models of unmyelinated axons (Rattay and Aberham 1993; Sundt et al. 2015; Tigerholm et al. 2014).
343.	Excitatory and inhibitory interactions in populations of model neurons (Wilson and Cowan 1972)
		Coupled nonlinear differential equations are derived for the dynamics of spatially localized populations containing both excitatory and inhibitory model neurons. Phase plane methods and numerical solutions are then used to investigate population responses to various types of stimuli. The results obtained show simple and multiple hysteresis phenomena and limit cycle activity. The latter is particularly interesting since the frequency of the limit cycle oscillation is found to be a monotonic function of stimulus intensity. Finally, it is proved that the existence of limit cycle dynamics in response to one class of stimuli implies the existence of multiple stable states and hysteresis in response to a different class of stimuli. The relation between these findings and a number of experiments is discussed.
344.	Excitatory synaptic interactions in pyramidal neuron dendrites (Behabadi et al. 2012)
		" ... We hypothesized that if two excitatory pathways bias their synaptic projections towards proximal vs. distal ends of the basal branches, the very different local spike thresholds and attenuation factors for inputs near and far from the soma might provide the basis for a classical-contextual functional asymmetry. Supporting this possibility, we found both in compartmental models and electrophysiological recordings in brain slices that the responses of basal dendrites to spatially separated inputs are indeed strongly asymmetric. ..."
345.	Extracellular Action Potential Simulations (Gold et al 2007)
		This package recreates the the principal experiments described in (Gold, Henze and Koch, 2007) and includes the core code necessary to create your own Extracellular Action Potential Simulations.
346.	Extracellular fields for a three-dimensional network of cells using NEURON (Appukuttan et al 2017)
		" ... In the present work, we demonstrate a technique to couple the extracellular fields of individual cells within the NEURON simulation environment. The existing features of the simulator are extended by explicitly defining current balance equations, resulting in the coupling of the extracellular fields of adjacent cells. ..."
347.	Extracellular stimulation of myelinated axon (Reilly 2016)
		This is an implementation of an established "electrostimulation model" subjected to a set of stimulation protocols. Such models and protocols are used to predict the response of neural tissue to stimulation by electromagnetic fields or direct application of extracellular current in order to "evaluate the efficacy and safety of medical devices, or to develop guidelines or standards on acceptible incidental exposure that may not be related to patient exposure for medical purposes."
348.	Facilitation by residual calcium (Stockbridge, Hines 1982)
		The residual calcium hypothesis is compatible with facilitation of transmitter release from the neuromuscular junction.
349.	Factors contribution to GDP-induced [Cl-]i transients (Lombardi et al 2019)
		This models are used to evaluate which factors influence the GDP (giant depolarizing potential) induced [Cl-]I transients based on a initial model of P. Jedlicka
350.	Fast AMPA receptor signaling (Geiger et al 1997)
		Glutamatergic transmission at a principal neuron-interneuron synapse was investigated by dual whole-cell patch-clamp recording in rat hippocampal slices combined with morphological analysis and modeling. Simulations based on a compartmental model of the interneuron indicated that the rapid postsynaptic conductance change determines the shape and the somatodendritic integration of EPSPs, thus enabling interneurons to detect synchronous principal neuron activity.
351.	Fast sodium channel gating in mossy fiber axons (Schmidt-Hieber et al. 2010)
		"... To study the mechanisms underlying AP initiation in unmyelinated hippocampal mossy fibers of adult mice, we recorded sodium currents in axonal and somatic membrane patches. We demonstrate that sodium channel density in the proximal axon is ~5 times higher than in the soma. Furthermore, sodium channel activation and inactivation are ~2 times faster. Modeling revealed that the fast activation localized the initiation site to the proximal axon even upon strong synaptic stimulation, while fast inactivation contributed to energy-efficient membrane charging during APs. ..."
352.	Fast Spiking Basket cells (Tzilivaki et al 2019)
		"Interneurons are critical for the proper functioning of neural circuits. While often morphologically complex, dendritic integration and its role in neuronal output have been ignored for decades, treating interneurons as linear point neurons. Exciting new findings suggest that interneuron dendrites support complex, nonlinear computations: sublinear integration of EPSPs in the cerebellum, coupled to supralinear calcium accumulations and supralinear voltage integration in the hippocampus. These findings challenge the point neuron dogma and call for a new theory of interneuron arithmetic. Using detailed, biophysically constrained models, we predict that dendrites of FS basket cells in both hippocampus and mPFC come in two flavors: supralinear, supporting local sodium spikes within large-volume branches and sublinear, in small-volume branches. Synaptic activation of varying sets of these dendrites leads to somatic firing variability that cannot be explained by the point neuron reduction. Instead, a 2-stage Artificial Neural Network (ANN), with both sub- and supralinear hidden nodes, captures most of the variance. We propose that FS basket cells have substantially expanded computational capabilities sub-served by their non-linear dendrites and act as a 2-layer ANN."
353.	Fast-spiking cortical interneuron (Golomb et al. 2007)
		Cortical fast-spiking (FS) interneurons display highly variable electrophysiological properties. We hypothesize that this variability emerges naturally if one assumes a continuous distribution of properties in a small set of active channels. We construct a minimal, single-compartment conductance-based model of FS cells that includes transient Na+, delayed-rectifier K+, and slowly inactivating d-type K+ conductances. The model may display delay to firing. Stuttering (elliptic bursting) and subthreshold oscillations may be observed for small Na+ window current.
354.	Febrile seizure-induced modifications to Ih (Chen et al 2001)
		Modeling and experiments in the paper Chen K,Aradi I, Thom N,Eghbal-Ahmadi M, Baram TZ, and Soltesz I (2001) support the hypothesis that modified Ih currents strongly influence inhibitory inputs in CA1 cells and that the depolarizing shift in Ih activation plays a primary role in this process. Please see the paper for details. Some modeling details are available at http://www.ucihs.uci.edu/anatomy/soltesz/supp.htm Correspondance should be addressed to isoltesz@uci.edu (modeling was done by Ildiko Aradi, iaradi@uci.edu)
355.	Feedforward heteroassociative network with HH dynamics (Lytton 1998)
		Using the original McCulloch-Pitts notion of simple on and off spike coding in lieu of rate coding, an Anderson-Kohonen artificial neural network (ANN) associative memory model was ported to a neuronal network with Hodgkin-Huxley dynamics.
356.	Feedforward inhibition in pyramidal cells (Ferrante & Ascoli 2015)
		"Feedforward inhibition (FFI) enables pyramidal cells in area CA1 of the hippocampus (CA1PCs) to remain easily excitable while faithfully representing a broad range of excitatory inputs without quickly saturating. Despite the cortical ubiquity of FFI, its specific function is not completely understood. FFI in CA1PCs is mediated by two physiologically and morphologically distinct GABAergic interneurons: fast-spiking, perisomatic-targeting basket cells and regular-spiking, dendritic-targeting bistratified cells. These two FFI pathways might create layer-specific computational sub-domains within the same CA1PC, but teasing apart their specific contributions remains experimentally challenging. We implemented a biophysically realistic model of CA1PCs using 40 digitally reconstructed morphologies and constraining synaptic numbers, locations, amplitude, and kinetics with available experimental data. ..."
357.	FHF2KO and Wild-Type Mouse Cardiomyocyte Strands (Park et al 2020)
		Fhf2WT and Fhf2KO mouse ventricular cardiomyocyte models differ only in the inactivation gating of voltage-gated sodium channels. Cardiomyocyte linear strands were constructed by electrically coupling 111 model cells. Action potential conduction through the Fhf2KO strand is blocked by a range of stressors, including temperature elevation or reduction in sodium, calcium, or gap junctional conductance densities. Conduction through the Fhf2WT model strand is resistant to these stresses.
358.	Firing neocortical layer V pyramidal neuron (Reetz et al. 2014; Stadler et al. 2014)
		Neocortical Layer V model with firing behaviour adjusted to in vitro observations. The model was used to investigate the effects of IFN and PKC on the excitability of neurons (Stadler et al 2014, Reetz et al. 2014). The model contains new channel simulations for HCN1, HCN2 and the big calcium dependent potassium channel BK.
359.	Firing patterns of CA3 hippocampal neurons (Soldado-Magraner et al. 2019)
		" ... Here we demonstrate that the intrinsic firing patterns of CA3 neurons of the rat hippocampus in vitro undergo rapid long-term plasticity in response to a few minutes of only subthreshold synaptic conditioning. This plasticity on the spike-timing could also be induced by intrasomatic injection of subthreshold depolarizing pulses and was blocked by kinase inhibitors, indicating that discharge dynamics are modulated locally. Cluster analysis of firing patterns before and after conditioning revealed systematic transitions towards adapting and intrinsic burst behaviours, irrespective of the patterns initially exhibited by the cells. We used a conductance-based model to decide appropriate pharmacological blockade, and found that the observed transitions are likely due to recruitment of low-voltage calcium and Kv7 potassium conductances. We conclude that CA3 neurons adapt their conductance profile to the subthreshold activity of their input, so that their intrinsic firing pattern is not a static signature, but rather a reflection of their history of subthreshold activity. In this way, recurrent output from CA3 neurons may collectively shape the temporal dynamics of their embedding circuits."
360.	Fluctuating synaptic conductances recreate in-vivo-like activity (Destexhe et al 2001)
		This model (and experiments) reported in Destexhe, Rudolh, Fellous, and Sejnowski (2001) support the hypothesis that many of the characteristics of cortical neurons in vivo can be explained by fast glutamatergic and GABAergic conductances varying stochastically. Some of these cortical neuron characteristics of fluctuating synaptic origin are a depolarized membrane potential, the presence of high-amplitude membrane potential fluctuations, a low input resistance and irregular spontaneous firing activity. In addition, the point-conductance model could simulate the enhancement of responsiveness due to background activity. For more information please contact Alain Destexhe. email: Destexhe@iaf.cnrs-gif.fr
361.	Fly lobular plate VS cell (Borst and Haag 1996, et al. 1997, et al. 1999)
		In a series of papers the authors conducted experiments to develop understanding and models of fly visual system HS, CS, and VS neurons. This model recreates the VS neurons from those papers with enough success to merit approval by Borst although some discrepancies remain (see readme).
362.	Four cortical interneuron subtypes (Kubota et al. 2011)
		" ... Using electron microscopy and serial reconstructions, we analyzed the dendritic trees of four morphologically distinct neocortical interneuron subtypes to reveal two underlying organizational principles common to all. First, cross-sectional areas at any given point within a dendrite were proportional to the summed length of all dendritic segments distal to that point. ... Second, dendritic cross-sections became progressively more elliptical at more proximal, larger diameter, dendritic locations. Finally, computer simulations revealed that these conserved morphological features limit distance dependent filtering of somatic EPSPs and facilitate distribution of somatic depolarization into all dendritic compartments. ..."
363.	Four-pathway phenomenological synaptic plasticity model (Ebner et al. 2019)
364.	Frog second-order vestibular neuron models (Rossert et al. 2011)
		This implements spiking Hodgkin-Huxley type models of tonic and phasic second-order vestibular neurons. Models fitted to intracellular spike and membrane potential recordings from frog (Rana temporaria). The models can be stimulated by intracellular step current, frequency current (ZAP) or synaptic stimulation.
365.	Fronto-parietal visuospatial WM model with HH cells (Edin et al 2007)
		1) J Cogn Neurosci: 3 structural mechanisms that had been hypothesized to underlie vsWM development during childhood were evaluated by simulating the model and comparing results to fMRI. It was concluded that inter-regional synaptic connection strength cause vsWM development. 2) J Integr Neurosci: Given the importance of fronto-parietal connections, we tested whether connection asymmetry affected resistance to distraction. We drew the conclusion that stronger frontal connections are beneficial. By comparing model results to EEG, we concluded that the brain indeed has stronger frontal-to-parietal connections than vice versa.
366.	Fully Implicit Parallel Simulation of Single Neurons (Hines et al. 2008)
		A 3-d reconstructed neuron model can be simulated in parallel on a dozen or so processors and experience almost linear speedup. Network models can be simulated when there are more processors than cells.
367.	Functional impact of dendritic branch point morphology (Ferrante et al., 2013)
		" ... Here, we first quantified the morphological variability of branch points from two-photon images of rat CA1 pyramidal neurons. We then investigated the geometrical features affecting spike initiation, propagation, and timing with a computational model validated by glutamate uncaging experiments. The results suggest that even subtle membrane readjustments at branch point could drastically alter the ability of synaptic input to generate, propagate, and time action potentials."
368.	Functional properties of dendritic gap junctions in Cerebellar Golgi cells (Szoboszlay et al. 2016)
		" ... We investigated the properties of gap junctions in cerebellar interneurons by combining paired somato-somatic and somato-dendritic recordings, anatomical reconstructions, immunohistochemistry, electron microscopy, and modeling. By fitting detailed compartmental models of Golgi cells to their somato-dendritic voltage responses, we determined their passive electrical properties and the mean gap junction conductance (0.9 nS). ..."
369.	Functional structure of mitral cell dendritic tuft (Djurisic et al. 2008)
		The computational modeling component of Djurisic et al. 2008 addressed two primary questions: whether amplification by active currents is necessary to explain the relatively mild attenuation suffered by tuft EPSPs spreading along the primary dendrite to the soma; what accounts for the relatively uniform peak EPSP amplitude throughout the tuft. These simulations show that passive spread from tuft to soma is sufficient to yield the low attenuation of tuft EPSPs, and that random distribution of a biologically plausible number of excitatory synapses throughout the tuft can produce the experimentally observed uniformity of depolarization.
370.	Gamma genesis in the basolateral amygdala (Feng et al 2019)
		Using in vitro and in vivo data we develop the first large-scale biophysically and anatomically realistic model of the basolateral amygdala nucleus (BL), which reproduces the dynamics of the in vivo local field potential (LFP). Significantly, it predicts that BL intrinsically generates the transient gamma oscillations observed in vivo. The model permitted exploration of the poorly understood synaptic mechanisms underlying gamma genesis in BL, and the model's ability to compute LFPs at arbitrary numbers of recording sites provided insights into the characteristics of the spatial properties of gamma bursts. Furthermore, we show how gamma synchronizes principal cells to overcome their low firing rates while simultaneously promoting competition, potentially impacting their afferent selectivity and efferent drive, and thus emotional behavior.
371.	Gamma oscillations in hippocampal interneuron networks (Bartos et al 2002)
		To examine whether an interneuron network with fast inhibitory synapses can act as a gamma frequency oscillator, we developed an interneuron network model based on experimentally determined properties. In comparison to previous interneuron network models, our model was able to generate oscillatory activity with higher coherence over a broad range of frequencies (20-110 Hz). In this model, high coherence and flexibility in frequency control emerge from the combination of synaptic properties, network structure, and electrical coupling.
372.	Gamma oscillations in hippocampal interneuron networks (Wang, Buzsaki 1996)
		The authors investigated the hypothesis that 20-80Hz neuronal (gamma) oscillations can emerge in sparsely connected network models of GABAergic fast-spiking interneurons. They explore model NN synchronization and compare their results to anatomical and electrophysiological data from hippocampal fast spiking interneurons.
373.	Gap junction subtypes (Appukuttan et al 2016)
		Computational models of various gap junction sub-types including accommodating differences in their unitary conductances, voltage sensitivity and gating kinetics.
374.	GC model (Beining et al 2017)
		A companion modeldb entry (NEURON only) to modeldb accession number 231862.
375.	Generalized Carnevale-Hines algorithm (van Elburg and van Ooyen 2009)
		Demo illustrating the behaviour of the integrate-and-fire model in the parameter regime relevant for the generalized event-based Carnevale-Hines integration scheme. The demo includes the improved implementation of the IntFire4 mechanism.
376.	Geometry-induced features of current transfer in neuronal dendrites (Korogod, Kulagina 1998)
		The impact of dendritic geometry on somatopetal transfer of the current generated by steady uniform activation of excitatory synaptic conductance distributed over passive, or active (Hodgkin-Huxley type), dendrites was studied in simulated neurons.
377.	Glutamate diffusion and AMPA receptor activation in the cerebellar glomerulus (Saftenku 2005)
		Synaptic conductances are influenced markedly by the geometry of the space surrounding the synapse since the transient glutamate concentration in the synaptic cleft is determined by this geometry. Our paper is an attempt to understand the reasons for slow glutamate diffusion in the cerebellar glomerulus, a structure situated around the enlarged mossy fiber terminal in the cerebellum and surrounded by a glial sheath. ... Our results suggest at least a 7- to 10-fold lower apparent diffusion coefficient of glutamate in the porous medium of the glomerulus than in water. ... See paper for details and more.
378.	Glutamate mediated dendritic and somatic plateau potentials in cortical L5 pyr cells (Gao et al '20)
		Our model was built on a reconstructed Layer 5 pyramidal neuron of the rat medial prefrontal cortex, and constrained by 4 sets of experimental data: (i) voltage waveforms obtained at the site of the glutamatergic input in distal basal dendrite, including initial sodium spikelet, fast rise, plateau phase and abrupt collapse of the plateau; (ii) a family of voltage traces describing dendritic membrane responses to gradually increasing intensity of glutamatergic stimulation; (iii) voltage waveforms of backpropagating action potentials in basal dendrites (Antic, 2003); and (iv) the change of backpropagating action potential amplitude in response to drugs that block Na+ or K+ channels (Acker and Antic, 2009). Both, synaptic AMPA/NMDA and extrasynaptic NMDA inputs were placed on basal dendrites to model the induction of local regenerative potentials termed "glutamate-mediated dendritic plateau potentials". The active properties of the cell were tuned to match the voltage waveform, amplitude and duration of experimentally observed plateau potentials. The effects of input location, receptor conductance, channel properties and membrane time constant during plateau were explored. The new model predicted that during dendritic plateau potential the somatic membrane time constant is reduced. This and other model predictions were then tested in real neurons. Overall, the results support our theoretical framework that dendritic plateau potentials bring neuronal cell body into a depolarized state ("UP state"), which lasts 200 - 500 ms, or more. Plateau potentials profoundly change neuronal state -- a plateau potential triggered in one basal dendrite depolarizes the soma and shortens membrane time constant, making the cell more susceptible to action potential firing triggered by other afferent inputs. Plateau potentials may allow cortical pyramidal neurons to tune into ongoing network activity and potentially enable synchronized firing, to form active neural ensembles.
379.	Goldfish Mauthner cell (Medan et al 2017)
		" ...In fish, evasion of a diving bird that breaks the water surface depends on integrating visual and auditory stimuli with very different characteristics. How do neurons process such differential sensory inputs at the dendritic level? For that we studied the Mauthner-cells (M-cells) in the goldfish startle circuit, which receive visual and auditory inputs via two separate dendrites, both accessible for in vivo recordings. We asked if electrophysiological membrane properties and dendrite morphology, studied in vivo, play a role in selective sensory processing in the M-cell. Our results show that anatomical and electrophysiological differences between the dendrites combine to produce stronger attenuation of visually evoked post synaptic potentials (PSPs) than to auditory evoked PSPs. Interestingly, our recordings showed also cross-modal dendritic interaction, as auditory evoked PSPs invade the ventral dendrite (VD) as well as the opposite, visual PSPs invade the lateral dendrite (LD). However, these interactions were asymmetrical with auditory PSPs being more prominent in the VD than visual PSPs in the LD. Modelling experiments imply that this asymmetry is caused by active conductances expressed in the proximal segments of the VD. ..."
380.	GPi/GPe neuron models (Johnson and McIntyre 2008)
		Model files for two types of non-human primate neurons used in the paper: simplified versions of 1) a GPi neuron and 2) a GPe axon collateralizing in GPi en route to STN.
381.	H-currents effect on the fluctuation of gamma/beta oscillations (Avella-Gonzalez et al., 2015)
		This model was designed to study the impact of H-currents on the dynamics of cortical oscillations, and in paticular on the occurrence of high and low amplitude episodes (HAE, LAE) in network oscillations. The H-current is a slow, hyperpolarization-activated, depolarizing current that contributes to neuronal resonance and membrane potential. We characterized amplitude fluctuations in network oscillations by measuring the average durations of HAEs and LAEs, and explored how these were modulated by trains of external spikes, both in the presence and absence of H-channels. We looked at HAE duration, the frequency and power of network oscillations, and the effect of H-channels on the temporal voltage profile in single cells. We found that H-currents increased the oscillation frequency and, in combination with external spikes, representing input from areas outside the network, strongly decreased the synchrony of firing. As a consequence, the oscillation power and the duration of episodes during which the network exhibited high-amplitude oscillations were greatly reduced in the presence of H-channels.
382.	High frequency oscillations in a hippocampal computational model (Stacey et al. 2009)
		"... Using a physiological computer model of hippocampus, we investigate random synaptic activity (noise) as a potential initiator of HFOs (high-frequency oscillations). We explore parameters necessary to produce these oscillations and quantify the response using the tools of stochastic resonance (SR) and coherence resonance (CR). ... Our results show that, under normal coupling conditions, synaptic noise was able to produce gamma (30–100 Hz) frequency oscillations. Synaptic noise generated HFOs in the ripple range (100–200 Hz) when the network had parameters similar to pathological findings in epilepsy: increased gap junctions or recurrent synaptic connections, loss of inhibitory interneurons such as basket cells, and increased synaptic noise. ... We propose that increased synaptic noise and physiological coupling mechanisms are sufficient to generate gamma oscillations and that pathologic changes in noise and coupling similar to those in epilepsy can produce abnormal ripples."
383.	High frequency oscillations induced in three gap-junction coupled neurons (Tseng et al. 2008)
		Here we showed experimentally that high frequency oscillations (up to 600 Hz) were easily induced in a purely gap-junction coupled network by simple two stimuli with very short interval. The root cause is that the second elicited spike suffered from slow propagation speed and failure to transmit through a low-conductance junction. Similiar results were also obtained in these simulation.
384.	Hippocampal basket cell gap junction network dynamics (Saraga et al. 2006)
		2 cell network of hippocampal basket cells connected by gap junctions. Paper explores how distal gap junctions and active dendrites can tune network dynamics.
385.	Hippocampal CA1 microcircuit model including somatic and dendritic inhibition
		Here, we investigate the role of (dis)inhibition on the lateral entorhinal cortex (LEC) induced dendritic spikes on hippocampal CA1 pyramidal cells. The circuit model consists of pyramidal, SST+, CCK+, CR+/VIP+, and CCK+/VIP+ cells.
386.	Hippocampal CA1 NN with spontaneous theta, gamma: full scale & network clamp (Bezaire et al 2016)
		This model is a full-scale, biologically constrained rodent hippocampal CA1 network model that includes 9 cells types (pyramidal cells and 8 interneurons) with realistic proportions of each and realistic connectivity between the cells. In addition, the model receives realistic numbers of afferents from artificial cells representing hippocampal CA3 and entorhinal cortical layer III. The model is fully scaleable and parallelized so that it can be run at small scale on a personal computer or large scale on a supercomputer. The model network exhibits spontaneous theta and gamma rhythms without any rhythmic input. The model network can be perturbed in a variety of ways to better study the mechanisms of CA1 network dynamics. Also see online code at http://bitbucket.org/mbezaire/ca1 and further information at http://mariannebezaire.com/models/ca1
387.	Hippocampal CA3 thorny and a-thorny principal neuron models (Linaro et al in review)
		This repository contains two populations of biophysically detailed models of murine hippocampal CA3 pyramidal neurons based on the two principal cell types that comprise this region. They are the result of a data-driven approach aimed at optimizing the model parameters by utilizing high-resolution morphological reconstructions and patch-clamp electrophysiology data together with a multi-objective optimization algorithm. The models quantitatively match the cell type-specific firing phenotypes and recapitulate the intrinsic population-level variability observed in the data. Additionally, the conductance values found by the optimization algorithm are consistent with differentially expressed ion channel genes in single-cell transcriptomic data for the two cell types. The models have further been employed to investigate the cell type-specific biophysical properties involved in the generation of complex-spiking output driven by synaptic input and to show that a-thorny bursting cells are capable of encoding more information in their firing output than their counterparts, thorny regular spiking neurons. Reference: Linaro D, Levy MJ, and Hunt, DL. Cell type-specific mechanisms of information transfer in data-driven biophysical models of hippocampal CA3 principal neurons. (2022) PLOS Computational Biology
388.	Hippocampal Mossy Fiber bouton: presynaptic KV7 channel function (Martinello et al 2019)
389.	Hippocampus CA1 Interneuron Specific 3 (IS3) in vivo-like virtual NN simulations (Luo et al 2020)
		"Disinhibition is a widespread circuit mechanism for information selection and transfer. In the hippocampus, disinhibition of principal cells is provided by the interneuron-specific interneurons that express the vasoactive intestinal polypeptide (VIP-IS) and innervate selectively inhibitory interneurons. By combining optophysiological experiments with computational models, we determined the impact of synaptic inputs onto the network state-dependent recruitment of VIP-IS cells. We found that VIP-IS cells fire spikes in response to both the Schaffer collateral and the temporoammonic pathway activation. Moreover, by integrating their intrinsic and synaptic properties into computational models, we predicted recruitment of these cells between the rising phase and peak of theta oscillation and during ripples. Two-photon Ca2+-imaging in awake mice supported in part the theoretical predictions, revealing a significant speed modulation of VIP-IS cells and their preferential albeit delayed recruitment during theta-run epochs, with estimated firing at the rising phase and peak of the theta cycle. However, it also uncovered that VIP-IS cells are not activated during ripples. Thus, given the preferential theta-modulated firing of VIP-IS cells in awake hippocampus, we postulate that these cells may be important for information gating during spatial navigation and memory encoding."
390.	Hippocampus CA1 pyramidal model with Na channel exhibiting slow inactivation (Menon et al. 2009)
		These NEURON simulations show the effect of prolonged inactivation of sodium channels on attenuation of trains of backpropagating action potentials (bAPs). The new sodium channel model is a Markov model derived using a state-mutating genetic algorithm, as described in the paper.
391.	Hippocampus temporo-septal engram shift model (Lytton 1999)
		Temporo-septal engram shift model of hippocampal memory. The model posits that memories gradually move along the hippocampus from a temporal encoding site to ever more septal sites from which they are recalled. We propose that the sense of time is encoded by the location of the engram along the temporo-septal axis.
392.	HMM of Nav1.7 WT and F1449V (Gurkiewicz et al. 2011)
		Neuron mod files for the WT and F1449V Na+ currents from the paper: Kinetic Modeling of Nav1.7 Provides Insight Into Erythromelalgia-associated F1449V Mutation M. Gurkiewicz, A. Korngreen, S. Waxman, and A. Lampert. J.Neurophysiol. (2011). The parameters for the K65, K53 and K63 transitions were derived from microscopic reversibility relationships in the model.
393.	Hodgkin-Huxley model of persistent activity in PFC neurons (Winograd et al. 2008) (NEURON python)
		The paper demonstrate a form of graded persistent activity activated by hyperpolarization. This phenomenon is modeled based on a slow calcium regulation of Ih, similar to that introduced earlier for thalamic neurons (see Destexhe et al., J Neurophysiol. 1996). The only difference is that the calcium signal is here provided by the high-threshold calcium current (instead of the low-threshold calcium current in thalamic neurons).
394.	Hodgkin-Huxley model of persistent activity in prefrontal cortex neurons (Winograd et al. 2008)
		The paper demonstrate a form of graded persistent activity activated by hyperpolarization. This phenomenon is modeled based on a slow calcium regulation of Ih, similar to that introduced earlier for thalamic neurons (see Destexhe et al., J Neurophysiol. 1996). The only difference is that the calcium signal is here provided by the high-threshold calcium current (instead of the low-threshold calcium current in thalamic neurons).
395.	Hodgkin-Huxley models of different classes of cortical neurons (Pospischil et al. 2008)
		"We review here the development of Hodgkin- Huxley (HH) type models of cerebral cortex and thalamic neurons for network simulations. The intrinsic electrophysiological properties of cortical neurons were analyzed from several preparations, and we selected the four most prominent electrophysiological classes of neurons. These four classes are 'fast spiking', 'regular spiking', 'intrinsically bursting' and 'low-threshold spike' cells. For each class, we fit 'minimal' HH type models to experimental data. ..."
396.	Homeostatic synaptic plasticity (Rabinowitch and Segev 2006a,b)
		(2006a): "We investigated analytically and numerically the interplay between two opposing forms of synaptic plasticity: positive-feedback, long-term potentiation/depression (LTP/LTD), and negative-feedback, homeostatic synaptic plasticity (HSP). A detailed model of a CA1 pyramidal neuron, with numerous HSP-modifiable dendritic synapses, demonstrates that HSP may have an important role in selecting which spatial patterns of LTP/LTD are to last. ... Despite the negative-feedback nature of HSP, under both local and global HSP, numerous synaptic potentiations/depressions can persist. These experimentally testable results imply that HSP could be significantly involved in shaping the spatial distribution of synaptic weights in the dendrites and not just normalizing it, as is currently believed." (2006b): "Homeostatic synaptic plasticity (HSP) is an important mechanism attributed with the slow regulation of the neuron's activity. Whenever activity is chronically enhanced, HSP weakens the weights of the synapses in the dendrites and vice versa. Because dendritic morphology and its electrical properties partition the dendritic tree into functional compartments, we set out to explore the interplay between HSP and dendritic compartmentalization. ... The spatial distribution of synaptic weights throughout the dendrites will markedly differ under the local versus global HSP mechanisms. We suggest an experimental paradigm to unravel which type of HSP mechanism operates in the dendritic tree. The answer to this question will have important implications to our understanding of the functional organization of the neuron."
397.	Hopfield and Brody model (Hopfield, Brody 2000)
		NEURON implementation of the Hopfield and Brody model from the papers: JJ Hopfield and CD Brody (2000) JJ Hopfield and CD Brody (2001). Instructions are provided in the below readme.txt file.
398.	Hopfield and Brody model (Hopfield, Brody 2000) (NEURON+python)
		Demonstration of Hopfield-Brody snychronization using artificial cells in NEURON+python.
399.	Human Cortical L5 Pyramidal Cell (Rich et al. 2021)
		This paper presents a full spiking, biophysically detailed multi-compartment model of a human cortical layer 5 (L5) pyramidal cell, where model development was primarily based on morphological and electrophysiological data from the same neuron. Focus was placed on capturing distinctly human dynamics of the h-channel and led to the articulation of a novel model of this channel's dynamics in humans. This led to an explanation for the surprising lack of subthreshold resonance seen in these cells in the human as opposed to rodent setting.
400.	Human L2/3 pyramidal cells with low Cm values (Eyal et al. 2016)
		The advanced cognitive capabilities of the human brain are often attributed to our recently evolved neocortex. However, it is not known whether the basic building blocks of human neocortex, the pyramidal neurons, possess unique biophysical properties that might impact on cortical computations. Here we show that layer 2/3 pyramidal neurons from human temporal cortex (HL2/3 PCs) have a specific membrane capacitance (Cm) of ~0.5 µF/cm2, half of the commonly accepted “universal” value (~1 µF/cm2) for biological membranes. This finding was predicted by fitting in vitro voltage transients to theoretical transients then validated by direct measurement of Cm in nucleated patch experiments. Models of 3D reconstructed HL2/3 PCs demonstrated that such low Cm value significantly enhances both synaptic charge-transfer from dendrites to soma and spike propagation along the axon. This is the first demonstration that human cortical neurons have distinctive membrane properties, suggesting important implications for signal processing in human neocortex.
401.	Human L5 Cortical Circuit (Guet-McCreight)
		We used L5 Pyr neuron models fit to electrophysiology data from younger and older individuals to simulate detailed human layer 5 microcircuits. These circuits also included detailed parvalbumin+ (PV), somatostatin+ (SST), and vasoactivate intestinal polypeptide+ (VIP) inhibitory interneuron models.
402.	Human layer 2/3 cortical microcircuits in health and depression (Yao et al, 2022)
403.	Human somatosensory and motor axon pair to compare thresholds (Gaines et al 2018)
		These motor and sensory axon models are based on the MRG axon model and the Howells motor and sensory compartment models. They take into account known differences in the channel properties between sensory and motor neurons.
404.	Hyperexcitability from Nav1.2 channel loss in neocortical pyramidal cells (Spratt et al 2021)
		Based on the Layer 5 thick-tufted pyramidal cell from the Blue Brain Project, we modify the distribution of the sodium channel Nav1.2 to recapitulate an increase in excitability observed in ex vivo slice experiments.
405.	Ih levels roles in bursting and regular-spiking subiculum pyramidal neurons (van Welie et al 2006)
		Pyramidal neurons in the subiculum typically display either bursting or regular-spiking behavior. ... Here we report that bursting neurons posses a hyperpolarization-activated cation current (Ih) that is two-fold larger (conductance: 5.3 ± 0.5 nS) than in regularspiking neurons (2.2 ± 0.6 nS), while Ih exhibits similar voltage-dependent and kinetic properties in both classes of neurons. Bursting and regular-spiking neurons display similar morphology. The difference in Ih between the two classes is not responsible for the distinct firing patterns, since neither pharmacological blockade of Ih nor enhancement of Ih using a dynamic clamp affects the qualitative firing patterns. Instead, the difference in Ih between bursting and regular-spiking neurons determines the temporal integration of evoked synaptic input from the CA1 area. In response to 50 Hz stimulation, bursting neurons, with a large Ih, show ~50% less temporal summation than regular-spiking neurons. ... A computer simulation model of a subicular neuron with the properties of either a bursting or a regular-spiking neuron confirmed the pivotal role of Ih in temporal integration of synaptic input. These data suggest that in the subicular network, bursting neurons are better suited to discriminate the content of high frequency input, such as that occurring during gamma oscillations, compared to regular-spiking neurons. See paper for more and details.
406.	Ih tunes oscillations in an In Silico CA3 model (Neymotin et al. 2013)
		" ... We investigated oscillatory control using a multiscale computer model of hippocampal CA3, where each cell class (pyramidal, basket, and oriens-lacunosum moleculare cells), contained type-appropriate isoforms of Ih. Our model demonstrated that modulation of pyramidal and basket Ih allows tuning theta and gamma oscillation frequency and amplitude. Pyramidal Ih also controlled cross-frequency coupling (CFC) and allowed shifting gamma generation towards particular phases of the theta cycle, effected via Ih’s ability to set pyramidal excitability. ..."
407.	Impact of dendritic atrophy on intrinsic and synaptic excitability (Narayanan & Chattarji, 2010)
		These simulations examined the atrophy induced changes in electrophysiological properties of CA3 pyramidal neurons. We found these neurons change from bursting to regular spiking as atrophy increases. Region-specific atrophy induced region-specific increases in synaptic excitability in a passive dendritic tree. All dendritic compartments of an atrophied neuron had greater synaptic excitability and a larger voltage transfer to the soma than the control neuron.
408.	Impact of dendritic size and topology on pyramidal cell burst firing (van Elburg and van Ooyen 2010)
		The code provided here was written to systematically investigate which of the physical parameters controlled by dendritic morphology underlies the differences in spiking behaviour observed in different realizations of the 'ping-pong'-model. Structurally varying dendritic topology and length in a simplified model allows us to separate out the physical parameters derived from morphology underlying burst firing. To perform the parameter scans we created a new NEURON tool the MultipleRunControl which can be used to easily set up a parameter scan and write the simulation results to file. Using this code we found that not input conductance but the arrival time of the return current, as measured provisionally by the average electrotonic path length, determines whether the pyramidal cell (with ping-pong model dynamics) will burst or fire single spikes.
409.	Impedance spectrum in cortical tissue: implications for LFP signal propagation (Miceli et al. 2017)
		" ... Here, we performed a detailed investigation of the frequency dependence of the conductivity within cortical tissue at microscopic distances using small current amplitudes within the typical (neuro)physiological micrometer and sub-nanoampere range. We investigated the propagation of LFPs, induced by extracellular electrical current injections via patch-pipettes, in acute rat brain slice preparations containing the somatosensory cortex in vitro using multielectrode arrays. Based on our data, we determined the cortical tissue conductivity over a 100-fold increase in signal frequency (5-500 Hz). Our results imply at most very weak frequency-dependent effects within the frequency range of physiological LFPs. Using biophysical modeling, we estimated the impact of different putative impedance spectra. Our results indicate that frequency dependencies of the order measured here and in most other studies have negligible impact on the typical analysis and modeling of LFP signals from extracellular brain recordings."
410.	In silico hippocampal modeling for multi-target pharmacotherapy in schizophrenia (Sherif et al 2020)
		"Using a hippocampal CA3 computer model with 1200 neurons, we examined the effects of alterations in NMDAR, HCN (Ih current), and GABAAR on information flow (measured with normalized transfer entropy), and in gamma activity in local field potential (LFP). We found that altering NMDARs, GABAAR, Ih, individually or in combination, modified information flow in an inverted-U shape manner, with information flow reduced at low and high levels of these parameters. Theta-gamma phase-amplitude coupling also had an inverted-U shape relationship with NMDAR augmentation. The strong information flow was associated with an intermediate level of synchrony, seen as an intermediate level of gamma activity in the LFP, and an intermediate level of pyramidal cell excitability"
411.	Increased computational accuracy in multi-compartmental cable models (Lindsay et al. 2005)
		Compartmental models of dendrites are the most widely used tool for investigating their electrical behaviour. Traditional models assign a single potential to a compartment. This potential is associated with the membrane potential at the centre of the segment represented by the compartment. All input to that segment, independent of its location on the segment, is assumed to act at the centre of the segment with the potential of the compartment. By contrast, the compartmental model introduced in this article assigns a potential to each end of a segment, and takes into account the location of input to a segment on the model solution by partitioning the effect of this input between the axial currents at the proximal and distal boundaries of segments. For a given neuron, the new and traditional approaches to compartmental modelling use the same number of locations at which the membrane potential is to be determined, and lead to ordinary differential equations that are structurally identical. However, the solution achieved by the new approach gives an order of magnitude better accuracy and precision than that achieved by the latter in the presence of point process input.
412.	Inferior Olive, subthreshold oscillations (Torben-Nielsen, Segev, Yarom 2012)
		The Inferior Olive is a brain structure in which neurons are solely connected to each other through gap-junctions. Its behavior is characterized by spontaneous subthreshold oscillation, frequency changes in the subthreshold oscillation, stable phase differences between neurons, and propagating waves of activity. Our model based on actual IO topology can reproduce these behaviors and provides a mechanistic explanation thereof.
413.	Inferring connection proximity in electrically coupled networks (Cali et al. 2007)
		In order to explore electrical coupling in the nervous system and its network-level organization, it is imperative to map the electrical synaptic microcircuits, in analogy with in vitro studies on monosynaptic and disynaptic chemical coupling. However, walking from cell to cell over large distances with a glass pipette is challenging, and microinjection of (fluorescent) dyes diffusing through gap-junctions remains so far the only method available to decipher such microcircuits even though technical limitations exist. Based on circuit theory, we derived analytical descriptions of the AC electrical coupling in networks of isopotential cells. We then proposed an operative electrophysiological protocol to distinguish between direct electrical connections and connections involving one or more intermediate cells. This method allows inferring the number of intermediate cells, generalizing the conventional coupling coefficient, which provides limited information. We provide here some analysis and simulation scripts that used to test our method through computer simulations, in vitro recordings, theoretical and numerical methods. Key words: Gap-Junctions; Electrical Coupling; Networks; ZAP current; Impedance.
414.	Influence of dendritic structure on neocortical neuron firing patterns (Mainen and Sejnowski 1996)
		This package contains compartmental models of four reconstructed neocortical neurons (layer 3 Aspiny, layer 4 Stellate, layer 3 and layer 5 Pyramidal neurons) with active dendritic currents using NEURON. Running this simulation demonstrates that an entire spectrum of firing patterns can be reproduced in this set of model neurons which share a common distribution of ion channels and differ only in their dendritic geometry. The reference paper is: Z. F. Mainen and T. J. Sejnowski (1996) Influence of dendritic structure on firing pattern in model neocortical neurons. Nature 382: 363-366. See also http://www.cnl.salk.edu/~zach/methods.html and http://www.cnl.salk.edu/~zach/ More info in readme.txt file below made visible by clicking on the patdemo folder and then on the readme.txt file.
415.	Information transmission in cerebellar granule cell models (Rossert et al. 2014)
		" ... In this modeling study we analyse how electrophysiological granule cell properties and spike sampling influence information coded by firing rate modulation, assuming no signal-related, i.e., uncorrelated inhibitory feedback (open-loop mode). A detailed one-compartment granule cell model was excited in simulation by either direct current or mossy-fiber synaptic inputs. Vestibular signals were represented as tonic inputs to the flocculus modulated at frequencies up to 20 Hz (approximate upper frequency limit of vestibular-ocular reflex, VOR). Model outputs were assessed using estimates of both the transfer function, and the fidelity of input-signal reconstruction measured as variance-accounted-for. The detailed granule cell model with realistic mossy-fiber synaptic inputs could transmit infoarmation faithfully and linearly in the frequency range of the vestibular-ocular reflex. ... "
416.	Infraslow intrinsic rhythmogenesis in a subset of AOB projection neurons (Gorin et al 2016)
		We investigated patterns of spontaneous neuronal activity in mouse accessory olfactory bulb mitral cells, the direct neural link between vomeronasal sensory input and limbic output. Both in vitro and in vivo, we identify a subpopulation of mitral cells that exhibit slow stereotypical rhythmic discharge. In intrinsically rhythmogenic neurons, these periodic activity patterns are maintained in absence of fast synaptic drive. The physiological mechanism underlying mitral cell autorhythmicity involves cyclic activation of three interdependent ionic conductances: subthreshold persistent Na(+) current, R-type Ca(2+) current, and Ca(2+)-activated big conductance K(+) current. Together, the interplay of these distinct conductances triggers infraslow intrinsic oscillations with remarkable periodicity, a default output state likely to affect sensory processing in limbic circuits. The model reproduces the intrinsic firing in a reconstructed single AOB mitral cell with ion channels kinetics fitted to experimental measurements of their steady state and time course.
417.	Inhibition of bAPs and Ca2+ spikes in a multi-compartment pyramidal neuron model (Wilmes et al 2016)
		"Synaptic plasticity is thought to induce memory traces in the brain that are the foundation of learning. To ensure the stability of these traces in the presence of further learning, however, a regulation of plasticity appears beneficial. Here, we take up the recent suggestion that dendritic inhibition can switch plasticity of excitatory synapses on and off by gating backpropagating action potentials (bAPs) and calcium spikes, i.e., by gating the coincidence signals required for Hebbian forms of plasticity. We analyze temporal and spatial constraints of such a gating and investigate whether it is possible to suppress bAPs without a simultaneous annihilation of the forward-directed information flow via excitatory postsynaptic potentials (EPSPs). In a computational analysis of conductance-based multi-compartmental models, we demonstrate that a robust control of bAPs and calcium spikes is possible in an all-or-none manner, enabling a binary switch of coincidence signals and plasticity. ..."
418.	Input Fluctuations effects on f-I curves (Arsiero et al. 2007)
		"... We examined in vitro frequency versus current (f-I) relationships of layer 5 (L5) pyramidal cells of the rat medial prefrontal cortex (mPFC) using fluctuating stimuli. ...our results show that mPFC L5 pyramidal neurons retain an increased sensitivity to input fluctuations, whereas their sensitivity to the input mean diminishes to near zero. This implies that the discharge properties of L5 mPFC neurons are well suited to encode input fluctuations rather than input mean in their firing rates, with important consequences for information processing and stability of persistent activity at the network level."
419.	Interacting synaptic conductances during, distorting, voltage clamp (Poleg-Polsky and Diamond 2011)
		This simulation examines the accuracy of the voltage clamp technique in detecting the excitatory and the inhibitory components of the synaptic drive.
420.	Interaural time difference detection by slowly integrating neurons (Vasilkov Tikidji-Hamburyan 2012)
		For localization of a sound source, animals and humans process the microsecond interaural time differences of arriving sound waves. How nervous systems, consisting of elements with time constants of about and more than 1 ms, can reach such high precision is still an open question. This model shows that population of 10000 slowly integrating Hodgkin-Huxley neurons with inhibitory and excitatory inputs (EI neurons) can detect minute temporal disparities in input signals which are significantly less than any time constant in the system.
421.	Interneuron Specific 3 Interneuron Model (Guet-McCreight et al, 2016)
		In this paper we develop morphologically detailed multi-compartment models of Hippocampal CA1 interneuron specific 3 interneurons using cell current-clamp recordings and dendritic calcium imaging data. In doing so, we developed several variant models, as outlined in the associated README.html file.
422.	Intracortical synaptic potential modulation by presynaptic somatic potential (Shu et al. 2006, 2007)
		" ... Here we show that the voltage fluctuations associated with dendrosomatic synaptic activity propagate significant distances along the axon, and that modest changes in the somatic membrane potential of the presynaptic neuron modulate the amplitude and duration of axonal action potentials and, through a Ca21- dependent mechanism, the average amplitude of the postsynaptic potential evoked by these spikes. These results indicate that synaptic activity in the dendrite and soma controls not only the pattern of action potentials generated, but also the amplitude of the synaptic potentials that these action potentials initiate in local cortical circuits, resulting in synaptic transmission that is a mixture of triggered and graded (analogue) signals."
423.	Intrinsic sensory neurons of the gut (Chambers et al. 2014)
		A conductance base model of intrinsic neurons neurons in the gastrointestinal tract. The model contains all the major voltage-gated and calcium-gated currents observed in these neurons. This model can reproduce physiological observations such as the response to multiple brief depolarizing currents, prolonged depolarizing currents and hyperpolarizing currents. This model can be used to predict how different currents influence the excitability of intrinsic sensory neurons in the gut.
424.	Inverse stochastic resonance of cerebellar Purkinje cell (Buchin et al. 2016)
		This code shows the simulations of the adaptive exponential integrate-and-fire model (http://www.scholarpedia.org/article/Adaptive_exponential_integrate-and-fire_model) at different stimulus conditions. The parameters of the model were tuned to the Purkinje cell of cerebellum to reproduce the inhibiion of these cells by noisy current injections. Similar experimental protocols were also applied to the detailed biophysical model of Purkinje cells, de Shutter & Bower (1994) model. The repository also includes the XPPaut version of the model with the corresponding bifurcation analysis.
425.	Ion channel modeling with whole cell and a genetic algorithm (Gurkiewicz and Korngreen 2007)
		"... Here we show that a genetic search algorithm in combination with a gradient descent algorithm can be used to fit whole-cell voltage-clamp data to kinetic models with a high degree of accuracy. Previously, ion channel stimulation traces were analyzed one at a time, the results of these analyses being combined to produce a picture of channel kinetics. Here the entire set of traces from all stimulation protocols are analysed simultaneously. The algorithm was initially tested on simulated current traces produced by several Hodgkin-Huxley–like and Markov chain models of voltage-gated potassium and sodium channels. ... Finally, the algorithm was used for finding the kinetic parameters of several voltage-gated sodium and potassium channels models by matching its results to data recorded from layer 5 pyramidal neurons of the rat cortex in the nucleated outside-out patch configuration. The minimization scheme gives electrophysiologists a tool for reproducing and simulating voltage-gated ion channel kinetics at the cellular level."
426.	Ionic mechanisms of dendritic spikes (Almog and Korngreen 2014)
		We used a combined experimental and numerical parameter peeling procedure was implemented to optimize a detailed ionic mechanism for the generation and propagation of dendritic spikes in neocortical L5 pyramidal neurons. Run the cc_run.hoc to get a demo for dendritic calcium spike generated by coincidence of a back-propagating AP and distal synaptic input.
427.	Irregular oscillations produced by cyclic recurrent inhibition (Friesen, Friesen 1994)
		Model of recurrent cyclic inhibition as described on p.119 of Friesen and Friesen (1994), which was slightly modified from Szekely's model (1965) of a network for producing alternating limb movements.
428.	Irregular spiking in NMDA-driven prefrontal cortex neurons (Durstewitz and Gabriel 2006)
		Slow N-Methyl-D-aspartic acid (NMDA) synaptic currents are assumed to strongly contribute to the persistently elevated firing rates observed in prefrontal cortex (PFC) during working memory. During persistent activity, spiking of many neurons is highly irregular. ... The highest interspike-interval (ISI) variability occurred in a transition regime where the subthreshold membrane potential distribution shifts from mono- to bimodality, ... Predictability within irregular ISI series was significantly higher than expected from a noise-driven linear process, indicating that it might best be described through complex (potentially chaotic) nonlinear deterministic processes. Accordingly, the phenomena observed in vitro could be reproduced in purely deterministic biophysical model neurons. High spiking irregularity in these models emerged within a chaotic, close-to-bifurcation regime characterized by a shift of the membrane potential distribution from mono- to bimodality and by similar ISI return maps as observed in vitro. ... NMDA-induced irregular dynamics may have important implications for computational processes during working memory and neural coding.
429.	JitCon: Just in time connectivity for large spiking networks (Lytton et al. 2008)
		This simulation is primarily an illustration and is not well optimized for actually running large networks. jitcon.mod contains a large amount of C level code, understanding of which requires some knowledge of Neuron internals
430.	Kernel method to calculate LFPs from networks of point neurons (Telenczuk et al 2020)
		"The local field potential (LFP) is usually calculated from current sources arising from transmembrane currents, in particular in asymmetric cellular morphologies such as pyramidal neurons. Here, we adopt a different point of view and relate the spiking of neurons to the LFP through efferent synaptic connections and provide a method to calculate LFPs. We show that the so-called unitary LFPs (uLFP) provide the key to such a calculation. We show experimental measurements and simulations of uLFPs in neocortex and hippocampus, for both excitatory and inhibitory neurons. We fit a “kernel” function to measurements of uLFPs, and we estimate its spatial and temporal spread by using simulations of morphologically detailed reconstructions of hippocampal pyramidal neurons. Assuming that LFPs are the sum of uLFPs generated by every neuron in the network, the LFP generated by excitatory and inhibitory neurons can be calculated by convolving the trains of action potentials with the kernels estimated from uLFPs. This provides a method to calculate the LFP from networks of spiking neurons, even for point neurons for which the LFP is not easily defined. We show examples of LFPs calculated from networks of point neurons."
431.	Ketamine disrupts theta modulation of gamma in a computer model of hippocampus (Neymotin et al 2011)
		"Abnormalities in oscillations have been suggested to play a role in schizophrenia. We studied theta-modulated gamma oscillations in a computer model of hippocampal CA3 in vivo with and without simulated application of ketamine, an NMDA receptor antagonist and psychotomimetic. Networks of 1200 multi-compartment neurons (pyramidal, basket and oriens-lacunosum moleculare, OLM, cells) generated theta and gamma oscillations from intrinsic network dynamics: basket cells primarily generated gamma and amplified theta, while OLM cells strongly contributed to theta. ..."
432.	Kinetic NMDA receptor model (Kampa et al 2004)
		This kinetic NMDA receptor model is based on voltage-clamp recordings of NMDA receptor-mediated currents in nucleated patches of rat neocortical layer 5 pyramidal neurons (Kampa et al 2004 J Physiol), this model was fit with AxoGraph directly to experimental recordings in order to obtain the optimal values for the parameters. The demo shows the behaviour of a kinetic NMDA receptor model reproducing the data in figure 2. The NMDA receptor model uses realistic rates of magnesium block and its effects on channel desensitisation. Presynaptic transmitter release is necessary for glutamate binding to the receptor. This model was written by Bjoern Kampa, Canberra, 2004.
433.	Kinetic synaptic models applicable to building networks (Destexhe et al 1998)
		Simplified AMPA, NMDA, GABAA, and GABAB receptor models useful for building networks are described in a book chapter. One reference paper synthesizes a comprehensive general description of synaptic transmission with Markov kinetic models which is applicable to modeling ion channels, synaptic release, and all receptors. Also a simple introduction to this method is given in a seperate paper Destexhe et al Neural Comput 6:14-18 , 1994). More information and papers at http://cns.iaf.cnrs-gif.fr/Main.html and through email: Destexhe@iaf.cnrs-gif.fr
434.	Knox implementation of Destexhe 1998 spike and wave oscillation model (Knox et al 2018)
		" ...The aim of this study was to use an established thalamocortical computer model to determine how T-type calcium channels work in concert with cortical excitability to contribute to pathogenesis and treatment response in CAE. METHODS: The model is comprised of cortical pyramidal, cortical inhibitory, thalamocortical relay, and thalamic reticular single-compartment neurons, implemented with Hodgkin-Huxley model ion channels and connected by AMPA, GABAA , and GABAB synapses. Network behavior was simulated for different combinations of T-type calcium channel conductance, inactivation time, steady state activation/inactivation shift, and cortical GABAA conductance. RESULTS: Decreasing cortical GABAA conductance and increasing T-type calcium channel conductance converted spindle to spike and wave oscillations; smaller changes were required if both were changed in concert. In contrast, left shift of steady state voltage activation/inactivation did not lead to spike and wave oscillations, whereas right shift reduced network propensity for oscillations of any type...."
435.	KV1 channel governs cerebellar output to thalamus (Ovsepian et al. 2013)
		The output of the cerebellum to the motor axis of the central nervous system is orchestrated mainly by synaptic inputs and intrinsic pacemaker activity of deep cerebellar nuclear (DCN) projection neurons. Herein, we demonstrate that the soma of these cells is enriched with KV1 channels produced by mandatory multi-merization of KV1.1, 1.2 alpha andKV beta2 subunits. Being constitutively active, the K+ current (IKV1) mediated by these channels stabilizes the rate and regulates the temporal precision of self-sustained firing of these neurons. ... Through the use of multi-compartmental modelling and ... the physiological significance of the described functions for processing and communication of information from the lateral DCN to thalamic relay nuclei is established.
436.	L5 PFC microcircuit used to study persistent activity (Papoutsi et al. 2014, 2013)
		Using a heavily constrained biophysical model of a L5 PFC microcircuit we investigate the mechanisms that underlie persistent activity emergence (ON) and termination (OFF) and search for the minimum network size required for expressing these states within physiological regimes.
437.	L5 PFC pyramidal neurons (Papoutsi et al. 2017)
		" ... Here, we use a modeling approach to investigate whether and how the morphology of the basal tree mediates the functional output of neurons. We implemented 57 basal tree morphologies of layer 5 prefrontal pyramidal neurons of the rat and identified morphological types which were characterized by different response features, forming distinct functional types. These types were robust to a wide range of manipulations (distribution of active ionic mechanisms, NMDA conductance, somatic and apical tree morphology or the number of activated synapses) and supported different temporal coding schemes at both the single neuron and the microcircuit level. We predict that the basal tree morphological diversity among neurons of the same class mediates their segregation into distinct functional pathways. ..."
438.	L5 pyr. cell spiking control by oscillatory inhibition in distal apical dendrites (Li et al 2013)
		This model examined how distal oscillatory inhibition influences the firing of a biophysically-detailed layer 5 pyramidal neuron model.
439.	L5 pyramidal neuron myelination increases analog-digital facilitation extent (Zbili & Debanne 2020)
		Analog-digital facilitations (ADFs) correspond to a class of phenomena describing how subthreshold variations of the presynaptic membrane potential influence the synaptic transmission. ADFs rely on the propagation of somatic membrane potential fluctuations to the presynaptic bouton where they modulate ion channels availability, inducing modifications of the presynaptic spike waveform, and threfore modifying the neurotransmitter release. In this simulation, we show that myelination can promote the propagation of somatic voltage subtheshold fluctuations into the axon, allowing the ADFs to impact distal presynaptic bouton (up to 3mm from the soma).
440.	L5b PC model constrained for BAC firing and perisomatic current step firing (Hay et al., 2011)
		"... L5b pyramidal cells have been the subject of extensive experimental and modeling studies, yet conductance-based models of these cells that faithfully reproduce both their perisomatic Na+-spiking behavior as well as key dendritic active properties, including Ca2+ spikes and back-propagating action potentials, are still lacking. Based on a large body of experimental recordings from both the soma and dendrites of L5b pyramidal cells in adult rats, we characterized key features of the somatic and dendritic firing and quantified their statistics. We used these features to constrain the density of a set of ion channels over the soma and dendritic surface via multi-objective optimization with an evolutionary algorithm, thus generating a set of detailed conductance-based models that faithfully replicate the back-propagating action potential activated Ca2+ spike firing and the perisomatic firing response to current steps, as well as the experimental variability of the properties. ... The models we present provide several experimentally-testable predictions and can serve as a powerful tool for theoretical investigations of the contribution of single-cell dynamics to network activity and its computational capabilities. "
441.	Large scale model of the olfactory bulb (Yu et al., 2013)
		The readme file currently contains links to the results for all the 72 odors investigated in the paper, and the movie showing the network activity during learning of odor k3-3 (an aliphatic ketone).
442.	Lateral dendrodenditic inhibition in the Olfactory Bulb (David et al. 2008)
		Mitral cells, the principal output neurons of the olfactory bulb, receive direct synaptic activation from primary sensory neurons. Shunting inhibitory inputs delivered by granule cell interneurons onto mitral cell lateral dendrites are believed to influence spike timing and underlie coordinated field potential oscillations. Lateral dendritic shunt conductances delayed spiking to a degree dependent on both their electrotonic distance and phase of onset. Recurrent inhibition significantly narrowed the distribution of mitral cell spike times, illustrating a tendency towards coordinated synchronous activity. This result suggests an essential role for early mechanisms of temporal coordination in olfaction. The model was adapted from Davison et al, 2003, but include additional noise mechanisms, long lateral dendrite, and specific synaptic point processes.
443.	Layer 5 Pyramidal Neuron (Shai et al., 2015)
		This work contains a NEURON model for a layer 5 pyramidal neuron (based on Hay et al., 2011) with distributed groups of synapses across the basal and tuft dendrites. The results of that simulation are used to fit a phenomenological model, which is also included in this file.
444.	Layer V PFC pyramidal neuron used to study persistent activity (Sidiropoulou & Poirazi 2012)
		"... Here, we use a compartmental modeling approach to search for discriminatory features in the properties of incoming stimuli to a PFC pyramidal neuron and/or its response that signal which of these stimuli will result in persistent activity emergence. Furthermore, we use our modeling approach to study cell-type specific differences in persistent activity properties, via implementing a regular spiking (RS) and an intrinsic bursting (IB) model neuron. ... Collectively, our results pinpoint to specific features of the neuronal response to a given stimulus that code for its ability to induce persistent activity and predict differential roles of RS and IB neurons in persistent activity expression. "
445.	Layer V pyramidal cell functions and schizophrenia genetics (Mäki-Marttunen et al 2019)
		Study on how GWAS-identified risk genes of shizophrenia affect excitability and integration of inputs in thick-tufted layer V pyramidal cells
446.	Layer V pyramidal cell model with reduced morphology (Mäki-Marttunen et al 2018)
		" ... In this work, we develop and apply an automated, stepwise method for fitting a neuron model to data with fine spatial resolution, such as that achievable with voltage sensitive dyes (VSDs) and Ca2+ imaging. ... We apply our method to simulated data from layer 5 pyramidal cells (L5PCs) and construct a model with reduced neuronal morphology. We connect the reduced-morphology neurons into a network and validate against simulated data from a high-resolution L5PC network model. ..."
447.	LCN-HippoModel: model of CA1 PCs deep-superficial theta firing dynamics (Navas-Olive et al 2020)
		Using a biophysically realistic model of CA1 pyramidal cells together with a combination of single-cell and multisite electrophysiological recordings, we have studied factors underlying the internal theta phase preference of identified cell types from the dorsal CA1. We found that perisomatic inhibition delivered by complementary populations of basket cells interacts with input pathways to shape phase-locked specificity of deep and superficial CA1 pyramidal cells. Somatodendritic integration of fluctuating glutamatergic inputs defined cycle-by-cycle by nested waveforms demonstrated that firing selection is tuneable across sublayers under the relevant influence of intrinsic factors. Our data identify a set of testable physiological mechanisms underlying a phase specific firing reservoir that can be repurposed for high-level flexible dynamical representations. Documentation in https://acnavasolive.github.io/LCN-HippoModel/. More info: http://hippo-circuitlab.es/
448.	Learning spatial transformations through STDP (Davison, Frégnac 2006)
		A common problem in tasks involving the integration of spatial information from multiple senses, or in sensorimotor coordination, is that different modalities represent space in different frames of reference. Coordinate transformations between different reference frames are therefore required. One way to achieve this relies on the encoding of spatial information using population codes. The set of network responses to stimuli in different locations (tuning curves) constitute a basis set of functions which can be combined linearly through weighted synaptic connections in order to approximate non-linear transformations of the input variables. The question then arises how the appropriate synaptic connectivity is obtained. This model shows that a network of spiking neurons can learn the coordinate transformation from one frame of reference to another, with connectivity that develops continuously in an unsupervised manner, based only on the correlations available in the environment, and with a biologically-realistic plasticity mechanism (spike timing-dependent plasticity).
449.	Leech Mechanosensory Neurons: Synaptic Facilitation by Reflected APs (Baccus 1998)
		This model by Stephen Baccus explores the phenomena of action potential (AP) propagation at branch boints in axons. APs are sometimes transmitted down the efferent processes and sometimes are reflected back to the axon of AP origin or neither. See the paper for details. The model zip file contains a readme.txt which list introductory steps to follow to run the simulation. Stephen Baccus's email address: baccus@fas.harvard.edu
450.	LFP in striatum (Tanaka & Nakamura 2019)
		The numerical simulations of LFP generation by cortical pyramidal neuron and medium-sized spiny neurons.
451.	LGMD - ON excitation to dendritic field C
		Neuron model code used in "Contrast-polarity specific mapping improves efficiency of neuronal computation for collision detection". This model adapts previous LGMD model to investigate the effects of newly discovered ON excitation impinging on dendritic field C
452.	LGMD impedance (Dewell & Gabbiani 2019)
		"How neurons filter and integrate their complex patterns of synaptic inputs is central to their role in neural information processing . Synaptic filtering and integration are shaped by the frequency-dependent neuronal membrane impedance. Using single and dual dendritic recordings in vivo, pharmacology, and computational modeling, we characterized the membrane impedance of a collision detection neuron in the grasshopper, Schistocerca americana. This neuron, the lobula giant movement detector (LGMD), exhibits consistent impedance properties across frequencies and membrane potentials. Two common active conductances gH and gM, mediated respectively by hyperpolarization-activated cyclic nucleotide gated (HCN) channels and by muscarine sensitive M-type K+ channels, promote broadband integration with high temporal precision over the LGMD's natural range of membrane potentials and synaptic input frequencies. Additionally, we found that a model based on the LGMD's branching morphology increased the gain and decreased the delay associated with the mapping of synaptic input currents to membrane potential. More generally, this was true for a wide range of model neuron morphologies, including those of neocortical pyramidal neurons and cerebellar Purkinje cells. These findings show the unexpected role played by two widespread active conductances and by dendritic morphology in shaping synaptic integration."
453.	LGMD Variability and logarithmic compression in dendrites (Jones and Gabbiani, 2012, 2012B)
		A compartmental model of the LGMD with a simplified, rake shaped, excitatory dendrite. It receives spontaneous input and excitatory and inhibitory synaptic inputs triggered by visual stimuli. It generates realistic responses to looming through the velocity dependent scaling and delay of individual excitatory synaptic inputs, with variability. We use the model to show that the key determinants of output variability are spontaneous input and temporal jitter of the excitatory inputs, rather than variability in magnitude of individual inputs (2012B, J Neurophysiol). We also use the model to analyze the transformation of the excitatory signals through the visual pathway; concluding that the representation of stimulus velocity is transformed from an expansive relationship at the level of the LGMD inputs to a logarithmic one at the level of its membrane potential (2012, J Neurosci).
454.	LGMD with 3D morphology and active dendrites (Dewell & Gabbiani 2018)
		This is a model of the locust LGMD looming sensitive neuron from Dewell & Gabbiani 2018. The morphology was constructed based on 2-photon imaging, and active conductances throughout the neuron were based on sharp electrode recordings in vivo.
455.	Library of biophysically detailed striatal projection neurons (Lindroos and Hellgren Kotaleski 2020)
		Library of compartmentalized models used to investigate dendritic integration in striatal projection neurons under neuromodulation.
456.	Lillie Transition: onset of saltatory conduction in myelinating axons (Young et al. 2013)
		Included are the NEURON (.hoc) files needed to generate the data used in our Young, Castelfranco, Hartline (2013) paper. The resulting .dat files are in the same folder as the MATLAB (.m) files that are used to sort the data.
457.	Linear vs non-linear integration in CA1 oblique dendrites (Gómez González et al. 2011)
		The hippocampus in well known for its role in learning and memory processes. The CA1 region is the output of the hippocampal formation and pyramidal neurons in this region are the elementary units responsible for the processing and transfer of information to the cortex. Using this detailed single neuron model, it is investigated the conditions under which individual CA1 pyramidal neurons process incoming information in a complex (non-linear) as opposed to a passive (linear) manner. This detailed compartmental model of a CA1 pyramidal neuron is based on one described previously (Poirazi, 2003). The model was adapted to five different reconstructed morphologies for this study, and slightly modified to fit the experimental data of (Losonczy, 2006), and to incorporate evidence in pyramidal neurons for the non-saturation of NMDA receptor-mediated conductances by single glutamate pulses. We first replicate the main findings of (Losonczy, 2006), including the very brief window for nonlinear integration using single-pulse stimuli. We then show that double-pulse stimuli increase a CA1 pyramidal neuron’s tolerance for input asynchrony by at last an order of magnitude. Therefore, it is shown using this model, that the time window for nonlinear integration is extended by more than an order of magnitude when inputs are short bursts as opposed to single spikes.
458.	Local variable time step method (Lytton, Hines 2005)
		The local variable time-step method utilizes separate variable step integrators for individual neurons in the network. It is most suitable for medium size networks in which average synaptic input intervals to a single cell are much greater than a fixed step dt.
459.	Locust olfactory network with GGN and full KC population in the mushroom body (Ray et al 2020)
		We reconstructed the GGN (giant GABAergic neuron) morphology from 3D confocal image stack, and built a passive model based on the morphology to study signal attenuation across this giant neuron. In order to study the effect of feedback inhibition from this cell on odor information processing, we created a model of the olfactory network in the locust mushroom body with 50,000 KCs (Kenyon cell) reciprocally connected to this neuron. Finally, we added a model of the IG (Inhibitor of GGN) to reproduce in vivo odor responses in GGN.
460.	Long time windows from theta modulated inhib. in entorhinal–hippo. loop (Cutsuridis & Poirazi 2015)
		"A recent experimental study (Mizuseki et al., 2009) has shown that the temporal delays between population activities in successive entorhinal and hippocampal anatomical stages are longer (about 70–80 ms) than expected from axon conduction velocities and passive synaptic integration of feed-forward excitatory inputs. We investigate via computer simulations the mechanisms that give rise to such long temporal delays in the hippocampus structures. ... The model shows that the experimentally reported long temporal delays in the DG, CA3 and CA1 hippocampal regions are due to theta modulated somatic and axonic inhibition..."
461.	Long-Term Inactivation of Na+ Channels as a Mech of Adaptation in CA1 Pyr Cells (Upchurch et al '22)
		"... Ramps were applied to CA1 pyramidal neurons from male rats in vitro (slice electrophysiology) and in silico (multi-compartmental NEURON model). Under control conditions, CA1 neurons fired more action potentials at higher frequencies on the up-ramp versus the down-ramp. This effect was more pronounced for dendritic compared to somatic ramps. We incorporated a four-state Markov scheme for NaV1.6 channels into our model and calibrated the spatial dependence of long-term inactivation according to the literature; this spatial dependence was sufficient to explain the difference in dendritic versus somatic ramps. Long-term inactivation reduced the firing frequency by decreasing open-state occupancy, and reduced spike amplitude during trains by decreasing occupancy in closed states, which comprise the available pool..."
462.	Look-Up Table Synapse (LUTsyn) models for AMPA and NMDA (Pham et al., 2021)
		Fast input-output synapse model of glutamatergic receptors AMPA and NMDA that can capture nonlinear interactions via look-up table abstraction. Speeds are comparable to 'linear' exponential synapses. Download LUT files at: https://senselab.med.yale.edu/modeldb/data/267103/LUTs.zip
463.	Low Threshold Calcium Currents in TC cells (Destexhe et al 1998)
		In Destexhe, Neubig, Ulrich, and Huguenard (1998) experiments and models examine low threshold calcium current's (IT, or T-current) distribution in thalamocortical (TC) cells. Multicompartmental modeling supports the hypothesis that IT currents have a density at least several fold higher in the dendrites than the soma. The IT current contributes significantly to rebound bursts and is thought to have important network behavior consequences. See the paper for details. See also http://cns.iaf.cnrs-gif.fr Correspondance may be addressed to Alain Destexhe: Destexhe@iaf.cnrs-gif.fr
464.	LP neuron model database (Zang and Marder 2023)
		Biological neurons show significant cell-to-cell variability but have the striking ability to maintain their key firing properties in the face of unpredictable perturbations and stochas- tic noise. Using a population of multi-compartment models consisting of soma, neurites, and axon for the lateral pyloric neuron in the crab stomatogastric ganglion, we explored how rebound bursting is preserved when the 14 channel conductances in each model are all randomly varied. The coupling between the axon and other compartments is critical for the ability of the axon to spike during bursts and consequently determines the set of successful solutions. When the coupling deviates from a biologically realistic range, the neuronal tolerance of conductance variations is lessened. Thus, the gross morphological features of these neurons enhance their robustness to perturbations of channel densities and expand the space of individual variability that can maintain a desired output pattern.
465.	LTP in cerebellar mossy fiber-granule cell synapses (Saftenku 2002)
		We simulated synaptic transmission and modified a simple model of long-term potentiation (LTP) and long-term depression (LTD) in order to describe long-term plasticity related changes in cerebellar mossy fiber-granule cell synapses. In our model, protein autophosphorylation, leading to the maintenance of long-term plasticity, is controlled by Ca2+ entry through the NMDA receptor channels. The observed nonlinearity in the development of long-term changes of EPSP in granule cells is explained by the difference in the rate constants of two independent autocatalytic processes.
466.	Mammalian Ventricular Cell (Beeler and Reuter 1977)
		This classic model of ventricular myocardial fibres was implemented by Francois Gannier. "... Four individual components of ionic current were formulated mathematically in terms of Hodgkin-Huxley type equations. The model incorporates two voltage- and time-dependent inward currents, the excitatory inward sodium current, illa, and a secondary or slow inward current, is, primarily carried by calcium ions. A time-independent outward potassium current, iK1, exhibiting inward-going rectification, and a voltage- and time-dependent outward current, i.1, primarily carried by potassium ions, are further elements of the model...."
467.	Mapping function onto neuronal morphology (Stiefel and Sejnowski 2007)
		"... We used an optimization procedure to find neuronal morphological structures for two computational tasks: First, neuronal morphologies were selected for linearly summing excitatory synaptic potentials (EPSPs); second, structures were selected that distinguished the temporal order of EPSPs. The solutions resembled the morphology of real neurons. In particular the neurons optimized for linear summation electrotonically separated their synapses, as found in avian nucleus laminaris neurons, and neurons optimized for spike-order detection had primary dendrites of significantly different diameter, as found in the basal and apical dendrites of cortical pyramidal neurons. ..."
468.	Mathematical model for windup (Aguiar et al. 2010)
		"Windup is characterized as a frequency-dependent increase in the number of evoked action potentials in dorsal horn neurons in response to electrical stimulation of afferent C-fibers. ... The approach presented here relies on mathematical and computational analysis to study the mechanism(s) underlying windup. From experimentally obtained windup profiles, we extract the time scale of the facilitation mechanisms that may support the characteristics of windup. Guided by these values and using simulations of a biologically realistic compartmental model of a wide dynamic range (WDR) neuron, we are able to assess the contribution of each mechanism for the generation of action potentials windup. ..."
469.	Maximal firing rate in midbrain dopamine neurons (Knowlton et al., 2021)
470.	MEC layer II stellate cell: Synaptic mechanisms of grid cells (Schmidt-Hieber & Hausser 2013)
		This study investigates the cellular mechanisms of grid field generation in Medial Entorhinal Cortex (MEC) layer II stellate cells.
471.	Mechanisms of fast rhythmic bursting in a layer 2/3 cortical neuron (Traub et al 2003)
		This simulation is based on the reference paper listed below. This port was made by Roger D Traub and Maciej T Lazarewicz (mlazarew at seas.upenn.edu) Thanks to Ashlen P Reid for help with porting a morphology of the cell.
472.	Mechanisms of magnetic stimulation of central nervous system neurons (Pashut et al. 2011)
		Transcranial magnetic stimulation (TMS) is a widely applied tool for probing cognitive function in humans and is one of the best tools for clinical treatments and interfering with cognitive tasks. Surprisingly, while TMS has been commercially available for decades, the cellular mechanisms underlying magnetic stimulation remain unclear. Here we investigate these mechanisms using compartmental modeling. We generated a numerical scheme allowing simulation of the physiological response to magnetic stimulation of neurons with arbitrary morphologies and active properties. Computational experiments using this scheme suggested that TMS affects neurons in the central nervous system (CNS) primarily by somatic stimulation.
473.	Mechanisms underlying subunit independence in pyramidal neuron dendrites (Behabadi and Mel 2014)
		"...Using a detailed compartmental model of a layer 5 pyramidal neuron, and an improved method for quantifying subunit independence that incorporates a more accurate model of dendritic integration, we first established that the output of each dendrite can be almost perfectly predicted by the intensity and spatial configuration of its own synaptic inputs, and is nearly invariant to the rate of bAP-mediated 'cross-talk' from other dendrites over a 100-fold range..."
474.	Medial vestibular neuron models (Quadroni and Knopfel 1994)
		The structure and the parameters of the model cells were chosen to reproduce the responses of type A and type B MVNns as described in electrophysiological recordings. The emergence of oscillatory firing under these two specific experimental conditions is consistent with electrophysiological recordings not used during construction of the model. We, therefore, suggest that these models have a high predictive value.
475.	MEG of Somatosensory Neocortex (Jones et al. 2007)
		"... To make a direct and principled connection between the SI (somatosensory primary neocortex magnetoencephalography) waveform and underlying neural dynamics, we developed a biophysically realistic computational SI model that contained excitatory and inhibitory neurons in supragranular and infragranular layers. ... our model provides a biophysically realistic solution to the MEG signal and can predict the electrophysiological correlates of human perception."
476.	Membrane electrical properties of mouse CA1 pyramidal cells during strong inputs (Bianchi et al 22)
		ABSTRACT: In this work we highlight an electrophysiological feature, often observed in recordings from mouse CA1 pyramidal cells, which has been so far ignored by experimentalists and modelers. It consists of a large and dynamic increase in the depolarization baseline (i.e. the minimum value of the membrane potential between successive action potentials during a sustained input) in response to strong somatic current injections. Such an increase can directly affect neurotransmitter release properties and, more generally, efficacy of synaptic transmission. However, it cannot be explained by any currently available conductance-based computational model. Here we present a model addressing this issue, demonstrating that experimental recordings can be reproduced by assuming that an input current modifies, in a time-dependent manner, the electrical and permeability properties of the neuron membrane by shifting the ionic reversal potentials and channel kinetics. For this reason, we propose that any detailed model of ion channel kinetics, for neurons exhibiting this characteristic, should be adapted to correctly represent the response and the synaptic integration process during strong and sustained inputs.
477.	Membrane potential changes in dendritic spines during APs and synaptic input (Palmer & Stuart 2009)
		" ... Finally, we used simulations of our experimental observations in morphologically realistic models to estimate spine neck resistance. These simulations indicated that spine neck resistance ranges up to ~500 M Ohm. Spine neck resistances of this magnitude reduce somatic EPSPs by ~15%, indicating that the spine neck is unlikely to act as a physical device to significantly modify synaptic strength."
478.	Mice Somatosensory L2/3 Pyramidal cells (Iascone et al 2020)
		Mice L2/3 pyramidal cells with full excitatory and inhibitory synaptic maps (Models used in Whole-neuron synaptic mapping reveals local balance between excitatory and inhibitory synapse organization - Iascone et at 2020)
479.	Microcircuits of L5 thick tufted pyramidal cells (Hay & Segev 2015)
		"... We simulated detailed conductance-based models of TTCs (Layer 5 thick tufted pyramidal cells) forming recurrent microcircuits that were interconnected as found experimentally; the network was embedded in a realistic background synaptic activity. ... Our findings indicate that dendritic nonlinearities are pivotal in controlling the gain and the computational functions of TTCs microcircuits, which serve as a dominant output source for the neocortex. "
480.	Midbrain dopamine neuron: firing patterns (Canavier 1999)
		Sodium dynamics drives the generation of slow oscillations postulated to underly NMDA-evoked bursting activity.
481.	Mirror Neuron (Antunes et al 2017)
		Modeling Mirror Neurons Through Spike-Timing Dependent Plasticity. This script reproduces Figure 3B.
482.	Mitral cell activity gating by respiration and inhibition in an olfactory bulb NN (Short et al 2016)
		To explore interactions between respiration, inhibition, and olfaction, experiments using light to active channel rhodopsin in sensory neurons expressing Olfactory Marker Protein were performed in mice and modeled in silico. This archive contains NEURON models that were run on parallel computers to explore the interactions between varying strengths of respiratory activity and olfactory sensory neuron input and the roles of periglomerular, granule, and external tufted cells in shaping mitral cell responses.
483.	MNTB Neuron: Kv3.1 currents (Wang et al 1998)
		Model of Medial Nucleus of the Trapezoid Body (MNTB) neurons described in Lu-Yang Wang, Li Gan, Ian D. Forsythe and Leonard K. Kaczmarek. Contribution of the Kv3.1 potassium channel to high-frequency firing in mouse auditory neurones. J. Physiol (1998) 509.1 183-194. Created by David Kornfeld, Byram Hills High School, Armonk NY. Please email dbk1@mindspring.com for questions about the model. See Readme.txt below for more info.
484.	Model of arrhythmias in a cardiac cells network (Casaleggio et al. 2014)
		" ... Here we explore the possible processes leading to the occasional onset and termination of the (usually) non-fatal arrhythmias widely observed in the heart. Using a computational model of a two-dimensional network of cardiac cells, we tested the hypothesis that an ischemia alters the properties of the gap junctions inside the ischemic area. ... In conclusion, our model strongly supports the hypothesis that non-fatal arrhythmias can develop from post-ischemic alteration of the electrical connectivity in a relatively small area of the cardiac cell network, and suggests experimentally testable predictions on their possible treatments."
485.	Model of CA1 activity during working memory task (Spera et al. 2016)
		"The cellular processes underlying individual differences in the Woring Memory Capacity (WMC) of humans are essentially unknown. Psychological experiments suggest that subjects with lower working memory capacity (LWMC), with respect to subjects with higher capacity (HWMC), take more time to recall items from a list because they search through a larger set of items and are much more susceptible to interference during retrieval. ... In this paper, we investigate the possible underlying mechanisms at the single neuron level by using a computational model of hippocampal CA1 pyramidal neurons, which have been suggested to be deeply involved in the recognition of specific items. ..."
486.	Model of peripheral nerve with ephaptic coupling (Capllonch-Juan & Sepulveda 2020)
		We built a computational model of a peripheral nerve trunk in which the interstitial space between the fibers and the tissues is modelled using a resistor network, thus enabling distance-dependent ephaptic coupling between myelinated axons and between fascicles as well. We used the model to simulate a) the stimulation of a nerve trunk model with a cuff electrode, and b) the propagation of action potentials along the axons. Results were used to investigate the effect of ephaptic interactions on recruitment and selectivity stemming from artificial (i.e., neural implant) stimulation and on the relative timing between action potentials during propagation.
487.	Model of repetitive firing in Grueneberg ganglion olfactory neurons (Liu et al., 2012)
		This model is constructed based on properties of Na+ and K+ currents observed in whole-cell patch clamp recordings of mouse Grueneberg ganglion neurons in acute slices. Two distinct Na+ conductances representing the TTX-sensitive and TTX-resistant currents and one delayed rectifier K+ currrent are included. By modulating the maximal conductances of Na+ currents, one can reproduce the regular, phasic, and sporadic patterns of repetitive firing found in the patch clamp experiments.
488.	Model of SK current`s influence on precision in Globus Pallidus Neurons (Deister et al. 2009)
		" ... In numerical simulations, the availability of both Na+ and A-type K+ channels during autonomous firing were reduced when SK channels were removed, and a nearly equal reduction in Na+ and K+ subthreshold-activated ion channel availability produced a large decrease in the neuron's slope conductance near threshold. This change made the neuron more sensitive to intrinsically generated noise. In vivo, this change would also enhance the sensitivity of GP (Globus Pallidus) neurons to small synaptic inputs."
489.	Model of the cerebellar granular network (Sudhakar et al 2017)
		"The granular layer, which mainly consists of granule and Golgi cells, is the first stage of the cerebellar cortex and processes spatiotemporal information transmitted by mossy fiber inputs with a wide variety of firing patterns. To study its dynamics at multiple time scales in response to inputs approximating real spatiotemporal patterns, we constructed a large-scale 3D network model of the granular layer. ..."
490.	Model of the Xenopus tadpole swimming spinal network (Roberts et al. 2014)
		This is a NEURON-python and MATLAB simulation code for generating anatomical or probabilistic connectivity and simulating the neuronal dynamics of the neuronal network controlling swimming in Xenopus tadpoles. For more details about this model, see Ferrario et al, 2018, eLife and Roberts et al, 2014, J of Neurosci
491.	Model of Type 3 firing in neurons (Clay et al 2008)
		An ionic model for Type 3 firing in neurons (Clay et al 2008) Some neurons fire only once in response to a sustained depolarizing current pulse, type 3 behavior. One example, surprisingly, is the squid giant axon. The Hodgkin-Huxley (HH) model of this preparation fires repetitively for these conditions – type 2, a result that is not observed experimentally as shown in the above paper. Changing one parameter of their model of IK is sufficient to mimic the result.
492.	Modeling a Nociceptive Neuro-Immune Synapse Activated by ATP and 5-HT in Meninges (Suleimanova et al., 2020)
		"Extracellular ATP and serotonin (5-HT) are powerful triggers of nociceptive firing in the meninges, a process supporting headache and whose cellular mechanisms are incompletely understood. The current study aimed to develop, with the neurosimulator NEURON, a novel approach to explore in silico the molecular determinants of the long-lasting, pulsatile nature of migraine attacks. The present model included ATP and 5-HT release, ATP diffusion and hydrolysis, 5-HT uptake, differential activation of ATP P2X or 5-HT3 receptors, and receptor subtype-specific desensitization. The model also tested the role of branched meningeal fibers with multiple release sites. Spike generation and propagation were simulated using variable contribution by potassium and sodium channels in a multi-compartment fiber environment. Multiple factors appeared important to ensure prolonged nociceptive firing potentially relevant to long-lasting pain. Crucial roles were observed in: (i) co-expression of ATP P2X2 and P2X3 receptor subunits; (ii) intrinsic activation/inactivation properties of sodium Nav1.8 channels; and (iii) temporal and spatial distribution of ATP/5-HT release sites along the branches of trigeminal nerve fibers. Based on these factors we could obtain either persistent activation of nociceptive firing or its periodic bursting mimicking the pulsating nature of pain. In summary, our model proposes a novel tool for the exploration of peripheral nociception to test the contribution of clinically relevant factors to headache including migraine pain." (paper abstract)
493.	Modeling dentate granule cells heterosynaptic plasticity using STDP-BCM rule (Jedlicka et al. 2015)
		... Here we study how key components of learning mechanisms in the brain, namely spike timing-dependent plasticity and metaplasticity, interact with spontaneous activity in the input pathways of the neuron. Using biologically realistic simulations we show that ongoing background activity is a key determinant of the degree of long-term potentiation and long-term depression of synaptic transmission between nerve cells in the hippocampus of freely moving animals. This work helps better understand the computational rules which drive synaptic plasticity in vivo. ...
494.	Modeling local field potentials (Bedard et al. 2004)
		This demo simulates a model of local field potentials (LFP) with variable resistivity. This model reproduces the low-pass frequency filtering properties of extracellular potentials. The model considers inhomogeneous spatial profiles of conductivity and permittivity, which result from the multiple media (fluids, membranes, vessels, ...) composing the extracellular space around neurons. Including non-constant profiles of conductivity enables the model to display frequency filtering properties, ie slow events such as EPSPs/IPSPs are less attenuated than fast events such as action potentials. The demo simulates Fig 6 of the paper.
495.	Modeling single neuron LFPs and extracellular potentials with LFPsim (Parasuram et al. 2016)
		LFPsim - Simulation scripts to compute Local Field Potentials (LFP) from cable compartmental models of neurons and networks implemented in the NEURON simulation environment.
496.	Modelling platform of the cochlear nucleus and other auditory circuits (Manis & Compagnola 2018)
		"Models of the auditory brainstem have been an invaluable tool for testing hypotheses about auditory information processing and for highlighting the most important gaps in the experimental literature. Due to the complexity of the auditory brainstem, and indeed most brain circuits, the dynamic behavior of the system may be difficult to predict without a detailed, biologically realistic computational model. Despite the sensitivity of models to their exact construction and parameters, most prior models of the cochlear nucleus have incorporated only a small subset of the known biological properties. This confounds the interpretation of modelling results and also limits the potential future uses of these models, which require a large effort to develop. To address these issues, we have developed a general purpose, bio-physically detailed model of the cochlear nucleus for use both in testing hypotheses about cochlear nucleus function and also as an input to models of downstream auditory nuclei. The model implements conductance-based Hodgkin-Huxley representations of cells using a Python-based interface to the NEURON simulator. ..."
497.	Modelling reduced excitability in aged CA1 neurons as a Ca-dependent process (Markaki et al. 2005)
		"We use a multi-compartmental model of a CA1 pyramidal cell to study changes in hippocampal excitability that result from aging-induced alterations in calcium-dependent membrane mechanisms. The model incorporates N- and L-type calcium channels which are respectively coupled to fast and slow afterhyperpolarization potassium channels. Model parameters are calibrated using physiological data. Computer simulations reproduce the decreased excitability of aged CA1 cells, which results from increased internal calcium accumulation, subsequently larger postburst slow afterhyperpolarization, and enhanced spike frequency adaptation. We find that aging-induced alterations in CA1 excitability can be modelled with simple coupling mechanisms that selectively link specific types of calcium channels to specific calcium-dependent potassium channels."
498.	Models of Na channels from a paper on the PKC control of I Na,P (Baker 2005)
		"The tetrodotoxin-resistant (TTX-r) persistent Na(+) current, attributed to Na(V)1.9, was recorded in small (< 25 mum apparent diameter) dorsal root ganglion (DRG) neurones cultured from P21 rats and from adult wild-type and Na(V)1.8 null mice. ... Numerical simulation of the up-regulation qualitatively reproduced changes in sensory neurone firing properties. ..." Note: models of NaV1.8 and NaV1.9 and also persistent and transient Na channels that collectively model Nav 1.1, 1.6, and 1.7 are present in this model.
499.	ModelView: online structural analysis of computational models (McDougal et al. 2015)
		" ... To aid users, we have developed ModelView, a web application for NEURON models in ModelDB that presents a graphical view of model structure augmented with contextual information. Web presentation provides a rich, simulator-independent environment for interacting with graphs. The necessary data is generated by combining manual curation, text-mining the source code, querying ModelDB, and simulator introspection. ... With this tool, researchers can examine the structure of hundreds of models in ModelDB in a standardized presentation without installing any software, downloading the model, or reading model source code."
500.	Modulation of hippocampal rhythms by electric fields and network topology (Berzhanskaya et al. 2013)
		“… Here we present experimental and computational evidence of the interplay among hippocampal synaptic circuitry, neuronal morphology, external electric fields, and network activity. Electrophysiological data are used to constrain and validate an anatomically and biophysically realistic model of area CA1 containing pyramidal cells and two interneuron types: dendritic- and perisomatic-targeting. We report two lines of results: addressing the network structure capable of generating theta-modulated gamma rhythms, and demonstrating electric field effects on those rhythms. First, theta-modulated gamma rhythms require specific inhibitory connectivity. … The second major finding is that subthreshold electric fields robustly alter the balance between different rhythms. …”
501.	Modulation of temporal integration window (Migliore, Shepherd 2002)
		Model simulation file from the paper M.Migliore and Gordon M. Shepherd Emerging rules for distributions of active dendritic properties underlying specific neuronal functions. Nature Rev. Neurosci. 3, 362-370 (2002).
502.	Molecular layer interneurons in cerebellum encode valence in associative learning (Ma et al 2020)
		We used two-photon microscopy to study the role of ensembles of cerebellar molecular layer interneurons (MLIs) in a go-no go task where mice obtain a sugar water reward. In order to begin understanding the circuit basis of our findings in changes in lick behavior with chemogenetics in the go-no go associative learning olfactory discrimination task we generated a simple computational model of MLI interaction with PCs.
503.	Morphological determinants of action potential dynamics in substantia nigra (Moubarak et al 2022)
		This model allows to simulate pacemaking activity in 37 fully reconstructed neurons. Calcium and sodium conductances vary by 11 increments in the Axon bearing dendrite part to simulate a 11*11*37 models. For each model Action potential (AP) properties are measured : frequency, amplitude, Threshold, Half duration, max first and second derivative. AP and conductances traces are then saved in a csv file.
504.	Motoneuron pool input-output function (Powers & Heckman 2017)
		"Although motoneurons have often been considered to be fairly linear transducers of synaptic input, recent evidence suggests that strong persistent inward currents (PICs) in motoneurons allow neuromodulatory and inhibitory synaptic inputs to induce large nonlinearities in the relation between the level of excitatory input and motor output. To try to estimate the possible extent of this nonlinearity, we developed a pool of model motoneurons designed to replicate the characteristics of motoneuron input-output properties measured in medial gastrocnemius motoneurons in the decerebrate cat with voltage- clamp and current-clamp techniques. We drove the model pool with a range of synaptic inputs consisting of various mixtures of excitation, inhibition, and neuromodulation. We then looked at the relation between excitatory drive and total pool output. Our results revealed that the PICs not only enhance gain but also induce a strong nonlinearity in the relation between the average firing rate of the motoneuron pool and the level of excitatory input. The relation between the total simulated force output and input was somewhat more linear because of higher force outputs in later-recruited units. ..."
505.	Motor cortex microcircuit simulation based on brain activity mapping (Chadderdon et al. 2014)
		"... We developed a computational model based primarily on a unified set of brain activity mapping studies of mouse M1. The simulation consisted of 775 spiking neurons of 10 cell types with detailed population-to-population connectivity. Static analysis of connectivity with graph-theoretic tools revealed that the corticostriatal population showed strong centrality, suggesting that would provide a network hub. ... By demonstrating the effectiveness of combined static and dynamic analysis, our results show how static brain maps can be related to the results of brain activity mapping."
506.	Motor system model with reinforcement learning drives virtual arm (Dura-Bernal et al 2017)
		"We implemented a model of the motor system with the following components: dorsal premotor cortex (PMd), primary motor cortex (M1), spinal cord and musculoskeletal arm (Figure 1). PMd modulated M1 to select the target to reach, M1 excited the descending spinal cord neurons that drove the arm muscles, and received arm proprioceptive feedback (information about the arm position) via the ascending spinal cord neurons. The large-scale model of M1 consisted of 6,208 spiking Izhikevich model neurons [37] of four types: regular-firing and bursting pyramidal neurons, and fast-spiking and low-threshold-spiking interneurons. These were distributed across cortical layers 2/3, 5A, 5B and 6, with cell properties, proportions, locations, connectivity, weights and delays drawn primarily from mammalian experimental data [38], [39], and described in detail in previous work [29]. The network included 486,491 connections, with synapses modeling properties of four different receptors ..."
507.	Multi-comp. CA1 O-LM interneuron model with varying dendritic Ih distributions (Sekulic et al 2015)
		The model presented here was used to investigate possible dendritic distributions of the HCN channel-mediated current (Ih) in models of oriens-lacunosum/moleculare (O-LM) CA1 hippocampal interneurons. Physiological effects of varying the dendritic distributions consisted of examining back-propagating action potential speeds.
508.	Multi-timescale adaptive threshold model (Kobayashi et al 2009) (NEURON)
		" ... In this study, we devised a simple, fast computational model that can be tailored to any cortical neuron not only for reproducing but also for predicting a variety of spike responses to greatly fluctuating currents. The key features of this model are a multi-timescale adaptive threshold predictor and a nonresetting leaky integrator. This model is capable of reproducing a rich variety of neuronal spike responses, including regular spiking, intrinsic bursting, fast spiking, and chattering, by adjusting only three adaptive threshold parameters. ..."
509.	Multicompartmental cerebellar granule cell model (Diwakar et al. 2009)
		A detailed multicompartmental model was used to study neuronal electroresponsiveness of cerebellar granule cells in rats. Here we show that, in cerebellar granule cells, Na+ channels are enriched in the axon, especially in the hillock, but almost absent from soma and dendrites. Numerical simulations indicated that granule cells have a compact electrotonic structure allowing EPSPs to diffuse with little attenuation from dendrites to axon. The spike arose almost simultaneously along the whole axonal ascending branch and invaded the hillock, whose activation promoted spike back-propagation with marginal delay (<200 micros) and attenuation (<20 mV) into the somato-dendritic compartment. For details check the cited article.
510.	Multiplexed coding in Purkinje neuron dendrites (Zang and De Schutter 2021)
		Neuronal firing patterns are crucial to underpin circuit level behaviors. In cerebellar Purkinje cells (PCs), both spike rates and pauses are used for behavioral coding, but the cellular mechanisms causing code transitions remain unknown. We use a well-validated PC model to explore the coding strategy that individual PCs use to process parallel fiber (PF) inputs. We find increasing input intensity shifts PCs from linear rate-coders to burst-pause timing-coders by triggering localized dendritic spikes. We validate dendritic spike properties with experimental data, elucidate spiking mechanisms, and predict spiking thresholds with and without inhibition. Both linear and burst-pause computations use individual branches as computational units, which challenges the traditional view of PCs as linear point neurons. Dendritic spike thresholds can be regulated by voltage state, compartmentalized channel modulation, between-branch interaction and synaptic inhibition to expand the dynamic range of linear computation or burst-pause computation. In addition, co-activated PF inputs between branches can modify somatic maximum spike rates and pause durations to make them carry analogue signals. Our results provide new insights into the strategies used by individual neurons to expand their capacity of information processing.
511.	Multiplication by NMDA receptors in Direction Selective Ganglion cells (Poleg-Polsky & Diamond 2016)
		The model demonstrates how signal amplification with NMDARs depends on the synaptic environment. When direction selectivity (DS) detection is mediated by DS inhibition, NMDARs multiply other synaptic conductances. In the case of DS tuned excitation, NMDARs contribute additively.
512.	MultiScale Optimized Neuronal Intramembrane Cavitation (SONIC) model (Lemaire et al. 2019)
		Jupyter Notebooks to reproduce data and figures of the SONIC paper (Lemaire et al. 2019) describing a computationally efficient variant to simulate ultrasound neuromodulation by intramembrane cavitation in cortical neurons.
513.	Multiscale simulation of the striatal medium spiny neuron (Mattioni & Le Novere 2013)
		"… We present a new event-driven algorithm to synchronize different neuronal models, which decreases computational time and avoids superfluous synchronizations. The algorithm is implemented in the TimeScales framework. We demonstrate its use by simulating a new multiscale model of the Medium Spiny Neuron of the Neostriatum. The model comprises over a thousand dendritic spines, where the electrical model interacts with the respective instances of a biochemical model. Our results show that a multiscale model is able to exhibit changes of synaptic plasticity as a result of the interaction between electrical and biochemical signaling. …"
514.	Multitarget pharmacology for Dystonia in M1 (Neymotin et al 2016)
		" ... We developed a multiscale model of primary motor cortex, ranging from molecular, up to cellular, and network levels, containing 1715 compartmental model neurons with multiple ion channels and intracellular molecular dynamics. We wired the model based on electrophysiological data obtained from mouse motor cortex circuit mapping experiments. We used the model to reproduce patterns of heightened activity seen in dystonia by applying independent random variations in parameters to identify pathological parameter sets. ..."
515.	Muscle spindle feedback circuit (Moraud et al, 2016)
		Here, we developed a computational model of the muscle spindle feedback circuits of the rat ankle that predicts the interactions between Epidural Stimulation and spinal circuit dynamics during gait.
516.	Myelinated axon conduction velocity (Brill et al 1977)
		Examines conduction velocity as function of internodal length.
517.	MyFirstNEURON (Houweling, Sejnowski 1997)
		MyFirstNEURON is a NEURON demo by Arthur Houweling and Terry Sejnowski. Perform experiments from the book 'Electrophysiology of the Neuron, A Companion to Shepherd's Neurobiology, An Interactive Tutorial' by John Huguenard & David McCormick, Oxford University Press 1997, or design your own one or two cell simulation.
518.	Na+ channel dependence of AP initiation in cortical pyramidal neuron (Kole et al. 2008)
		In this simulation action potential initiation, action potential properties and the role of axon initial segment Na+ channels are investigated in a realistic model of a layer 5 pyramidal neuron axon initial segment. The main Na+ channel properties were constrained by experimental data and the axon initial segment was reconstructed. Model parameters were constrained by direct recordings at the axon initial segment.
519.	Na+ Signals in olfactory bulb neurons (granule cell model) (Ona-Jodar et al. 2017)
		Simulations of Na+ during action potentials in granule cells replicated the behaviors observed in experiments.
520.	NAcc medium spiny neuron: effects of cannabinoid withdrawal (Spiga et al. 2010)
		Cannabinoid withdrawal produces a hypofunction of dopaminergic neurons targeting medium spiny neurons (MSN) of the forebrain. Administration of a CB1 receptor antagonist to control rats provoked structural abnormalities, reminiscent of those observed in withdrawal conditions and support the regulatory role of cannabinoids in neurogenesis, axonal growth and synaptogenesis. Experimental observations were incorporated into a realistic computational model which predicts a strong reduction in the excitability of morphologically-altered MSN, yielding a significant reduction in action potential output. These paper provided direct morphological evidence for functional abnormalities associated with cannabinoid dependence at the level of dopaminergic neurons and their post synaptic counterpart, supporting a hypodopaminergic state as a distinctive feature of the “addicted brain”.
521.	Nav1.6 sodium channel model in globus pallidus neurons (Mercer et al. 2007)
		Model files for the paper Mercer JN, Chan CS, Tkatch T, Held J, Surmeier DJ. Nav1.6 sodium channels are critical to pacemaking and fast spiking in globus pallidus neurons.,J Neurosci. 2007 Dec 5;27(49):13552-66.
522.	Neocort. pyramidal cells subthreshold somatic voltage controls spike propagation (Munro Kopell 2012)
		There is suggestive evidence that pyramidal cell axons in neocortex may be coupled by gap junctions into an ``axonal plexus" capable of generating Very Fast Oscillations (VFOs) with frequencies exceeding 80 Hz. It is not obvious, however, how a pyramidal cell in such a network could control its output when action potentials are free to propagate from the axons of other pyramidal cells into its own axon. We address this problem by means of simulations based on 3D reconstructions of pyramidal cells from rat somatosensory cortex. We show that somatic depolarization enables propagation via gap junctions into the initial segment and main axon, while somatic hyperpolarization disables it. We show further that somatic voltage cannot effectively control action potential propagation through gap junctions on minor collaterals; action potentials may therefore propagate freely from such collaterals regardless of somatic voltage. In previous work, VFOs are all but abolished during the hyperpolarization phase of slow-oscillations induced by anesthesia in vivo. This finding constrains the density of gap junctions on collaterals in our model and suggests that axonal sprouting due to cortical lesions may result in abnormally high gap junction density on collaterals, leading in turn to excessive VFO activity and hence to epilepsy via kindling.
523.	Neocortical Layer I: I-A and I-K (Zhou, Hablitz 1996)
		NEURON mod files for the I-A and I-K currents from the paper: Zhou FM, Hablitz JJ. Layer I neurons of the rat neocortex. II. Voltage-dependent outward currents. J Neurophysiol 1996 76:668-82.
524.	Neocortical pyramidal neuron: deep; effects of dopamine (Durstewitz et al 2000)
		"... Simulated dopamine strongly enhanced high, delay-type activity but not low, spontaneous activity in the model network. Furthermore the strength of an afferent stimulation needed to disrupt delay-type activity increased with the magnitude of the dopamine-induced shifts in network parameters, making the currently active representation much more stable. Stability could be increased by dopamine-induced enhancements of the persistent Na(+) and N-methyl-D-aspartate (NMDA) conductances. Stability also was enhanced by a reduction in AMPA conductances. The increase in GABA(A) conductances that occurs after stimulation of dopaminergic D1 receptors was necessary in this context to prevent uncontrolled, spontaneous switches into high-activity states (i.e., spontaneous activation of task-irrelevant representations). In conclusion, the dopamine-induced changes in the biophysical properties of intrinsic ionic and synaptic conductances conjointly acted to highly increase stability of activated representations in PFC networks and at the same time retain control over network behavior and thus preserve its ability to adequately respond to task-related stimuli. ..." See paper and references for more and details.
525.	Nerve terminal currents at lizard neuromuscular junction (Lindgren, Moore 1989)
		Loose patch clamp measurement of presynaptic ionic currents at lizard neuromuscular junction compared with computer simulations.
526.	Network recruitment to coherent oscillations in a hippocampal model (Stacey et al. 2011)
		"... Here we demonstrate, via a detailed computational model, a mechanism whereby physiological noise and coupling initiate oscillations and then recruit neighboring tissue, in a manner well described by a combination of Stochastic Resonance and Coherence Resonance. We develop a novel statistical method to quantify recruitment using several measures of network synchrony. This measurement demonstrates that oscillations spread via preexisting network connections such as interneuronal connections, recurrent synapses, and gap junctions, provided that neighboring cells also receive sufficient inputs in the form of random synaptic noise. ..."
527.	Networks of spiking neurons: a review of tools and strategies (Brette et al. 2007)
		This package provides a series of codes that simulate networks of spiking neurons (excitatory and inhibitory, integrate-and-fire or Hodgkin-Huxley type, current-based or conductance-based synapses; some of them are event-based). The same networks are implemented in different simulators (NEURON, GENESIS, NEST, NCS, CSIM, XPP, SPLIT, MVAspike; there is also a couple of implementations in SciLab and C++). The codes included in this package are benchmark simulations; see the associated review paper (Brette et al. 2007). The main goal is to provide a series of benchmark simulations of networks of spiking neurons, and demonstrate how these are implemented in the different simulators overviewed in the paper. See also details in the enclosed file Appendix2.pdf, which describes these different benchmarks. Some of these benchmarks were based on the Vogels-Abbott model (Vogels TP and Abbott LF 2005).
528.	Neural Query System NQS Data-Mining From Within the NEURON Simulator (Lytton 2006)
		NQS is a databasing program with a query command modeled loosely on the SQL select command. Please see the manual NQS.pdf for details of use. An NQS database must be populated with data to be used. This package includes MFP (model fingerprint) which provides an example of NQS use with the model provided in the modeldb folder (see readme for usage).
529.	NeuroGPU example on L5_TTPC1_cADpyr232_1 (Ben-Shalom 2022)(Ramaswamy et al., 2015)
		This shows an example use case of building NeuroGPU simulation around a model pyramidal cell from the BBP portal. While the simulation can be run without python, we show how to update the parameters and run the simulation in python.
530.	Neuromusculoskeletal modeling with neural and finite element models (Volk et al, 2021)
		"In this study, we present a predictive NMS model that uses an embedded neural architecture within a finite element (FE) framework to simulate muscle activation. A previously developed neuromuscular model of a motor neuron was embedded into a simple FE musculoskeletal model. Input stimulation profiles from literature were simulated in the FE NMS model to verify effective integration of the software platforms. Motor unit recruitment and rate coding capabilities of the model were evaluated. The integrated model reproduced previously published output muscle forces with an average error of 0.0435 N. The integrated model effectively demonstrated motor unit recruitment and rate coding in the physiological range based upon motor unit discharge rates and muscle force output."
531.	NEURON + Python (Hines et al. 2009)
		The NEURON simulation program now allows Python to be used alone or in combination with NEURON's traditional Hoc interpreter. Adding Python to NEURON has the immediate benefit of making available a very extensive suite of analysis tools written for engineering and science. It also catalyzes NEURON software development by offering users a modern programming tool that is recognized for its flexibility and power to create and maintain complex programs. At the same time, nothing is lost because all existing models written in Hoc, including GUI tools, continue to work without change and are also available within the Python context. An example of the benefits of Python availability is the use of the xml module in implementing NEURON's Import3D and CellBuild tools to read MorphML and NeuroML model specifications.
532.	NEURON interfaces to MySQL and the SPUD feature extraction algorithm (Neymotin et al. 2008)
		See the readme.txt for information on setting up this interface to a MySQL server from the NEURON simulator. Note the SPUD feature extraction algorithm includes its own readme in the spud directory.
533.	Neuronal dendrite calcium wave model (Neymotin et al, 2015)
		"... We developed a reaction-diffusion model of an apical dendrite with diffusible inositol triphosphate (IP3 ), diffusible Ca2+, IP3 receptors (IP3 Rs), endoplasmic reticulum (ER) Ca2+ leak, and ER pump (SERCA) on ER. ... At least two modes of Ca2+ wave spread have been suggested: a continuous mode based on presumed relative homogeneity of ER within the cell; and a pseudo-saltatory model where Ca2+ regeneration occurs at discrete points with diffusion between them. We compared the effects of three patterns of hypothesized IP3 R distribution: 1. continuous homogeneous ER, 2. hotspots with increased IP3R density (IP3 R hotspots), 3. areas of increased ER density (ER stacks). All three modes produced Ca2+ waves with velocities similar to those measured in vitro (~50 - 90µm /sec). ... The measures were sensitive to changes in density and spacing of IP3 R hotspots and stacks. ... An extended electrochemical model, including voltage gated calcium channels and AMPA synapses, demonstrated that membrane priming via AMPA stimulation enhances subsequent Ca2+ wave amplitude and duration. Our modeling suggests that pharmacological targeting of IP3 Rs and SERCA could allow modulation of Ca2+ wave propagation in diseases where Ca2+ dysregulation has been implicated. "
534.	Neuronal morphology goes digital ... (Parekh & Ascoli 2013)
		An illustration of a NEURON model and why reconstructing morphologies is useful in this regard (i.e. investigating spatial/temporal aspect of how different currents and voltage propagate in dendrites).
535.	Neurophysiological impact of inactivation pathways in A-type K+ channels (Fineberg et al 2012)
		These models predict the differential effects of varying pathways of inactivation (closed state inactivation, CSI, or open state inactivation, OSI). Specifically, Markov models of Kv4 potassium channels with CSI or CSI+OSI were inserted into the CA1 pyramidal neuron model from Migliore et al (1999; ModelDB accession #2796) to determine the neurophysiological impact of inactivation pathways. Furthermore, Markov models of Kv4.2 and Kv3.4 channels are used to illustrate a method by which to test what pathway of inactivation a channel uses.
536.	Nigral dopaminergic neurons: effects of ethanol on Ih (Migliore et al. 2008)
		We use a realistic computational model of dopaminergic neurons in vivo to suggest that ethanol, through its effects on Ih, modifies the temporal structure of the spiking activity. The model predicts that the dopamine level may increase much more during bursting than pacemaking activity, especially in those brain regions with a slow dopamine clearance rate. The results suggest that a selective pharmacological remedy could thus be devised against the rewarding effects of ethanol that are postulated to mediate alcohol abuse and addiction, targeting the specific HCN genes expressed in dopaminergic neurons.
537.	NMDA receptor saturation (Chen et al 2001)
		Experiments and modeling reported in the paper Chen N, Ren J, Raymond LA, and Murphy T (2001) support the hypothesis that glutamate has a relatively lower potency at NMDARs than previously thought from agonist application under equilibrium conditions. Further information and reprint requests are available from Dr T.H. Murphy thmurphy at interchange.ubc.ca
538.	NMDA receptors enhance the fidelity of synaptic integration (Li and Gulledge 2021)
		Excitatory synaptic transmission in many neurons is mediated by two co-expressed ionotropic glutamate receptor subtypes, AMPA and NMDA receptors, that differ in their kinetics, ion-selectivity, and voltage-sensitivity. AMPA receptors have fast kinetics and are voltage-insensitive, while NMDA receptors have slower kinetics and increased conductance at depolarized membrane potentials. Here we report that the voltage-dependency and kinetics of NMDA receptors act synergistically to stabilize synaptic integration of excitatory postsynaptic potentials (EPSPs) across spatial and voltage domains. Simulations of synaptic integration in simplified and morphologically realistic dendritic trees revealed that the combined presence of AMPA and NMDA conductances reduces the variability of somatic responses to spatiotemporal patterns of excitatory synaptic input presented at different initial membrane potentials and/or in different dendritic domains. This moderating effect of the NMDA conductance on synaptic integration was robust across a wide range of AMPA-to-NMDA ratios, and results from synergistic interaction of NMDA kinetics (which reduces variability across membrane potential) and voltage-dependence (which favors stabilization across dendritic location). When combined with AMPA conductance, the NMDA conductance balances voltage- and impedance-dependent changes in synaptic driving force, and distance-dependent attenuation of synaptic potentials arriving at the axon, to increase the fidelity of synaptic integration and EPSP-spike coupling across neuron state (i.e., initial membrane potential) and dendritic location of synaptic input. Thus, synaptic NMDA receptors convey advantages for synaptic integration that are independent of, but fully compatible with, their importance for coincidence detection and synaptic plasticity.
539.	NMDA spikes in basal dendrites of L5 pyramidal neurons (Polsky et al. 2009)
		"... In apical dendrites of neocortical pyramidal neurons, calcium spikes are known to contribute to burst generation, but a comparable understanding of basal dendritic mechanisms is lacking. Here we show that NMDA spikes in basal dendrites mediate both detection and generation of bursts through a postsynaptic mechanism. High-frequency inputs to basal dendrites markedly facilitated NMDA spike initiation compared with low-frequency activation or single inputs. ..."
540.	NN activity impact on neocortical pyr. neurons integrative properties in vivo (Destexhe & Pare 1999)
		"During wakefulness, neocortical neurons are subjected to an intense synaptic bombardment. To assess the consequences of this background activity for the integrative properties of pyramidal neurons, we constrained biophysical models with in vivo intracellular data obtained in anesthetized cats during periods of intense network activity similar to that observed in the waking state. In pyramidal cells of the parietal cortex (area 5–7), synaptic activity was responsible for an approximately fivefold decrease in input resistance (Rin), a more depolarized membrane potential (Vm), and a marked increase in the amplitude of Vm fluctuations, as determined by comparing the same cells before and after microperfusion of tetrodotoxin (TTX). ..."
541.	Nonlinear dendritic processing in barrel cortex spiny stellate neurons (Lavzin et al. 2012)
		This is a multi-compartmental simulation of a spiny stellate neuron which is stimulated by a thalamocortical (TC) and cortico-cortical (CC) inputs. No other cells are explicitly modeled; the presynaptic network activation is represented by the number of active synapses. Preferred and non –preferred thalamic directions thus correspond to larder/smaller number of TC synapses. This simulation revealed that randomly activated synapses can cooperatively trigger global NMDA spikes, which involve participation of most of the dendritic tree. Surprisingly, we found that although the voltage profile of the cell was uniform, the calcium influx was restricted to ‘hot spots’ which correspond to synaptic clusters or large conductance synapses
542.	Norepinephrine stimulates glycogenolysis in astrocytes to fuel neurons (Coggan et al 2018)
		"The mechanism of rapid energy supply to the brain, especially to accommodate the heightened metabolic activity of excited states, is not well-understood. We explored the role of glycogen as a fuel source for neuromodulation using the noradrenergic stimulation of glia in a computational model of the neural-glial-vasculature ensemble (NGV). The detection of norepinephrine (NE) by the astrocyte and the coupled cAMP signal are rapid and largely insensitive to the distance of the locus coeruleus projection release sites from the glia, implying a diminished impact for volume transmission in high affinity receptor transduction systems. Glucosyl-conjugated units liberated from glial glycogen by NE-elicited cAMP second messenger transduction winds sequentially through the glycolytic cascade, generating robust increases in NADH and ATP before pyruvate is finally transformed into lactate. This astrocytic lactate is rapidly exported by monocarboxylate transporters to the associated neuron, demonstrating that the astrocyte-to-neuron lactate shuttle activated by glycogenolysis is a likely fuel source for neuromodulation and enhanced neural activity. Altogether, the energy supply for both astrocytes and neurons can be supplied rapidly by glycogenolysis upon neuromodulatory stimulus."
543.	Normal ripples, abnormal ripples, and fast ripples in a hippocampal model (Fink et al. 2015)
		"...We use a computational model of hippocampus to investigate possible network mechanisms underpinning normal ripples, pathological ripples, and fast ripples. Our results unify several prior findings regarding HFO mechanisms, and also make several new predictions regarding abnormal HFOs. We show that HFOs are generic, emergent phenomena whose characteristics reflect a wide range of connectivity and network input. Although produced by different mechanisms, both normal and abnormal HFOs generate similar ripple frequencies, underscoring that peak frequency is unable to distinguish the two. Abnormal ripples are generic phenomena that arise when input to pyramidal cells overcomes network inhibition, resulting in high-frequency, uncoordinated firing. In addition, fast ripples transiently and sporadically arise from the precise conditions that produce abnormal ripples. Lastly, we show that such abnormal conditions do not require any specific network structure to produce coherent HFOs, as even completely asynchronous activity is capable of producing abnormal ripples and fast ripples in this manner. These results provide a generic, network-based explanation for the link between pathological ripples and fast ripples, and a unifying description for the entire spectrum from normal ripples to pathological fast ripples."
544.	Novel Na current with slow de-inactivation (Tsutsui, Oka 2002)
		The authors found a novel Na current in teleost thalamic nuclei was well described by the m^3 h Hodgkin-Huxley model. The kinetic parameters derived from their experiments (see the reference for details) revealed that the h gate had a large time constant (~100ms at -80 to -50mV). This explains the thalamic neurons long refractory period and the gradual recovery of AP amplitude as the inter spike interval grows.
545.	O-LM interneuron model (Lawrence et al. 2006)
		Exploring the kinetics and distribution of the muscarinic potassium channel, IM, in 2 O-LM interneuron morphologies. Modulation of the ion channel by drugs such as XE991 (antagonist) and retigabine (agonist) are simulated in the models to examine the role of IM in spiking properties.
546.	Olfactory bulb cluster formation (Migliore et al. 2010)
		Functional roles of distributed synaptic clusters in the mitral-granule cell network of the olfactory bulb.
547.	Olfactory bulb granule cell: effects of odor deprivation (Saghatelyan et al 2005)
		The model supports the experimental findings on the effects of postnatal odor deprivation, and shows that a -10mV shift in the Na activation or a reduction in the dendritic length of newborn GC could independently explain the observed increase in excitability.
548.	Olfactory bulb mitral and granule cell column formation (Migliore et al. 2007)
		In the olfactory bulb, the processing units for odor discrimination are believed to involve dendrodendritic synaptic interactions between mitral and granule cells. There is increasing anatomical evidence that these cells are organized in columns, and that the columns processing a given odor are arranged in widely distributed arrays. Experimental evidence is lacking on the underlying learning mechanisms for how these columns and arrays are formed. We have used a simplified realistic circuit model to test the hypothesis that distributed connectivity can self-organize through an activity-dependent dendrodendritic synaptic mechanism. The results point to action potentials propagating in the mitral cell lateral dendrites as playing a critical role in this mechanism, and suggest a novel and robust learning mechanism for the development of distributed processing units in a cortical structure.
549.	Olfactory bulb mitral and granule cell: dendrodendritic microcircuits (Migliore and Shepherd 2008)
		This model shows how backpropagating action potentials in the long lateral dendrites of mitral cells, together with granule cell actions on mitral cells within narrow columns forming glomerular units, can provide a mechanism to activate strong local inhibition between arbitrarily distant mitral cells. The simulations predict a new role for the dendrodendritic synapses in the multicolumnar organization of the granule cells.
550.	Olfactory bulb mitral cell gap junction NN model: burst firing and synchrony (O`Connor et al. 2012)
		In a network of 6 mitral cells connected by gap junction in the apical dendrite tuft, continuous current injections of 0.06 nA are injected into 20 locations in the apical tufts of two of the mitral cells. The current injections into one of the cells starts 10 ms after the other to generate asynchronous firing in the cells (Migliore et al. 2005 protocol). Firing of the cells is asynchronous for the first 120 ms. However after the burst firing phase is completed the firing in all cells becomes synchronous.
551.	Olfactory bulb mitral cell: synchronization by gap junctions (Migliore et al 2005)
		In a realistic model of two electrically connected mitral cells, the paper shows that the somatically-measured experimental properties of Gap Junctions (GJs) may correspond to a variety of different local coupling strengths and dendritic distributions of GJs in the tuft. The model suggests that the propagation of the GJ-induced local tuft depolarization is a major mechanim for intraglomerular synchronization of mitral cells.
552.	Olfactory Bulb Network (Davison et al 2003)
		A biologically-detailed model of the mammalian olfactory bulb, incorporating the mitral and granule cells and the dendrodendritic synapses between them. The results of simulation experiments with electrical stimulation agree closely in most details with published experimental data. The model predicts that the time course of dendrodendritic inhibition is dependent on the network connectivity as well as on the intrinsic parameters of the synapses. In response to simulated odor stimulation, strongly activated mitral cells tend to suppress neighboring cells, the mitral cells readily synchronize their firing, and increasing the stimulus intensity increases the degree of synchronization. For more details, see the reference below.
553.	Olfactory Computations in Mitral-Granule cell circuits (Migliore & McTavish 2013)
		Model files for the entry "Olfactory Computations in Mitral-Granule Cell Circuits" of the Springer Encyclopedia of Computational Neuroscience by Michele Migliore and Tom Mctavish. The simulations illustrate two typical Mitral-Granule cell circuits in the olfactory bulb of vertebrates: distance-independent lateral inhibition and gating effects.
554.	Olfactory Mitral Cell (Bhalla, Bower 1993)
		This is a conversion to NEURON of the mitral cell model described in Bhalla and Bower (1993). The original model was written in GENESIS and is available by joining BABEL, the GENESIS users' group here http://www.genesis-sim.org/GENESIS/babel.html
555.	Olfactory Mitral Cell (Davison et al 2000)
		A four-compartment model of a mammalian olfactory bulb mitral cell, reduced from the complex 286-compartment model described by Bhalla and Bower (1993). The compartments are soma/axon, secondary dendrites, primary dendrite shaft and primary dendrite tuft. The reduced model runs 75 or more times faster than the full model, making its use in large, realistic network models of the olfactory bulb practical.
556.	Olfactory Mitral cell: AP initiation modes (Chen et al 2002)
		The mitral cell primary dendrite plays an important role in transmitting distal olfactory nerve input from olfactory glomerulus to the soma-axon initial segment. To understand how dendritic active properties are involved in this transmission, we have combined dual soma and dendritic patch recordings with computational modeling to analyze action-potential initiation and propagation in the primary dendrite.
557.	Olfactory Mitral Cell: I-A and I-K currents (Wang et al 1996)
		NEURON mod files for the I-A and I-K currents from the paper: X.Y. Wang, J.S. McKenzie and R.E. Kemm, Whole-cell K+ currents in identified olfactory bulb output neurones of rats. J Physiol. 1996 490.1:63-77. Please see the readme.txt included in the model file for more information.
558.	Olfactory Periglomerular Cells: I-h kinetics (Cadetti, Belluzzi 2001)
		NEURON mod files for the Ih current from the paper: Cadetti L, Belluzzi O. Hyperpolarisation-activated current in glomerular cells of the rat olfactory bulb. Neuroreport 12:3117-20 (2001).
559.	Optical stimulation of a channelrhodopsin-2 positive pyramidal neuron model (Foutz et al 2012)
		A computational tool to explore the underlying principles of optogenetic neural stimulation. This "light-neuron" model consists of theoretical representations of the light dynamics generated by a fiber optic in brain tissue, coupled to a multicompartment cable model of a cortical pyramidal neuron (Hu et al. 2009, ModelDB #123897) embedded with channelrhodopsin-2 (ChR2) membrane dynamics. Simulations predict that the activation threshold is sensitive to many of the properties of ChR2 (density, conductivity, and kinetics), tissue medium (scattering and absorbance), and the fiber-optic light source (diameter and numerical aperture). This model system represents a scientific instrument to characterize the effects of optogenetic neuromodulation, as well as an engineering design tool to help guide future development of optogenetic technology.
560.	Optimal balance predicts/explains amplitude and decay time of iPSGs (Kim & Fiorillo 2017)
		"Synaptic inhibition counterbalances excitation, but it is not known what constitutes optimal inhibition. We previously proposed that perfect balance is achieved when the peak of an excitatory postsynaptic potential (EPSP) is exactly at spike threshold, so that the slightest variation in excitation determines whether a spike is generated. Using simulations, we show that the optimal inhibitory postsynaptic conductance (IPSG) increases in amplitude and decay rate as synaptic excitation increases from 1 to 800 Hz. As further proposed by theory, we show that optimal IPSG parameters can be learned through anti-Hebbian rules. ..."
561.	Orientation preference in L23 V1 pyramidal neurons (Park et al 2019)
		"Pyramidal neurons integrate synaptic inputs from basal and apical dendrites to generate stimulus-specific responses. It has been proposed that feed-forward inputs to basal dendrites drive a neuron’s stimulus preference, while feedback inputs to apical dendrites sharpen selectivity. However, how a neuron’s dendritic domains relate to its functional selectivity has not been demonstrated experimentally. We performed 2-photon dendritic micro-dissection on layer-2/3 pyramidal neurons in mouse primary visual cortex. We found that removing the apical dendritic tuft did not alter orientation-tuning. Furthermore, orientation-tuning curves were remarkably robust to the removal of basal dendrites: ablation of 2 basal dendrites was needed to cause a small shift in orientation preference, without significantly altering tuning width. Computational modeling corroborated our results and put limits on how orientation preferences among basal dendrites differ in order to reproduce the post-ablation data. In conclusion, neuronal orientation-tuning appears remarkably robust to loss of dendritic input."
562.	Oscillating neurons in the cochlear nucleus (Bahmer Langner 2006a, b, and 2007)
		"Based on the physiological and anatomical data, we propose a model consisting of a minimum network of two choppers that are interconnected with a synaptic delay of 0.4 ms (Bahmer and Langner 2006a) . Such minimum delays have been found in different systems and in various animals (e.g. Hackett, Jackson, and Rubel 1982; Borst, Helmchen, and Sakmann 1995). The choppers receive input from both the auditory nerve and an onset neuron. This model can reproduce the mean, standard deviation, and coefficient of variation of the ISI and the dynamic features of AM coding of choppers."
563.	Paradoxical effect of fAHP amplitude on gain in dentate gyrus granule cells (Jaffe & Brenner 2018)
		The afterhyperpolarization (AHP) is canonically viewed as a major factor underlying the refractory period, serving to limit neuronal firing rate. We recently reported (Wang et al, J. Neurophys. 116:456, 2016) that enhancing the amplitude of the fast AHP in a relatively slowly firing neuron (versus fast spiking neurons), augments neuronal excitability in dentate gyrus granule neurons expressing gain-of-function BK channels. Here we present a novel, quantitative hypothesis for how varying the amplitude of the fast AHP (fAHP) can, paradoxically, influence a subsequent spike tens of milliseconds later.
564.	Parallel network simulations with NEURON (Migliore et al 2006)
		The NEURON simulation environment has been extended to support parallel network simulations. The performance of three published network models with very different spike patterns exhibits superlinear speedup on Beowulf clusters.
565.	Parallel odor processing by mitral and middle tufted cells in the OB (Cavarretta et al 2016, 2018)
		"[...] experimental findings suggest that MC and mTC may encode parallel and complementary odor representations. We have analyzed the functional roles of these pathways by using a morphologically and physiologically realistic three-dimensional model to explore the MC and mTC microcircuits in the glomerular layer and deeper plexiform layers. [...]"
566.	Parallelizing large networks in NEURON (Lytton et al. 2016)
		"Large multiscale neuronal network simulations and innovative neurotechnologies are required for development of these models requires development of new simulation technologies. We describe here the current use of the NEURON simulator with MPI (message passing interface) for simulation in the domain of moderately large networks on commonly available High Performance Computers (HPCs). We discuss the basic layout of such simulations, including the methods of simulation setup, the run-time spike passing paradigm and post-simulation data storage and data management approaches. We also compare three types of networks, ..."
567.	Parametric computation and persistent gamma in a cortical model (Chambers et al. 2012)
		Using the Traub et al (2005) model of the cortex we determined how 33 synaptic strength parameters control gamma oscillations. We used fractional factorial design to reduce the number of runs required to 4096. We found an expected multiplicative interaction between parameters.
568.	Parvalbumin-positive basket cells differentiate among hippocampal pyramidal cells (Lee et al. 2014)
		This detailed microcircuit model explores the network level effects of sublayer specific connectivity in the mouse CA1. The differences in strengths and numbers of synapses between PV+ basket cells and either superficial sublayer or deep sublayer pyramidal cells enables a routing of inhibition from superficial to deep pyramidal cells. At the network level of this model, the effects become quite prominent when one compares the effect on firing rates when either the deep or superficial pyramidal cells receive a selective increase in excitation.
569.	Phase response curve of a globus pallidal neuron (Fujita et al. 2011)
		We investigated how changes in ionic conductances alter the phase response curve (PRC) of a globus pallidal (GP) neuron and stability of a synchronous activity of a GP network, using a single-compartmental conductance-based neuron model. The results showed the PRC and the stability were influenced by changes in the persistent sodium current, the Kv3 potassium, the M-type potassium and the calcium-dependent potassium current.
570.	Phase response curves firing rate dependency of rat purkinje neurons in vitro (Couto et al 2015)
		NEURON implementation of stochastic gating in the Khaliq-Raman Purkinje cell model. NEURON implementation of the De Schutter and Bower model of a Purkinje Cell. Matlab scripts to compute the Phase Response Curve (PRC). LCG configuration files to experimentally determine the PRC. Integrate and Fire models (leaky and non-leaky) implemented in BRIAN to see the influence of the PRC in a network of unconnected neurons receiving sparse common input.
571.	Phase response theory in sparsely + strongly connected inhibitory NNs (Tikidji-Hamburyan et al 2019)
572.	Phenomenological models of NaV1.5: Hodgkin-Huxley and kinetic formalisms (Andreozzi et al 2019)
		"Computational models of ion channels represent the building blocks of conductance-based, biologically inspired models of neurons and neural networks. Ion channels are still widely modelled by means of the formalism developed by the seminal work of Hodgkin and Huxley (HH), although the electrophysiological features of the channels are currently known to be better fitted by means of kinetic Markov-type models. The present study is aimed at showing why simplified Markov-type kinetic models are more suitable for ion channels modelling as compared to HH ones, and how a manual optimization process can be rationally carried out for both. ..."
573.	PIR gamma oscillations in network of resonators (Tikidji-Hamburyan et al. 2015)
		" ... The coupled oscillator model implemented with Wang–Buzsaki model neurons is not sufficiently robust to heterogeneity in excitatory drive, and therefore intrinsic frequency, to account for in vitro models of ING. Similarly, in a tightly synchronized regime, the stochastic population oscillator model is often characterized by sparse firing, whereas interneurons both in vivo and in vitro do not fire sparsely during gamma,but rather on average every other cycle. We substituted so-called resonator neural models, which exhibit class 2 excitability and postinhibitory rebound (PIR), for the integrators that are typically used. This results in much greater robustness to heterogeneity that actually increases as the average participation in spikes per cycle approximates physiological levels. Moreover, dynamic clamp experiments that show autapse-induced firing in entorhinal cortical interneurons support the idea that PIR can serve as a network gamma mechanism. ..."
574.	Pleiotropic effects of SCZ-associated genes (Mäki-Marttunen et al. 2017)
		Python and MATLAB scripts for studying the dual effects of SCZ-related genes on layer 5 pyramidal cell firing and sinoatrial node cell pacemaking properties. The study is based on two L5PC models (Hay et al. 2011, Almog & Korngreen 2014) and SANC models (Kharche et al. 2011, Severi et al. 2012).
575.	Potjans-Diesmann cortical microcircuit model in NetPyNE (Romaro et al 2021)
		The Potjans-Diesmann cortical microcircuit model is a widely used model originally implemented in NEST. Here, we re-implemented the model using NetPyNE, a high-level Python interface to the NEURON simulator, and reproduced the findings of the original publication. We also implemented a method for rescaling the network size which preserves first and second order statistics, building on existing work on network theory. The new implementation enables using more detailed neuron models with multicompartment morphologies and multiple biophysically realistic channels. This opens the model to new research, including the study of dendritic processing, the influence of individual channel parameters, and generally multiscale interactions in the network. The rescaling method provides flexibility to increase or decrease the network size if required when running these more realistic simulations. Finally, NetPyNE facilitates modifying or extending the model using its declarative language; optimizing model parameters; running efficient large-scale parallelized simulations; and analyzing the model through built-in methods, including local field potential calculation and information flow measures.
576.	pre-Bötzinger complex variability (Fietkiewicz et al. 2016)
		" ... Based on experimental observations, we developed a computational model that can be embedded in more comprehensive models of respiratory and cardiovascular autonomic control. Our simulation results successfully reproduce the variability we observed experimentally. The in silico model suggests that age-dependent variability may be due to a developmental increase in mean synaptic conductance between preBötC neurons. We also used simulations to explore the effects of stochastic spiking in sensory relay neurons. Our results suggest that stochastic spiking may actually stabilize modulation of both respiratory rate and its variability when the rate changes due to physiological demand. "
577.	Preserving axosomatic spiking features despite diverse dendritic morphology (Hay et al., 2013)
		The authors found that linearly scaling the ion channel conductance densities of a reference model with the conductance load in 28 3D reconstructed layer 5 thick-tufted pyramidal cells was necessary to match the experimental statistics of these cells electrical firing properties.
578.	Presynaptic calcium dynamics at neuromuscular junction (Stockbridge, Moore 1984)
		The diffusion of calcium is effectively reduced by the ratio of bound to free calcium. Treating the release magnitude as proportional to the fourth power of calcium concentration next to the membrane gives reasonable facilitation with very little release between spikes.
579.	Principles governing the operation of synaptic inhibition in dendrites (Gidon & Segev 2012)
		A simple result of Gidon & Segev 2012 was provided where distal (off-path) inhibition is demonstrated to be more effective than proximal (on-path) inhibition in a ball and stick neuron.
580.	Prosthetic electrostimulation for information flow repair in a neocortical simulation (Kerr 2012)
		This model is an extension of a model ( http://modeldb.yale.edu/138379 ) recently published in Frontiers in Computational Neuroscience. This model consists of 4700 event-driven, rule-based neurons, wired according to anatomical data, and driven by both white-noise synaptic inputs and a sensory signal recorded from a rat thalamus. Its purpose is to explore the effects of cortical damage, along with the repair of this damage via a neuroprosthesis.
581.	Purkinje cell: Synaptic activation predicts voltage control of burst-pause (Masoli & D'Angelo 2017)
		"The dendritic processing in cerebellar Purkinje cells (PCs), which integrate synaptic inputs coming from hundreds of thousands granule cells and molecular layer interneurons, is still unclear. Here we have tested a leading hypothesis maintaining that the significant PC output code is represented by burst-pause responses (BPRs), by simulating PC responses in a biophysically detailed model that allowed to systematically explore a broad range of input patterns. BPRs were generated by input bursts and were more prominent in Zebrin positive than Zebrin negative (Z+ and Z-) PCs. Different combinations of parallel fiber and molecular layer interneuron synapses explained type I, II and III responses observed in vivo. BPRs were generated intrinsically by Ca-dependent K channel activation in the somato-dendritic compartment and the pause was reinforced by molecular layer interneuron inhibition. BPRs faithfully reported the duration and intensity of synaptic inputs, such that synaptic conductance tuned the number of spikes and release probability tuned their regularity in the millisecond range. ..."
582.	Purkinje neuron network (Zang et al. 2020)
		Both spike rate and timing can transmit information in the brain. Phase response curves (PRCs) quantify how a neuron transforms input to output by spike timing. PRCs exhibit strong firing-rate adaptation, but its mechanism and relevance for network output are poorly understood. Using our Purkinje cell (PC) model we demonstrate that the rate adaptation is caused by rate-dependent subthreshold membrane potentials efficiently regulating the activation of Na+ channels. Then we use a realistic PC network model to examine how rate-dependent responses synchronize spikes in the scenario of reciprocal inhibition-caused high-frequency oscillations. The changes in PRC cause oscillations and spike correlations only at high firing rates. The causal role of the PRC is confirmed using a simpler coupled oscillator network model. This mechanism enables transient oscillations between fast-spiking neurons that thereby form PC assemblies. Our work demonstrates that rate adaptation of PRCs can spatio-temporally organize the PC input to cerebellar nuclei.
583.	Pyramidal neuron coincidence detection tuned by dendritic branching pattern (Schaefer et al 2003)
		"... We examined the relationship between dendritic arborization and the coupling between somatic and dendritic action potential (AP) initiation sites in layer 5 (L5) neocortical pyramidal neurons. Coupling was defined as the relative reduction in threshold for initiation of a dendritic calcium AP due to a coincident back-propagating AP. Simulations based on reconstructions of biocytin-filled cells showed that addition of oblique branches of the main apical dendrite in close proximity to the soma (d < 140 um) increases the coupling between the apical and axosomatic AP initiation zones, whereas incorporation of distal branches decreases coupling. ... We conclude that variation in dendritic arborization may be a key determinant of variability in coupling (49+-17%; range 19-83%; n = 37) and is likely to outweigh the contribution made by variations in active membrane properties. Thus coincidence detection of inputs arriving from different cortical layers is strongly regulated by differences in dendritic arborization."
584.	Pyramidal neuron conductances state and STDP (Delgado et al. 2010)
		Neocortical neurons in vivo process each of their individual inputs in the context of ongoing synaptic background activity, produced by the thousands of presynaptic partners a typical neuron has. That background activity affects multiple aspects of neuronal and network function. However, its effect on the induction of spike-timing dependent plasticity (STDP) is not clear. Using the present biophysically-detailed computational model, it is not only able to replicate the conductance-dependent shunting of dendritic potentials (Delgado et al,2010), but show that synaptic background can truncate calcium dynamics within dendritic spines, in a way that affects potentiation more strongly than depression. This program uses a simplified layer 2/3 pyramidal neuron constructed in NEURON. It was similar to the model of Traub et al., J Neurophysiol. (2003), and consisted of a soma, an apical shaft, distal dendrites, five basal dendrites, an axon, and a single spine. The spine’s location was variable along the apical shaft (initial 50 &#956;m) and apical. The axon contained an axon hillock region, an initial segment, segments with myelin, and nodes of Ranvier, in order to have realistic action potential generation. For more information about the model see supplemental material, Delgado et al 2010.
585.	Pyramidal Neuron Deep: attenuation in dendrites (Stuart, Spruston 1998)
		Stuart, G. and Spruston, N. Determinants of voltage attenuation in neocortical pyramidal neuron dendrites. Journal of Neuroscience 18:3501-3510, 1998.
586.	Pyramidal Neuron Deep: K+ kinetics (Korngreen, Sakmann 2000)
		NEURON mod files for the slow and fast K+ currents from the paper: Voltage-gated K+ channels in layer 5 neocortical pyramidal neurones from young rats: subtypes and gradients A. Korngreen and B. Sakmann, J.Physiol. 525.3, 621-639 (2000).
587.	Pyramidal neuron, fast, regular, and irregular spiking interneurons (Konstantoudaki et al 2014)
		This is a model network of prefrontal cortical microcircuit based primarily on rodent data. It includes 16 pyramidal model neurons, 2 fast spiking interneuron models, 1 regular spiking interneuron model and 1 irregular spiking interneuron model. The goal of the paper was to use this model network to determine the role of specific interneuron subtypes in persistent activity
588.	Pyramidal Neuron: Deep, Thalamic Relay and Reticular, Interneuron (Destexhe et al 1998, 2001)
		This package shows single-compartment models of different classes of cortical neurons, such as the "regular-spiking", "fast-spiking" and "bursting" (LTS) neurons. The mechanisms included are the Na+ and K+ currents for generating action potentials (INa, IKd), the T-type calcium current (ICaT), and a slow voltage-dependent K+ current (IM). See http://cns.fmed.ulaval.ca/alain_demos.html
589.	Pyramidal neurons with mutated SCN2A gene (Nav1.2) (Ben-Shalom et al 2017)
		Model of pyramidal neurons that either hyper or hypo excitable due to SCN2A mutations. Mutations are taken from patients with ASD or Epilepsy
590.	Rat LGN Thalamocortical Neuron (Connelly et al 2015, 2016)
		" ... Here, combining data from fluorescence-targeted dendritic recordings and Ca2+ imaging from low-threshold spiking cells in rat brain slices with computational modeling, the cellular mechanism responsible for LTS (Low Threshold Spike) generation is established. ..." " ... Using dendritic recording, 2-photon glutamate uncaging, and computational modeling, we investigated how rat dorsal lateral geniculate nucleus thalamocortical neurons integrate excitatory corticothalamic feedback. ..."
591.	Rat subthalamic projection neuron (Gillies and Willshaw 2006)
		A computational model of the rat subthalamic nucleus projection neuron is constructed using electrophysiological and morphological data and a restricted set of channel specifications. The model cell exhibits a wide range of electrophysiological behaviors characteristic of rat subthalamic neurons. It reveals that a key set of three channels play a primary role in distinguishing behaviors: a high-voltage-activated calcium channel (Cav 1.2.-1.3), a low-voltage-activated calcium channel (Cav 3.-), and a small current calcium-activated potassium channel (KCa 2.1-2.3). See paper for more and details.
592.	Reaction-diffusion in the NEURON simulator (McDougal et al 2013)
		"In order to support research on the role of cell biological principles (genomics, proteomics, signaling cascades and reaction dynamics) on the dynamics of neuronal response in health and disease, NEURON's Reaction-Diffusion (rxd) module in Python provides specification and simulation for these dynamics, coupled with the electrophysiological dynamics of the cell membrane. Arithmetic operations on species and parameters are overloaded, allowing arbitrary reaction formulas to be specified using Python syntax. These expressions are then transparently compiled into bytecode that uses NumPy for fast vectorized calculations. At each time step, rxd combines NEURON's integrators with SciPy's sparse linear algebra library."
593.	Realistic amplifier model (Oláh et al. 2021)
		"... we built a model that was verified by small axonal recordings. The model accurately recreated actual action potential measurements with typical recording artefacts and predicted the native electrical behavior. The simulations verified that recording instruments substantially filter voltage recordings. Moreover, we revealed that instrumentation directly interferes with local signal generation depending on the size of the recorded structures, which complicates the interpretation of recordings from smaller structures, such as axons. However, our model offers a straightforward approach that predicts the native waveforms of fast voltage signals and the underlying conductances even from the smallest neuronal structures..."
594.	Reciprocal regulation of rod and cone synapse by NO (Kourennyi et al 2004)
		We constructed models of rod and cone photoreceptors using NEURON software to predict how changes in Ca channels would affect the light response in these cells and in postsynaptic horizontal cells.
595.	Reconstructing cerebellar granule layer evoked LFP using convolution (ReConv) (Diwakar et al. 2011)
		The model allows reconstruction of evoked local field potentials as seen in the cerebellar granular layer. The approach uses a detailed model of cerebellar granule neuron to generate data traces and then uses a "ReConv" or jittered repetitive convolution technique to reproduce post-synaptic local field potentials in the granular layer. The algorithm was used to generate both in vitro and in vivo evoked LFP and reflected the changes seen during LTP and LTD, when such changes were induced in the underlying neurons by modulating release probability of synapses and sodium channel regulated intrinsic excitability of the cells.
596.	Recording from rod bipolar axon terminals in situ (Oltedal et al 2007)
		"... Whole cell recordings from axon terminals and cell bodies were used to investigate the passive membrane properties of rod bipolar cells and analyzed with a two-compartment equivalent electrical circuit model developed by Mennerick et al. For both terminal- and soma-end recordings, capacitive current decays were well fitted by biexponential functions. Computer simulations of simplified models of rod bipolar cells demonstrated that estimates of the capacitance of the axon terminal compartment can depend critically on the recording location, with terminal-end recordings giving the best estimates. Computer simulations and whole cell recordings demonstrated that terminal-end recordings can yield more accurate estimates of the peak amplitude and kinetic properties of postsynaptic currents generated at the axon terminals due to increased electrotonic filtering of these currents when recorded at the soma. ..." See paper for more and details.
597.	Recurrent discharge in a reduced model of cat spinal motoneuron (Balbi et al, 2013)
		Following a distal stimulation of a motor fibre, only a fraction of spinal motoneurons are able to produce a re-excitation of the initial segment leading to an orthodromically conducted action potential, known as recurrent discharge. In order to show the reciprocal interplay of the axonal initial segment and the soma leading to recurrent discharge in detail, a reduced model of a cat spinal motoneuron was developed.
598.	Reduced-morphology model of CA1 pyramidal cells optimized + validated w/ HippoUnit (Tomko et al '21)
		Here we employ the HippoUnit tests to optimize and validate our new compartmental model with reduced morphology. We show that our model is able to account for the following six well-established characteristic anatomical and physiological properties of CA1 pyramidal cells: (1) The reduced dendritic morphology contains all major dendritic branch classes. In addition to anatomy, the model reproduces also 5 key physiological features, including (2) somatic electrophysiological responses, (3) depolarization block, (4) EPSP attenuation (5) action potential (AP) backpropagation, and (6) synaptic integration at oblique dendrites.
599.	Regulation of a slow STG rhythm (Nadim et al 1998)
		Frequency regulation of a slow rhythm by a fast periodic input. Nadim, F., Manor, Y., Nusbaum, M. P., Marder, E. (1998) J. Neurosci. 18: 5053-5067
600.	Regulation of firing frequency in a midbrain dopaminergic neuron model (Kuznetsova et al. 2010)
		A dopaminergic (DA) neuron model with a morphologicaly realistic dendritic architecture. The model captures several salient features of DA neurons under different pharmacological manipulations and exhibits depolarization block for sufficiently high current pulses applied to the soma.
601.	Regulation of motoneuron excitability by KCNQ/Kv7 modulators (Lombardo & Harrington 2016)
		" ... Computer simulations confirmed that pharmacological enhancement of KCNQ/Kv7 channel (M current) activity decreases excitability and also suggested that the effects of inhibition of KCNQ/Kv7 channels on the excitability of spinal MNs do not depend on a direct effect in these neurons but likely on spinal cord synaptic partners. These results indicate that KCNQ/Kv7 channels have a fundamental role in the modulation of the excitability of spinal MNs acting both in these neurons and in their local presynaptic partners. ..."
602.	Regulation of the firing pattern in dopamine neurons (Komendantov et al 2004)
		Midbrain dopaminergic (DA) neurons in vivo exhibit two major firing patterns: single-spike firing and burst firing. The firing pattern expressed is dependent on both the intrinsic properties of the neurons and their excitatory and inhibitory synaptic inputs. Experimental data suggest that the activation of NMDA and GABAA receptors is crucial contributor to the initiation and suppression of burst firing, respectively, and that blocking calcium-activated potassium channels can facilitate burst firing. This multi-compartmental model of a DA neuron with a branching structure was developed and calibrated based on in vitro experimental data to explore the effects of different levels of activation of NMDA and GABAA receptors as well as the modulation of the SK current on the firing activity.
603.	Reinforcement learning of targeted movement (Chadderdon et al. 2012)
		"Sensorimotor control has traditionally been considered from a control theory perspective, without relation to neurobiology. In contrast, here we utilized a spiking-neuron model of motor cortex and trained it to perform a simple movement task, which consisted of rotating a single-joint “forearm” to a target. Learning was based on a reinforcement mechanism analogous to that of the dopamine system. This provided a global reward or punishment signal in response to decreasing or increasing distance from hand to target, respectively. Output was partially driven by Poisson motor babbling, creating stochastic movements that could then be shaped by learning. The virtual forearm consisted of a single segment rotated around an elbow joint, controlled by flexor and extensor muscles. ..."
604.	Rejuvenation model of dopamine neuron (Chan et al. 2007)
		Model files for the paper C. Savio Chan, et al. 'Rejuvenation' protects neurons in mouse models of Parkinson's disease, Nature 447, 1081-1086(28 June 2007).
605.	Resonance properties through Chirp stimulus responses (Narayanan Johnston 2007, 2008)
		...we constructed a simple, single-compartment model with Ih as the only active current... we found that both resonance frequency and resonance strength increased monotonically with the increase in the h conductance, supporting the notion of a direct, graded relationship between h conductance and resonance properties... (Narayanan and Johnston, 2007). ...we show that the h channels introduce an apparent negative delay in the local voltage response of these neurons with respect to the injected current within the theta frequency range... we found that the total inductive phase increased monotonically with the h conductance, whereas it had a bell-shaped dependence on both the membrane voltage and the half-maximal activation voltage for the h conductance. (Narayanan and Johnston, 2008).
606.	Response properties of neocort. neurons to temporally modulated noisy inputs (Koendgen et al. 2008)
		Neocortical neurons are classified by current–frequency relationship. This is a static description and it may be inadequate to interpret neuronal responses to time-varying stimuli. Theoretical studies (Brunel et al., 2001; Fourcaud-Trocmé et al. 2003; Fourcaud-Trocmé and Brunel 2005; Naundorf et al. 2005) suggested that single-cell dynamical response properties are necessary to interpret ensemble responses to fast input transients. Further, it was shown that input-noise linearizes and boosts the response bandwidth, and that the interplay between the barrage of noisy synaptic currents and the spike-initiation mechanisms determine the dynamical properties of the firing rate. In order to allow a reader to explore such simulations, we prepared a simple NEURON implementation of the experiments performed in Köndgen et al., 2008 (see also Fourcaud-Trocmé al. 2003; Fourcaud-Trocmé and Brunel 2005). In addition, we provide sample MATLAB routines for exploring the sandwich model proposed in Köndgen et al., 2008, employing a simple frequdency-domain filtering. The simulations and the MATLAB routines are based on the linear response properties of layer 5 pyramidal cells estimated by injecting a superposition of a small-amplitude sinusoidal wave and a background noise, as in Köndgen et al., 2008.
607.	Retinal Ganglion Cell: I-A (Benison et al 2001)
		NEURON mod files for the K-A current from the papers: (model) Benison G, Keizer J, Chalupa LM, Robinson DW. Modeling temporal behavior of postnatal cat retinal ganglion cells. J.Theor.Biol. 210:187-199 (2001) and (experiment) Skaliora I, Robinson DW, Scobey RP, Chalupa LM., Properties of K+ conductances in cat retinal ganglion cells during the period of activity-mediated refinements in retinofugal pathways. Eur.J.Neurosci. 7:1558-1568 (1995).
608.	Retinal Ganglion Cell: I-CaN and I-CaL (Benison et al. 2001)
		NEURON mod files for the CaN and CaL currents from the papers: Huang, S.-J. & Robinson, D.W. (1998). Activation and Inactivation properties of voltage-gated calcium currents in developing cat retinal ganglion cells. Neuroscience 85:239-247 (experimental) and Benison G. Keizer J., Chalupa L.M., Robinson D.W., (2001) J. theor. Biol. 210:187-199 (theoretical).
609.	Retinal Ganglion Cell: I-K (Skaliora et al 1995)
		NEURON mod files for the K-DR current from the paper: Skaliora I, Robinson DW, Scobey RP, Chalupa LM. Properties of K+ conductances in cat retinal ganglion cells during the period of activity-mediated refinements in retinofugal pathways. Eur J Neurosci 1995 7(7):1558-1568. See the readme.txt file below for more information.
610.	Retinal Ganglion Cell: I-Na,t (Benison et al 2001)
		NEURON mod files for the Na current from the papers: (model) Benison G, Keizer J, Chalupa LM, Robinson DW. Modeling temporal behavior of postnatal cat retinal ganglion cells. J Theor Biol. 2001 210:187-99 and a reference from this paper: (experimental) Skaliora I, Scobey RP, Chalupa LM. Prenatal development of excitability in cat retinal ganglion cells: action potentials and sodium currents. J Neurosci 1993 13:313-23. See the readme.txt file below for more information.
611.	Retinal ganglion cells responses and activity (Tsai et al 2012, Guo et al 2016)
		From the abstracts: "Retinal ganglion cells (RGCs), which survive in large numbers following neurodegenerative diseases, could be stimulated with extracellular electric pulses to elicit artificial percepts. How do the RGCs respond to electrical stimulation at the sub-cellular level under different stimulus configurations, and how does this influence the whole-cell response? At the population level, why have experiments yielded conflicting evidence regarding the extent of passing axon activation? We addressed these questions through simulations of morphologically and biophysically detailed computational RGC models on high performance computing clusters. We conducted the analyses on both large-field RGCs and small-field midget RGCs. ...", "... In this study, an existing RGC ionic model was extended by including a hyperpolarization activated non-selective cationic current as well as a T-type calcium current identified in recent experimental findings. Biophysically-defined model parameters were simultaneously optimized against multiple experimental recordings from ON and OFF RGCs. ...
612.	Retinal Photoreceptor: I Potassium (Beech, Barnes 1989)
		NEURON mod files for a Potassium current from the paper: Beech DJ, Barnes S. Characterization of a voltage-gated K+ channel that accelerates the rod response to dim light. Neuron 3:573-81 (1989).
613.	Rhesus Monkey Layer 3 Pyramidal Neurons: V1 vs PFC (Amatrudo, Weaver et al. 2012)
		Whole-cell patch-clamp recordings and high-resolution 3D morphometric analyses of layer 3 pyramidal neurons in in vitro slices of monkey primary visual cortex (V1) and dorsolateral granular prefrontal cortex (dlPFC) revealed that neurons in these two brain areas possess highly distinctive structural and functional properties. ... Three-dimensional reconstructions of V1 and dlPFC neurons were incorporated into computational models containing Hodgkin-Huxley and AMPA- and GABAA-receptor gated channels. Morphology alone largely accounted for observed passive physiological properties, but led to AP firing rates that differed more than observed empirically, and to synaptic responses that opposed empirical results. Accordingly, modeling predicts that active channel conductances differ between V1 and dlPFC neurons. The unique features of V1 and dlPFC neurons are likely fundamental determinants of area-specific network behavior. The compact electrotonic arbor and increased excitability of V1 neurons support the rapid signal integration required for early processing of visual information. The greater connectivity and dendritic complexity of dlPFC neurons likely support higher level cognitive functions including working memory and planning.
614.	Rhesus Monkey Layer 3 Pyramidal Neurons: Young vs aged PFC (Coskren et al. 2015)
		Layer 3 (L3) pyramidal neurons in the lateral prefrontal cortex (LPFC) of rhesus monkeys exhibit dendritic regression, spine loss and increased action potential (AP) firing rates during normal aging. The relationship between these structural and functional alterations, if any, is unknown. Computational models using the digital reconstructions with Hodgkin-Huxley and AMPA channels allowed us to assess relationships between demonstrated age-related changes and to predict physiological changes that have not yet been tested empirically. Tuning passive parameters for each model predicted significantly higher membrane resistance (Rm) in aged versus young neurons. This Rm increase alone did not account for the empirically observed fI-curves, but coupling these Rm values with subtle differences in morphology and membrane capacitance Cm did. The predicted differences in passive parameters (or other parameters with similar effects) are mathematically plausible, but must be tested empirically.
615.	Rhesus Monkey Young and Aged L3 PFC Pyramidal Neurons (Rumbell et al. 2016)
		A stereotypical pyramidal neuron morphology with ion channel parameter combinations that reproduce firing patterns of one young and one aged rhesus monkey L3 PFC pyramidal neurons. Parameters were found through an automated optimization method.
616.	Ribbon Synapse (Sikora et al 2005)
		A model of the ribbon synapse was developed to replicate both pre- and postsynaptic functions of this glutamatergic juncture. The presynaptic portion of the model is rich in anatomical and physiological detail and includes multiple release sites for each ribbon based on anatomical studies of presynaptic terminals, presynaptic voltage at the terminal, the activation of voltage-gated calcium channels and a calcium-dependent release mechanism whose rate varies as a function of the calcium concentration that is monitored at two different sites which control both an ultrafast, docked pool of vesicles and a release ready pool of tethered vesicles. See paper for more and details.
617.	Rod photoreceptor (Barnes and Hille 1989, Publio et al. 2006, Kourennyi and Liu et al. 2004)
		This a conductance-based model of a rod photoreceptor cell based on other modeling works (Barnes and Hille 1989 and Publio et al. 2006 and Kourennyi and Liu et al. 2004 ). In this model four types of ionic channels identified in the inner segment of the rod: nonselective cation channel (h), delayed rectifying potassium channel (Kv), noninactivating potassium channel (Kx) and calcium channel (Ca) was used. The model accurately reproduces the rod response when stimulated with a simulated photocurrent signal. We can show the effect of nonselective cation channel. The absence of this channel cause increasing the peak amplitude and the time to reach the peak of voltage response and absence of transient mode in this response.
618.	Role for short term plasticity and OLM cells in containing spread of excitation (Hummos et al 2014)
		This hippocampus model was developed by matching experimental data, including neuronal behavior, synaptic current dynamics, network spatial connectivity patterns, and short-term synaptic plasticity. Furthermore, it was constrained to perform pattern completion and separation under the effects of acetylcholine. The model was then used to investigate the role of short-term synaptic depression at the recurrent synapses in CA3, and inhibition by basket cell (BC) interneurons and oriens lacunosum-moleculare (OLM) interneurons in containing the unstable spread of excitatory activity in the network.
619.	Role of afferent-hair cell connectivity in determining spike train regularity (Holmes et al 2017)
		"Vestibular bouton afferent terminals in turtle utricle can be categorized into four types depending on their location and terminal arbor structure: lateral extrastriolar (LES), striolar, juxtastriolar, and medial extrastriolar (MES). The terminal arbors of these afferents differ in surface area, total length, collecting area, number of boutons, number of bouton contacts per hair cell, and axon diameter (Huwe JA, Logan CJ, Williams B, Rowe MH, Peterson EH. J Neurophysiol 113: 2420 –2433, 2015). To understand how differences in terminal morphology and the resulting hair cell inputs might affect afferent response properties, we modeled representative afferents from each region, using reconstructed bouton afferents. ..."
620.	Role of Ih in firing patterns of cold thermoreceptors (Orio et al., 2012)
		" ... Here we investigated the role of Ih in cold-sensitive (CS) nerve endings, where cold sensory transduction actually takes place. Corneal CS nerve endings in mice show a rhythmic spiking activity at neutral skin temperature that switches to bursting mode when the temperature is lowered. ... Mathematical modeling shows that the firing phenotype of CS nerve endings from HCN1-/- mice can be reproduced by replacing HCN1 channels with the slower HCN2 channels rather than by abolishing Ih. We propose that Ih carried by HCN1 channels helps tune the frequency of the oscillation and the length of bursts underlying regular spiking in cold thermoreceptors, having important implications for neural coding of cold sensation. "
621.	Role of the AIS in the control of spontaneous frequency of dopaminergic neurons (Meza et al 2017)
		Computational modeling showed that the size of the Axon Initial Segment (AIS), but not its position within the somatodendritic domain, is the major causal determinant of the tonic firing rate in the intact model, by virtue of the higher intrinsic frequency of the isolated AIS. Further mechanistic analysis of the relationship between neuronal morphology and firing rate showed that dopaminergic neurons function as a coupled oscillator whose frequency of discharge results from a compromise between AIS and somatodendritic oscillators.
622.	Salamander retinal ganglian cells: morphology influences firing (Sheasby, Fohlmeister 1999)
		Nerve impulse entrainment and other excitation and passive phenomena are analyzed for a morphologically diverse and exhaustive data set (n=57) of realistic (3-dimensional computer traced) soma-dendritic tree structures of ganglion cells in the tiger salamander (Ambystoma tigrinum) retina.
623.	Salamander retinal ganglion cell: ion channels (Fohlmeister, Miller 1997)
		A realistic five (5) channel spiking model reproduces the bursting behavior of tiger salamander ganglion cells in the retina. Please see the readme for more information.
624.	Schiz.-linked gene effects on intrinsic single-neuron excitability (Maki-Marttunen et al. 2016)
		Python scripts for running NEURON simulations that model a layer V pyramidal cell with certain genetic variants implemented. The genes included are obtained from genome-wide association studies of schizophrenia.
625.	SCN1A gain-of-function in early infantile encephalopathy (Berecki et al 2019)
		"OBJECTIVE: To elucidate the biophysical basis underlying the distinct and severe clinical presentation in patients with the recurrent missense SCN1A variant, p.Thr226Met. Patients with this variant show a well-defined genotype-phenotype correlation and present with developmental and early infantile epileptic encephalopathy that is far more severe than typical SCN1A Dravet syndrome. METHODS: Whole cell patch clamp and dynamic action potential clamp were used to study T226M Nav 1.1 channels expressed in mammalian cells. Computational modeling was used to explore the neuronal scale mechanisms that account for altered action potential firing. RESULTS: T226M channels exhibited hyperpolarizing shifts of the activation and inactivation curves and enhanced fast inactivation. Dynamic action potential clamp hybrid simulation showed that model neurons containing T226M conductance displayed a left shift in rheobase relative to control. At current stimulation levels that produced repetitive action potential firing in control model neurons, depolarization block and cessation of action potential firing occurred in T226M model neurons. Fully computationally simulated neuron models recapitulated the findings from dynamic action potential clamp and showed that heterozygous T226M models were also more susceptible to depolarization block. ..."
626.	SCZ-associated variant effects on L5 pyr cell NN activity and delta osc. (Maki-Marttunen et al 2018)
		" … Here, using computational modeling, we show that a common biomarker of schizophrenia, namely, an increase in delta-oscillation power, may be a direct consequence of altered expression or kinetics of voltage-gated ion channels or calcium transporters. Our model of a circuit of layer V pyramidal cells highlights multiple types of schizophrenia-related variants that contribute to altered dynamics in the delta frequency band. Moreover, our model predicts that the same membrane mechanisms that increase the layer V pyramidal cell network gain and response to delta-frequency oscillations may also cause a decit in a single-cell correlate of the prepulse inhibition, which is a behavioral biomarker highly associated with schizophrenia."
627.	Selective control of cortical axonal spikes by a slowly inactivating K+ current (Shu et al. 2007)
		We discovered a low-threshold, slowly inactivating K+ current, containing Kv1.2 alpha subunits, in axon initial segment, playing a key role in the modulation of spike threshold and spike duration as well as the spike timing in prefrontal cortex layer V pyramidal cell of ferrets and rats. A kd.mod file implements this D current and put it in the axonal model: Neuron_Dcurrent.hoc. Run the model to see the gradual modulation effect over seconds on spike shape.
628.	Sensorimotor cortex reinforcement learning of 2-joint virtual arm reaching (Neymotin et al. 2013)
		"... We developed a model of sensory and motor neocortex consisting of 704 spiking model-neurons. Sensory and motor populations included excitatory cells and two types of interneurons. Neurons were interconnected with AMPA/NMDA, and GABAA synapses. We trained our model using spike-timing-dependent reinforcement learning to control a 2-joint virtual arm to reach to a fixed target. ... "
629.	Sensory-evoked responses of L5 pyramidal tract neurons (Egger et al 2020)
		This is the L5 pyramidal tract neuron (L5PT) model from Egger, Narayanan et al., Neuron 2020. It allows investigating how synaptic inputs evoked by different sensory stimuli are integrated by the complex intrinsic properties of L5PTs. The model is constrained by anatomical measurements of the subcellular synaptic input patterns to L5PT neurons, in vivo measurements of sensory-evoked responses of different populations of neurons providing these synaptic inputs, and in vitro measurements constraining the biophysical properties of the soma, dendrites and axon (note: the biophysical model is based on the work by Hay et al., Plos Comp Biol 2011). The model files provided here allow performing simulations and analyses presented in Figures 3, 4 and 5.
630.	Shaping NMDA spikes by timed synaptic inhibition on L5PC (Doron et al. 2017)
		This work (published in "Timed synaptic inhibition shapes NMDA spikes, influencing local dendritic processing and global I/O properties of cortical neurons", Doron et al, Cell Reports, 2017), examines the effect of timed inhibition over dendritic NMDA spikes on L5PC (Based on Hay et al., 2011) and CA1 cell (Based on Grunditz et al. 2008 and Golding et al. 2001).
631.	Shaping of action potentials by different types of BK channels (Jaffe et al., 2011)
		Dentate gyrus granule cells highly express the beta4 accessory subunit which confer BK channels with type II properties. The properties of heterologously-expressed BK channels (with and without the beta4 subunit) were used to construct channel models. These were then used to study how they affect single action potentials and trains of spikes in a model dentate gyrus granule cells (based on Aradi and Holmes, 1999).
632.	Short term plasticity at the cerebellar granule cell (Nieus et al. 2006)
		The model reproduces short term plasticity of the mossy fibre to granule cell synapse. To reproduce synaptic currents recorded in experiments, a model of presynaptic release was used to determine the concentration of glutamate in the synaptic cleft that ultimately determined a synaptic response. The parameters of facilitation and depression were determined deconvolving AMPA EPSCs.
633.	Short term plasticity of synapses onto V1 layer 2/3 pyramidal neuron (Varela et al 1997)
		This archive contains 3 mod files for NEURON that implement the short term synaptic plasticity model described in Varela, J.A., Sen, K., Gibson, J., Fost, J., Abbott, L.R., and Nelson, S.B.. A quantitative description of short-term plasticity at excitatory synapses in layer 2/3 of rat primary visual cortex. Journal of Neuroscience 17:7926-7940, 1997. Contact ted.carnevale@yale.edu if you have questions about this implementation of the model.
634.	Signal integration in a CA1 pyramidal cell (Graham 2001)
		This model investigates signal integration in the dendritic tree of a hippocampal CA1 pyramidal cell when different combinations of active channels are present in the tree (Graham, 2001)
635.	Signal integration in LGN cells (Briska et al 2003)
		Computer models were used to investigate passive properties of lateral geniculate nucleus thalamocortical cells and thalamic interneurons based on in vitro whole-cell study. Two neurons of each type were characterized physiologically and morphologically. Differences in the attenuation of propagated signals depend on both cell morphology and signal frequency. See the paper for details.
636.	Simple and accurate Diffusion Approximation algor. for stochastic ion channels (Orio & Soudry 2012)
		" ... We derived the (Stochastic Differential Equations) SDE explicitly for any given ion channel kinetic scheme. The resulting generic equations were surprisingly simple and interpretable – allowing an easy, transparent and efficient (Diffusion Approximation) DA implementation, avoiding unnecessary approximations. The algorithm was tested in a voltage clamp simulation and in two different current clamp simulations, yielding the same results as (Markov Chains) MC modeling. Also, the simulation efficiency of this DA method demonstrated considerable superiority over MC methods, except when short time steps or low channel numbers were used."
637.	Simulated cortical color opponent receptive fields self-organize via STDP (Eguchi et al., 2014)
		"... In this work, we address the problem of understanding the cortical processing of color information with a possible mechanism of the development of the patchy distribution of color selectivity via computational modeling. ... Our model of the early visual system consists of multiple topographically-arranged layers of excitatory and inhibitory neurons, with sparse intra-layer connectivity and feed-forward connectivity between layers. Layers are arranged based on anatomy of early visual pathways, and include a retina, lateral geniculate nucleus, and layered neocortex. ... After training with natural images, the neurons display heightened sensitivity to specific colors. ..."
638.	Simulated light response in rod photoreceptors (Liu and Kourennyi 2004)
		We developed a complete computer model of the rod, which accurately reproduced the main features of the light response and allowed us to demonstrate that it was suppression of Kx channels that was essential for slowing SLR and increasing excitability of rods. The results reported in this work further establish the importance of Kx channels in rod photoreceptor function.
639.	Simulations of modulation of HCN channels in L5PCs (Mäki-Marttunen and Mäki-Marttunen, 2022)
		"... In this work, we build upon existing biophysically detailed models of thick-tufted layer V pyramidal cells and model the effects of over- and under-expression of Ih channels as well as their neuromodulation by dopamine (gain of Ih function) and acetylcholine (loss of Ih function). We show that Ih channels facilitate the action potentials of layer V pyramidal cells in response to proximal dendritic stimulus while they hinder the action potentials in response to distal dendritic stimulus at the apical dendrite. We also show that the inhibitory action of the Ih channels in layer V pyramidal cells is due to the interactions between Ih channels and a hot zone of low voltage-activated Ca2+ channels at the apical dendrite. Our simulations suggest that a combination of Ih-enhancing neuromodulation at the proximal apical dendrite and Ih-inhibiting modulation at the distal apical dendrite can increase the layer V pyramidal excitability more than any of the two neuromodulators alone..."
640.	Simulations of motor unit discharge patterns (Powers et al. 2011)
		" ... To estimate the potential contributions of PIC (Persistent Inward Current) activation and synaptic input patterns to motor unit discharge patterns, we examined the responses of a set of cable motoneuron models to different patterns of excitatory and inhibitory inputs. The models were first tuned to approximate the current- and voltage-clamp responses of low- and medium-threshold spinal motoneurons studied in decerebrate cats and then driven with different patterns of excitatory and inhibitory inputs. The responses of the models to excitatory inputs reproduced a number of features of human motor unit discharge. However, the pattern of rate modulation was strongly influenced by the temporal and spatial pattern of concurrent inhibitory inputs. Thus, even though PIC activation is likely to exert a strong influence on firing rate modulation, PIC activation in combination with different patterns of excitatory and inhibitory synaptic inputs can produce a wide variety of motor unit discharge patterns."
641.	Single compartment Dorsal Lateral Medium Spiny Neuron w/ NMDA and AMPA (Biddell and Johnson 2013)
		A biophysical single compartment model of the dorsal lateral striatum medium spiny neuron is presented here. The model is an implementation then adaptation of a previously described model (Mahon et al. 2002). The model has been adapted to include NMDA and AMPA receptor models that have been fit to dorsal lateral striatal neurons. The receptor models allow for excitation by other neuron models.
642.	Single compartment: nonlinear a5-GABAAR controls synaptic NMDAR activation (Schulz et al 2018)
		This study shows that IPSCs mediated by a5-subunit containing GABAA receptors are strongly outward-rectifying generating 4-fold larger conductances above -50?mV than at rest. This model shows that synaptic activation of these receptors can very effectively control voltage-dependent NMDA-receptor activation. The files contain the NEURON code for Fig.6 and Fig.7. The model is a single dendritic compartment with one glutamatergic and GABAergic synapse. Physiological properties of GABA synapses were modeled as determined by optogenetic activation of inputs during voltage-clamp recordings in Schulz et al. 2018.
643.	Single E-I oscillating network with amplitude modulation (Avella Gonzalez et al. 2012)
		"... Intriguingly, the amplitude of ongoing oscillations, such as measured in EEG recordings, fluctuates irregularly, with episodes of high amplitude (HAE) alternating with episodes of low amplitude (LAE). ... Here, we show that transitions between HAE and LAE in the alpha/beta frequency band occur in a generic neuronal network model consisting of interconnected inhibitory (I) and excitatory (E) cells that are externally driven by sustained depolarizing currents(cholinergic input) and trains of action potentials that activate excitatory synapses. In the model, action potentials onto inhibitory cells represent input from other brain areas and desynchronize network activity, being crucial for the emergence of amplitude fluctuations. ..."
644.	Single excitatory axons form clustered synapses onto CA1 pyramidal cell dendrites (Bloss et al 2018)
		" ... Here we show that single presynaptic axons form multiple, spatially clustered inputs onto the distal, but not proximal, dendrites of CA1 pyramidal neurons. These compound connections exhibit ultrastructural features indicative of strong synapses and occur much more commonly in entorhinal than in thalamic afferents. Computational simulations revealed that compound connections depolarize dendrites in a biophysically efficient manner, owing to their inherent spatiotemporal clustering. ..."
645.	Site of impulse initiation in a neuron (Moore et al 1983)
		Examines the effect of temperature, the taper of the axon hillock, and HH channel density on antidromic spike invasion into the soma and spike initiation under dendritic stimulation.
646.	Small world networks of Type I and Type II Excitable Neurons (Bogaard et al. 2009)
		Implemented with NEURON 5.9, four model neurons with varying excitability properties affect the spatiotemporal patterning of small world networks of homogeneous and heterogeneous cell population.
647.	Sodium channel mutations causing generalized epilepsy with febrile seizures + (Barela et al. 2006)
		A novel mutation, R859C, in the Nav1.1 sodium channel was identified in a 4-generation, 33-member Caucasian family with a clinical presentation consistent with GEFS+. The mutation neutralizes a positively charged arginine in the domain 2 S4 voltage sensor of the Nav1.1 channel Ą subunit. When the mutation was placed in the rat Nav1.1 channel and expressed in Xenopus oocytes, the mutant channel displayed a positive shift in the voltage-dependence of sodium channel activation, slower recovery from slow inactivation, and lower levels of current compared to the wild-type channel. Computational analysis suggests that neurons expressing the mutant channel have higher thresholds for firing a single action potential and for firing multiple action potentials, along with decreased repetitive firing. Therefore, this mutation should lead to decreased neuronal excitability, in contrast to most previous GEFS+ sodium channel mutations that have changes predicted to increase neuronal firing.
648.	Sodium currents activate without a delay (Baranauskas and Martina 2006)
		Hodgkin and Huxley established that sodium currents in the squid giant axons activate after a delay, which is explained by the model of a channel with three identical independent gates that all have to open before the channel can pass current (the HH model). It is assumed that this model can adequately describe the sodium current activation time course in all mammalian central neurons, although there is no experimental evidence to support such a conjecture. We performed high temporal resolution studies of sodium currents gating in three types of central neurons. ... These results can be explained by a model with two closed states and one open state. ... This model captures all major properties of the sodium current activation. In addition, the proposed model reproduces the observed action potential shape more accurately than the traditional HH model. See paper for more and details.
649.	Sodium potassium ATPase pump (Chapman et al. 1983)
		The electrochemical properties of a widely accepted six-step reaction scheme for the Na,K-ATPase have been studied by computer simulation.
650.	Sound-evoked activity in peripheral axons of type I spiral ganglion neurons (Budak et al. 2021)
		Using this model, we investigated the implications of two mechanisms underlying the auditory neuropathy known as hidden hearing loss, namely synaptopathy and myelinopathy, on sound-evoked spike generation and timing in the peripheral axons of type I spiral ganglion neurons (SGNs). The model is a reduced biophysical model consisting of a population of myelinated SGN axonal fibers whose firing activity is driven by a previously developed, well accepted model for cochlear sound processing. Using the model, we investigated how synapse loss (synaptopathy) or disruption of myelin organization (myelinopathy) affected spike generation on the axons and the profile of the compound action potential (CAP) signal computed from the spike activity. Synaptopathy and myelinopathy were implemented by removing synapses and by varying the position of SGN heminodes (the nodal structures closest to the inner hair cell synapse where action potentials are generated), respectively. Model results showed that heminode disruption caused decreased amplitude and increased latency of sound-evoked CAPs. In addition, significant elongation of the initial axon segment caused spike generation failure leading to decreased spiking probability. In contrast, synaptopathy, solely decreased probability of firing, subsequently decreasing CAP peak amplitude without affecting its latency, similar to observations in noise exposed animals. Model results reveal the disruptive effect of synaptopathy or myelinopathy on neural activity in the peripheral auditory system that may contribute to perceptual deficits.
651.	Space clamp problems in neurons with voltage-gated conductances (Bar-Yehuda and Korngreen 2008)
		" ... using numerical simulations, we show that the distortions of voltage-gated K+ and Ca2+ currents are substantial even in neurons with short dendrites. The simulations also demonstrate that passive cable theory cannot be used to justify voltage-clamping of neurons, due to significant shunting to the reversal potential of the voltage-gated conductance during channel activation. ... "
652.	Spatial constrains of GABAergic rheobase shift (Lombardi et al., 2021)
		In this models we investigated how the threshold eGABA, at which GABAergic inhibition switches to excitation, depends on the spatiotemporal constrains in a ball-and-stick neurons and a neurons with a topology derived from an reconstructed neuron.
653.	Spatial gridding and temporal accuracy in NEURON (Hines and Carnevale 2001)
		A heuristic for compartmentalization based on the space constant at 100 Hz is proposed. The paper also discusses spatio/temporal accuracy and the use of CVODE.
654.	Spike burst-pause dynamics of Purkinje cells regulate sensorimotor adaptation (Luque et al 2019)
		"Cerebellar Purkinje cells mediate accurate eye movement coordination. However, it remains unclear how oculomotor adaptation depends on the interplay between the characteristic Purkinje cell response patterns, namely tonic, bursting, and spike pauses. Here, a spiking cerebellar model assesses the role of Purkinje cell firing patterns in vestibular ocular reflex (VOR) adaptation. The model captures the cerebellar microcircuit properties and it incorporates spike-based synaptic plasticity at multiple cerebellar sites. ..."
655.	Spike exchange methods for a Blue Gene/P supercomputer (Hines et al., 2011)
		Tests several spike exchange methods on a Blue Gene/P supercomputer on up to 64K cores.
656.	Spike frequency adaptation in spinal sensory neurones (Melnick et al 2004)
		Using tight-seal recordings from rat spinal cord slices, intracellular labelling and computer simulation, we analysed the mechanisms of spike frequency adaptation in substantia gelatinosa (SG) neurones. Adapting-firing neurones (AFNs) generated short bursts of spikes during sustained depolarization and were mostly found in lateral SG. ... Ca2 + -dependent conductances do not contribute to adapting firing. Transient KA current was small and completely inactivated at resting potential suggesting that adapting firing was mainly generated by voltage-gated Na+ and delayed-rectifier K+ (KDR ) currents. ... Computer simulation has further revealed that down-regulation of Na+ conductance represents an effective mechanism for the induction of firing adaptation. It is suggested that the cell-specific regulation of Na+ channel expression can be an important factor underlying the diversity of firing patterns in SG neurones. See paper for more and details.
657.	Spike Initiation in Neocortical Pyramidal Neurons (Mainen et al 1995)
		This model reproduces figure 3A from the paper Mainen ZF, Joerges J, Huguenard JR, Sejnowski TJ (1995). Please see the paper for detail whose full text is available at http://www.cnl.salk.edu/~zach/methods.html Email Zach Mainen for questions: mainen@cshl.org
658.	Spike propagation in dendrites with stochastic ion channels (Diba et al. 2006)
		"We investigate the effects of the stochastic nature of ion channels on the faithfulness, precision and reproducibility of electrical signal transmission in weakly active, dendritic membrane under in vitro conditions. ... We numerically simulate the effects of stochastic ion channels on the forward and backward propagation of dendritic spikes in Monte-Carlo simulations on a reconstructed layer 5 pyramidal neuron. We report that in most instances there is little variation in timing or amplitude for a single BPAP, while variable backpropagation can occur for trains of action potentials. Additionally, we find that the generation and forward propagation of dendritic Ca2+ spikes are susceptible to channel variability. This indicates limitations on computations that depend on the precise timing of Ca2+ spikes."
659.	Spike repolarization in axon collaterals (Foust et al. 2011)
		Voltage sensing dye experiments and simulations characterize the location and re-polarizing function of Kv1 channels in cortical neurons. "... (the papers) results indicate that action potential-induced synaptic transmission may operate through a mix of analog–digital transmission owing to the properties of Kv1 channels in axon collaterals and presynaptic boutons."
660.	Spike-timing dependent inhibitory plasticity for gating bAPs (Wilmes et al 2017)
		"Inhibition is known to influence the forward-directed flow of information within neurons. However, also regulation of backward-directed signals, such as backpropagating action potentials (bAPs), can enrich the functional repertoire of local circuits. Inhibitory control of bAP spread, for example, can provide a switch for the plasticity of excitatory synapses. Although such a mechanism is possible, it requires a precise timing of inhibition to annihilate bAPs without impairment of forward-directed excitatory information flow. Here, we propose a specific learning rule for inhibitory synapses to automatically generate the correct timing to gate bAPs in pyramidal cells when embedded in a local circuit of feedforward inhibition. Based on computational modeling of multi-compartmental neurons with physiological properties, we demonstrate that a learning rule with anti-Hebbian shape can establish the required temporal precision. ..."
661.	Spikelet generation and AP initiation in a L5 neocortical pyr neuron (Michalikova et al. 2017) Fig 1
		The article by Michalikova et al. (2017) explores the generation of spikelets in cortical pyramidal neurons. The model cell, adapted from Hu et al. (2009), is a layer V pyramidal neuron. The cell is stimulated by fluctuating synaptic inputs and generates somatic APs and spikelets in response. The spikelets are initiated as APs at the AIS that do not activate the soma.
662.	Spikelet generation and AP initiation in a simplified pyr neuron (Michalikova et al. 2017) Fig 3
		The article by Michalikova et al. (2017) explores the generation of spikelets in cortical pyramidal neurons. This package contains code for simulating the model with simplified morphology shown in Figs 3 and S2.
663.	Spinal Dorsal Horn Network Model (Medlock et al 2022)
		To explore spinal dorsal horn (SDH) network function, we developed a computational model of the circuit that is tightly constrained by experimental data. Our model comprises conductance-based model neurons that reproduce the characteristic firing patterns of excitatory and inhibitory spinal neurons. Excitatory spinal neuron subtypes defined by calretinin, somatostatin, delta-opioid receptor, protein kinase C gamma, or vesicular glutamate transporter 3 expression or by transient/central spiking/morphology and inhibitory neuron subtypes defined by parvalbumin or dynorphin expression or by islet morphology were synaptically connected according to available qualitative data. Synaptic weights were adjusted to produce firing in projection neurons, defined by neurokinin-1 expression, matching experimentally measured responses to a range of mechanical stimulus intensities. Input to the circuit was provided by three types of afferents (Aß, Ad, and C-fibres) whose firing rates were also matched to experimental data.
664.	Spinal motoneuron recruitment regulated by ionic channels during fictive locomotion (Zhang & Dai 20)
		"... we investigated the channel mechanism regulating the motoneuron recruitment. Three types of motoneuron pools including slow (S), fatigue-resistant (FR) and fast-fatigable (FF) motoneurons were constructed based on the membrane proprieties of cat lumbar motoneurons. The transient sodium (NaT), persistent sodium (NaP), delayed-rectifier potassium [K(DR)], Ca2+-dependent K+ [K(AHP)] and L-type calcium (CaL) channels were included in the models..."
665.	Spinal Motor Neuron (Dodge, Cooley 1973)
		"The excitability of various regions of the spinal motorneuron can be specified by solving the partial differential equation of a nerve fiber whose diameter and membrane properties vary with distance. For our model geometrical factors for the myelinated axon, initial segment and cell body were derived from anatomical measurements, the dendritic tree was represented by its equivalent cylinder, and the current-voltage relations of the membrane were described by a modification of the Hodgkin-Huxley model that fits voltage-clamp data from the motorneuron. ..."
666.	Spinal Motor Neuron (McIntyre et al 2002)
		Simulation of peripheral nervous system (PNS) mylelinated axon. This model is described in detail in: McIntyre CC, Richardson AG, and Grill WM.(2002)
667.	Spinal Motor Neuron: Na, K_A, and K_DR currents (Safronov, Vogel 1995)
		NEURON mod files for the Na, K-A, and K-DR currents from the paper: Safronov, B.V. and Vogel,W. Single voltage-activated Na+ and K+ channels in the somata of rat motorneurons. Journal of Physiology 487.1:91-106 (1995). See the readme.txt file for more information.
668.	Spine fusion and branching affects synaptic response (Rusakov et al 1996, 1997)
		This compartmental model of a hippocampal granule cell has spinous synapses placed on the second-order dendrites. Changes in shape and connectivity of the spines usually does not effect the synaptic response of the cell unless active conductances are incorporated into the spine membrane (e.g. voltage-dependent Ca2+ channels). With active conductances, spines can generate spike-like events. We showed that changes like fusion and branching, or in fact any increase in the equivalent spine neck resistance, could trigger a dramatic increase in the spine's influence on the dendritic shaft potential.
669.	Spine head calcium in a CA1 pyramidal cell model (Graham et al. 2014)
		"We use a computational model of a hippocampal CA1 pyramidal cell to demonstrate that spine head calcium provides an instantaneous readout at each synapse of the postsynaptic weighted sum of all presynaptic activity impinging on the cell. The form of the readout is equivalent to the functions of weighted, summed inputs used in neural network learning rules. Within a dendritic layer, peak spine head calcium levels are either a linear or sigmoidal function of the number of coactive synapses, with nonlinearity depending on the ability of voltage spread in the dendrites to reach calcium spike threshold. ..."
670.	Spine neck plasticity controls postsynaptic calcium signals (Grunditz et al. 2008)
		This model was set up to dissect the relative contribution of different channels to the spine calcium transients measured at single spines.
671.	Spiny neuron model with dopamine-induced bistability (Gruber et al 2003)
		These files implement a model of dopaminergic modulation of voltage-gated currents (called kir2 and caL in the original paper). See spinycell.html for details of usage and implementation. For questions about this implementation, contact Ted Carnevale (ted.carnevale@yale.edu)
672.	Spontaneous firing caused by stochastic channel gating (Chow, White 1996)
		NEURON implementation of model of stochastic channel gating, resulting in spontaneous firing. Qualitatively reproduces the phenomena described in the reference.
673.	Spreading Depolarization in Brain Slices (Kelley et al. 2022)
		A tissue-scale model of spreading depolarization (SD) in brain slices. We used the NEURON simulator's reaction-diffusion framework to implement embed thousands of neurons (based on the the model from Wei et al. 2014) in the extracellular space of a brain slice, which is itself embedded in an bath solution. We initiate SD in the slice by elevating extracellular K+ in a spherical region at the center of the slice. Effects of hypoxia and propionate on the slice were modeled by appropriate changes to the volume fraction and tortuosity of the extracellular space and oxygen/chloride concentrations.
674.	Squid axon (Hodgkin, Huxley 1952) (NEURON)
		The classic HH model of squid axon membrane implemented in NEURON. Hodgkin, A.L., Huxley, A.F. (1952)
675.	State and location dependence of action potential metabolic cost (Hallermann et al., 2012)
		With this model of a layer 5 pyramidal neuron the state and location dependence of the ATP usage and the metabolic efficiency of action potentials can be analyzed. Model parameters were constrained by direct subcellular recordings at dendritic, somatic and axonal compartments.
676.	State dependent drug binding to sodium channels in the dentate gyrus (Thomas & Petrou 2013)
		A Markov model of sodium channels was developed that includes drug binding to fast inactivated states. This was incorporated into a model of the dentate gyrus to investigate the effects of anti-epileptic drugs on neuron and network properties.
677.	Status epilepticus alters dentate basket cell tonic inhibition (Yu J et al 2013)
		Status epilepticus (SE) leads to changes in dentate inhibitory neuronal networks and alters synaptic and tonic inhibition in granule cells. Recently, we identified that one week after pilocarpine-induced status epilepticus, dentate fast-spiking basket cells (FS-BCs), which underlie fast perisomatic inhibition, show two distinct changes in inhibition: (1) enhanced tonic currents (IGABA) and (2)depolarizing shift in GABA reversal (EGABA) following SE. These two changes can have opposing effects on neuronal inhibition with increases in tonic GABA conductance (gGABA) reducing excitability when the GABA currents are shunting (or hyperpolarizing) and potentially enhancing excitability when GABA currents are depolarizing. The following model is used to examine the post-SE changes in tonic GABA conductance, together with the depolarized GABA reversal potential modify FS-BC excitability and dentate network activity.
678.	STD-dependent and independent encoding of Input irregularity as spike rate (Luthman et al. 2011)
		"... We use a conductance-based model of a CN neuron to study the effect of the regularity of Purkinje cell spiking on CN neuron activity. We find that increasing the irregularity of Purkinje cell activity accelerates the CN neuron spike rate and that the mechanism of this recoding of input irregularity as output spike rate depends on the number of Purkinje cells converging onto a CN neuron. ..."
679.	STDP and BDNF in CA1 spines (Solinas et al. 2019)
		Storing memory traces in the brain is essential for learning and memory formation. Memory traces are created by joint electrical activity in neurons that are interconnected by synapses and allow transferring electrical activity from a sending (presynaptic) to a receiving (postsynaptic) neuron. During learning, neurons that are co-active can tune synapses to become more effective. This process is called synaptic plasticity or long-term potentiation (LTP). Timing-dependent LTP (t-LTP) is a physiologically relevant type of synaptic plasticity that results from repeated sequential firing of action potentials (APs) in pre- and postsynaptic neurons. T-LTP is observed during learning in vivo and is a cellular correlate of memory formation. T-LTP can be elicited by different rhythms of synaptic activity that recruit distinct synaptic growth processes underlying t-LTP. The protein brain-derived neurotrophic factor (BDNF) is released at synapses and mediates synaptic growth in response to specific rhythms of t-LTP stimulation, while other rhythms mediate BDNF-independent t-LTP. Here, we developed a realistic computational model that accounts for our previously published experimental results of BDNF-independent 1:1 t-LTP (pairing of 1 presynaptic with 1 postsynaptic AP) and BDNF-dependent 1:4 t-LTP (pairing of 1 presynaptic with 4 postsynaptic APs). The model explains the magnitude and time course of both t-LTP forms and allows predicting t-LTP properties that result from altered BDNF turnover. Since BDNF levels are decreased in demented patients, understanding the function of BDNF in memory processes is of utmost importance to counteract Alzheimer’s disease.
680.	STDP depends on dendritic synapse location (Letzkus et al. 2006)
		This model was published in Letzkus, Kampa & Stuart (2006) J Neurosci 26(41):10420-9. The simulation creates several plots showing voltage and NMDA current and conductance changes at different apical dendritic locations in layer 5 pyramidal neurons during STDP induction protocols. Created by B. Kampa (2006).
681.	Steady-state Vm distribution of neurons subject to synaptic noise (Rudolph, Destexhe 2005)
		This package simulates synaptic background activity similar to in vivo measurements using a model of fluctuating synaptic conductances, and compares the simulations with analytic estimates. The steady-state membrane potential (Vm) distribution is calculated numerically and compared with the "extended" analytic expression provided in the reference (see this paper for details).
682.	Stochastic 3D model of neonatal rat spinal motoneuron (Ostroumov 2007)
		" ... Although existing models of motoneurons have indicated the distributed role of certain conductances in regulating firing, it is unclear how the spatial distribution of certain currents is ultimately shaping motoneuron output. Thus, it would be helpful to build a bridge between histological and electrophysiological data. The present report is based on the construction of a 3D motoneuron model based on available parameters applicable to the neonatal spinal cord. ..."
683.	Stochastic Ih and Na-channels in pyramidal neuron dendrites (Kole et al 2006)
		The hyperpolarization-activated cation current (Ih) plays an important role in regulating neuronal excitability, yet its native single-channel properties in the brain are essentially unknown. Here we use variance-mean analysis to study the properties of single Ih channels in the apical dendrites of cortical layer 5 pyramidal neurons in vitro. ... In contrast to the uniformly distributed single-channel conductance, Ih channel number increases exponentially with distance, reaching densities as high as approximately 550 channels/microm2 at distal dendritic sites. These high channel densities generate significant membrane voltage noise. By incorporating a stochastic model of Ih single-channel gating into a morphologically realistic model of a layer 5 neuron, we show that this channel noise is higher in distal dendritic compartments and increased threefold with a 10-fold increased single-channel conductance (6.8 pS) but constant Ih current density. ... These data suggest that, in the face of high current densities, the small single-channel conductance of Ih is critical for maintaining the fidelity of action potential output. See paper for more and details.
684.	Stochastic layer V pyramidal neuron: interpulse interval coding and noise (Singh & Levy 2017)
		Layer V pyramidal neuron with stochastic Na channels. Supports evidence for interpulse interval coding and has very detailed AIS with Nav1.2 and Nav1.6 channels.
685.	Stoney vs Histed: Quantifying spatial effects of intracortical microstims (Kumaravelu et al 2022)
		"...We implemented a biophysically-based computational model of a cortical column comprising neurons with realistic morphology and representative synapses. We quantified the spatial effects of single pulses and short trains of ICMS, including the volume of activated neurons and the density of activated neurons as a function of stimulation intensity..."
686.	Storing serial order in intrinsic excitability: a working memory model (Conde-Sousa & Aguiar 2013)
		" … Here we present a model for working memory which relies on the modulation of the intrinsic excitability properties of neurons, instead of synaptic plasticity, to retain novel information for periods of seconds to minutes. We show that it is possible to effectively use this mechanism to store the serial order in a sequence of patterns of activity. … The presented model exhibits properties which are in close agreement with experimental results in working memory. ... "
687.	Striatal D1R medium spiny neuron, including a subcellular DA cascade (Lindroos et al 2018)
		We are investigating how dopaminergic modulation of single channels can be combined to make the D1R possitive MSN more excitable. We also connect multiple channels to substrates of a dopamine induced subcellular cascade to highlight that the classical pathway is too slow to explain DA induced kinetics in the subsecond range (Howe and Dombeck, 2016. doi: 10.1038/nature18942)
688.	Striatal Output Neuron (Mahon, Deniau, Charpier, Delord 2000)
		Striatal output neurons (SONs) integrate glutamatergic synaptic inputs originating from the cerebral cortex. In vivo electrophysiological data have shown that a prior depolarization of SONs induced a short-term (1 sec)increase in their membrane excitability, which facilitated the ability of corticostriatal synaptic potentials to induce firing. Here we propose, using a computational model of SONs, that the use-dependent, short-term increase in the responsiveness of SONs mainly results from the slow kinetics of a voltage-dependent, slowly inactivating potassium A-current. This mechanism confers on SONs a form of intrinsic short-term memory that optimizes the synaptic input–output relationship as a function of their past activation.
689.	Submyelin Potassium accumulation in Subthalamic neuron (STN) axons (Bellinger et al. 2008)
		"To better understand the direct effects of DBS (Deep brain stimulation) on central neurons, a computational model of a myelinated axon has been constructed which includes the effects of K+ accumulation within the peri-axonal space. Using best estimates of anatomic and electrogenic model parameters for in vivo STN axons, the model predicts a functional block along the axon due to K+ accumulation in the submyelin space. ... These results suggest that therapeutic DBS of the STN likely results in a functional block for many STN axons, although a subset of STN axons may also be activated at the stimulating frequency. "
690.	Subthreshold inact. of K channels modulates APs in bitufted interneurons (Korngreen et al 2005)
		... In this study we show that in bitufted interneurones from layer 2/3 of the somatosensory cortex, the height and width of APs recorded at the soma are sensitive to changes in the resting membrane potential, suggesting subthreshold activity of voltage-gated conductances. Attributes of K+ currents examined in nucleated patches revealed a fast subthreshold-inactivating K+ conductance (Kf ) and a slow suprathreshold-inactivating K+ conductance (Ks ). Simulations of these K+ conductances, incorporated into a Hodgkin–Huxley-type model, suggested that during a single AP or during low frequency trains of APs, subthreshold inactivation of Kf was the primary modulator of AP shape, whereas during trains of APs the shape was governed to a larger degree by Ks resulting in the generation of smaller and broader APs. ... Compartmental simulation of the back-propagating AP suggested a mechanism for the modulation of the back-propagating AP height and width by subthreshold activation of Kf . We speculate that this signal may modulate retrograde GABA release and consequently depression of synaptic ef&#64257;cacy of excitatory input from neighbouring pyramidal neurones.
691.	Superior paraolivary nucleus neuron (Kopp-Scheinpflug et al. 2011)
		This is a model of neurons in the brainstem superior paraolivary nucleus (SPN), which produce very salient offset firing during sound stimulation. Rebound offset firing is triggered by IPSPs coming from the medial nucleus of the trapezoid body (MNTB). This model shows that AP firing can emerge from inhibition through integration of large IPSPs, driven by an extremely negative chloride reversal potential, combined with a large hyperpolarization- activated non-specific cationic current (IH), with a secondary contribution from a T-type calcium conductance (ITCa). As a result, tiny gaps in sound stimuli of just 3-4ms can elicit reliable APs that signal such brief offsets.
692.	Survey of electrically evoked responses in the retina (Tsai et al 2017)
		"Cones and horizontal cells are interconnected to adjacent cones and horizontal cells, respectively, with gap junctions. In particular, the horizontal cell gap junctional conductance is modulated by exogenous factors. What roles does this conductance play in the electrically evoked responses of horizontal cells? To address this question, we constructed a computational model consisting of the cone and horizontal cell layer..."
693.	Sympathetic Preganglionic Neurone (Briant et al. 2014)
		A model of a sympathetic preganglionic neurone of muscle vasoconstrictor-type.
694.	Synaptic gating at axonal branches, and sharp-wave ripples with replay (Vladimirov et al. 2013)
		The computational model of in vivo sharp-wave ripples with place cell replay. Excitatory post-synaptic potentials at dendrites gate antidromic spikes arriving from the axonal collateral, and thus determine when the soma and the main axon fire. The model allows synchronous replay of pyramidal cells during sharp-wave ripple event, and the replay is possible in both forward and reverse directions.
695.	Synaptic information transfer in computer models of neocortical columns (Neymotin et al. 2010)
		"... We sought to measure how the activity of the network alters information flow from inputs to output patterns. Information handling by the network reflected the degree of internal connectivity. ... With greater connectivity strength, the recurrent network translated activity and information due to contribution of activity from intrinsic network dynamics. ... At still higher internal synaptic strength, the network corrupted the external information, producing a state where little external information came through. The association of increased information retrieved from the network with increased gamma power supports the notion of gamma oscillations playing a role in information processing."
696.	Synaptic integration by MEC neurons (Justus et al. 2017)
		Pyramidal cells, stellate cells and fast-spiking interneurons receive running speed dependent glutamatergic input from septo-entorhinal projections. These models simulate the integration of this input by the different MEC celltypes.
697.	Synaptic integration in a model of granule cells (Gabbiani et al 1994)
		We have developed a compartmental model of a turtle cerebellar granule cell consisting of 13 compartments that represent the soma and 4 dendrites. We used this model to investigate the synaptic integration of mossy fiber inputs in granule cells. See reference or abstract at PubMed link below for more information.
698.	Synaptic integration in tuft dendrites of layer 5 pyramidal neurons (Larkum et al. 2009)
		Simulations used in the paper. Voltage responses to current injections in different tuft locations; NMDA and calcium spike generation. Summation of multiple input distribution.
699.	Synaptic plasticity: pyramid->pyr and pyr->interneuron (Tsodyks et al 1998)
		An implementation of a model of short-term synaptic plasticity with NEURON. The model was originally described by Tsodyks et al., who assumed that the synapse acted as a current source, but this implementation treats it as a conductance change. Tsodyks, M., Pawelzik, K., Markram, H. Neural networks with dynamic synapses. Neural Computation 10:821-835, 1998. Tsodyks, M., Uziel, A., Markram, H. Synchrony generation in recurrent networks with frequency-dependent synapses. J. Neurosci. 2000 RC50.
700.	Synaptic scaling balances learning in a spiking model of neocortex (Rowan & Neymotin 2013)
		Learning in the brain requires complementary mechanisms: potentiation and activity-dependent homeostatic scaling. We introduce synaptic scaling to a biologically-realistic spiking model of neocortex which can learn changes in oscillatory rhythms using STDP, and show that scaling is necessary to balance both positive and negative changes in input from potentiation and atrophy. We discuss some of the issues that arise when considering synaptic scaling in such a model, and show that scaling regulates activity whilst allowing learning to remain unaltered.
701.	Synaptic transmission at the calyx of Held (Graham et al 2001)
		This model allows the user to investigate faciliation and depression in a complex Monte Carlo model of the calyx of Held, a giant synapse in the mammalian auditory system (Graham et al, 2001)
702.	Synchrony by synapse location (McTavish et al. 2012)
		This model considers synchrony between mitral cells induced via shared granule cell interneurons while taking into account the spatial constraints of the system. In particular, since inhibitory inputs decay passively along the lateral dendrites, this model demonstrates that an optimal arrangement of the inhibitory synapses will be near the cell bodies of the relevant mitral cells.
703.	Synthesis of spatial tuning functions from theta cell spike trains (Welday et al., 2011)
		A single compartment model reproduces the firing rate maps of place, grid, and boundary cells by receiving inhibitory inputs from theta cells. The theta cell spike trains are modulated by the rat's movement velocity in such a way that phase interference among their burst pattern creates spatial envelope function which simulate the firing rate maps.
704.	T channel currents (Vitko et al 2005)
		Computer simulations predict that seven of the SNPs would increase firing of neurons, with three of them inducing oscillations at similar frequencises. 3 representative models from the paper have been submited: a wild-type (WT) recombinant Cav3.2 T-channel, and two of the mutants described in the Vitko et al., 2005 paper (C456S and R788C). See the paper for more and details.
705.	T-type Ca current in thalamic neurons (Wang et al 1991)
		A model of the transient, low-threshold voltage-dependent (T-type) Ca2+ current is constructed using whole-cell voltage-clamp data from enzymatically isolated rat thalamocortical relay neurons. The T-type Ca2+ current is described according to the Hodgkin-Huxley scheme, using the m3h format, with rate constants determined from the experimental data.
706.	T-type Calcium currents (McRory et al 2001)
		NEURON mod files for CaT currents from the paper McRory et al., J.Biol.Chem. 276:3999 (2001). In this paper, three members (alpha-1G, -1H, and -1I) of the LVA calcium channels family were studied. Kinetic parameters were derived from functional expression in transfected cells.
707.	Temperature sensitive axon models (DeMaegd & Stein 2020)
708.	Temperature-Sensitive conduction at axon branch points (Westerfield et al 1978)
		Propagation of impulses through branching regions of squid axons was examined experimentally and with computer simulations. The ratio of postbranch/prebranch diameters at which propagation failed was very sensitive to temperature.
709.	Thalamic interneuron multicompartment model (Zhu et al. 1999)
		This is an attempt to recreate a set of simulations originally performed in 1994 under NEURON version 3 and last tested in 1999. When I ran it now it did not behave exactly the same as previously which I suspect is due to some minor mod file changes on my side rather than due to any differences among versions. After playing around with the parameters a little bit I was able to get something that looks generally like a physiological trace in J Neurophysiol, 81:702--711, 1999, fig. 8b top trace. This sad preface is simply offered in order to encourage anyone who is interested in this model to make and post fixes. I'm happy to help out. Simulation by JJ Zhu To run nrnivmodl nrngui.hoc
710.	Thalamic network model of deep brain stimulation in essential tremor (Birdno et al. 2012)
		"... Thus the decreased effectiveness of temporally irregular DBS trains is due to long pauses in the stimulus trains, not the degree of temporal irregularity alone. We also conducted computer simulations of neuronal responses to the experimental stimulus trains using a biophysical model of the thalamic network. Trains that suppressed tremor in volunteers also suppressed fluctuations in thalamic transmembrane potential at the frequency associated with cerebellar burst-driver inputs. Clinical and computational findings indicate that DBS suppresses tremor by masking burst-driver inputs to the thalamus and that pauses in stimulation prevent such masking. Although stimulation of other anatomic targets may provide tremor suppression, we propose that the most relevant neuronal targets for effective tremor suppression are the afferent cerebellar fibers that terminate in the thalamus."
711.	Thalamic neuron: Modeling rhythmic neuronal activity (Meuth et al. 2005)
		The authors use an in vitro cell model of a single acutely isolated thalamic neuron in the NEURON simulation environment to address and discuss questions in an undergraduate course. Topics covered include passive electrical properties, composition of action potentials, trains of action potentials, multicompartment modeling, and research topics. The paper includes detailed instructions on how to run the simulations in the appendix.
712.	Thalamic quiescence of spike and wave seizures (Lytton et al 1997)
		A phase plane analysis of a two cell interaction between a thalamocortical neuron (TC) and a thalamic reticularis neuron (RE).
713.	Thalamic Relay Neuron: I-h (McCormick, Pape 1990)
		NEURON mod files for the Ih current from the paper: McCormick DA, Pape HC. Properties of a hyperpolarization-activated cation current and its role in rhythmic oscillation in thalamic relay neurones. J. Physiol. 1990 431:291-318.
714.	Thalamic Relay Neuron: I-T current (Williams, Stuart 2000)
		NEURON mod files for the Ca-T current from the paper: Williams SR, Stuart GJ, Action potential backpropagation and somato-dendritic distribution of ion channels in thalamocortical neurons. J Neurosci. 2000 20:1307-17. Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model.
715.	Thalamic Reticular Network (Destexhe et al 1994)
		Demo for simulating networks of thalamic reticular neurons (reproduces figures from Destexhe A et al 1994)
716.	Thalamic reticular neurons: the role of Ca currents (Destexhe et al 1996)
		The experiments and modeling reported in this paper show how intrinsic bursting properties of RE cells may be explained by dendritic calcium currents.
717.	Thalamocortical and Thalamic Reticular Network (Destexhe et al 1996)
		NEURON model of oscillations in networks of thalamocortical and thalamic reticular neurons in the ferret. (more applications for a model quantitatively identical to previous DLGN model; updated for NEURON v4 and above)
718.	Thalamocortical augmenting response (Bazhenov et al 1998)
		In the cortical model, augmenting responses were more powerful in the "input" layer compared with those in the "output" layer. Cortical stimulation of the network model produced augmenting responses in cortical neurons in distant cortical areas through corticothalamocortical loops and low-threshold intrathalamic augmentation. ... The predictions of the model were compared with in vivo recordings from neurons in cortical area 4 and thalamic ventrolateral nucleus of anesthetized cats. The known intrinsic properties of thalamic cells and thalamocortical interconnections can account for the basic properties of cortical augmenting responses. See reference for details. NEURON implementation note: cortical SU cells are getting slightly too little stimulation - reason unknown.
719.	Thalamocortical Relay cell under current clamp in high-conductance state (Zeldenrust et al 2018)
		Mammalian thalamocortical relay (TCR) neurons switch their firing activity between a tonic spiking and a bursting regime. In a combined experimental and computational study, we investigated the features in the input signal that single spikes and bursts in the output spike train represent and how this code is influenced by the membrane voltage state of the neuron. Identical frozen Gaussian noise current traces were injected into TCR neurons in rat brain slices to adjust, fine-tune and validate a three-compartment TCR model cell (Destexhe et al. 1998, accession number 279). Three currents were added: an h-current (Destexhe et al. 1993,1996, accession number 3343), a high-threshold calcium current and a calcium- activated potassium current (Huguenard & McCormick 1994, accession number 3808). The information content carried by the various types of events in the signal as well as by the whole signal was calculated. Bursts phase-lock to and transfer information at lower frequencies than single spikes. On depolarization the neuron transits smoothly from the predominantly bursting regime to a spiking regime, in which it is more sensitive to high-frequency fluctuations. Finally, the model was used to in the more realistic “high-conductance state” (Destexhe et al. 2001, accession number 8115), while being stimulated with a Poisson input (Brette et al. 2007, Vogels & Abbott 2005, accession number 83319), where fluctuations are caused by (synaptic) conductance changes instead of current injection. Under “standard” conditions bursts are difficult to initiate, given the high degree of inactivation of the T-type calcium current. Strong and/or precisely timed inhibitory currents were able to remove this inactivation.
720.	Thalamocortical relay neuron models constrained by experiment and optimization (Iavarone et al 2019)
721.	The APP in C-terminal domain alters CA1 neuron firing (Pousinha et al 2019)
		"The amyloid precursor protein (APP) is central to AD pathogenesis and we recently showed that its intracellular domain (AICD) could modify synaptic signal integration. We now hypothezise that AICD modifies neuron firing activity, thus contributing to the disruption of memory processes. Using cellular, electrophysiological and behavioural techniques, we showed that pathological AICD levels weakens CA1 neuron firing activity through a gene transcription-dependent mechanism. Furthermore, increased AICD production in hippocampal neurons modifies oscillatory activity, specifically in the gamma frequency range, and disrupts spatial memory task. Collectively, our data suggest that AICD pathological levels, observed in AD mouse models and in human patients, might contribute to progressive neuron homeostatic failure, driving the shift from normal ageing to AD."
722.	The cannula artifact (Chandler & Hodgkin 1965)
		Chandler and Hodgkin 1965 describes how using a high impedance electrode can lead to squid axon recordings that appear to overshoot the sodium reversal potential, thus resolving controversial recordings at the time.
723.	The STN-GPe network; subthalamic nucleus, prototypic GPe, and arkypallidal GPe neurons (Kitano 2023)
724.	The subcellular distribution of T-type Ca2+ channels in LGN interneurons (Allken et al. 2014)
		" ...To study the relationship between the (Ca2+ channel) T-distribution and several (LGN interneuron) IN response properties, we here run a series of simulations where we vary the T-distribution in a multicompartmental IN model with a realistic morphology. We find that the somatic response to somatic current injection is facilitated by a high T-channel density in the soma-region. Conversely, a high T-channel density in the distal dendritic region is found to facilitate dendritic signalling in both the outward direction (increases the response in distal dendrites to somatic input) and the inward direction (the soma responds stronger to distal synaptic input). ..."
725.	The virtual slice setup (Lytton et al. 2008)
		"In an effort to design a simulation environment that is more similar to that of neurophysiology, we introduce a virtual slice setup in the NEURON simulator. The virtual slice setup runs continuously and permits parameter changes, including changes to synaptic weights and time course and to intrinsic cell properties. The virtual slice setup permits shocks to be applied at chosen locations and activity to be sampled intra- or extracellularly from chosen locations. ..."
726.	Tight junction model of CNS myelinated axons (Devaux and Gow 2008)
		Two models are included: 1) a myelinated axon is represented by an equivalent circuit with a double cable design but includes a tight junction in parallel with the myelin membrane RC circuit (called double cable model, DCM). 2) a myelinated axon is represented by an equivalent circuit with a double cable design but includes a tight junction in series with the myelin RC circuit (called tight junction model, TJM). These models have been used to simulate data from compound action potentials measured in mouse optic nerve from Claudin 11-null mice in Fig. 6 of: Devaux, J.J. & Gow, A. (2008) Tight Junctions Potentiate The Insulative Properties Of Small CNS Myelinated Axons. J Cell Biol 183, 909-921.
727.	Tonic firing in substantia gelatinosa neurons (Melnick et al 2004)
		Ionic conductances underlying excitability in tonically firing neurons (TFNs) from substantia gelatinosa (SG) were studied by the patch-clamp method in rat spinal cord slices. ... Suppression of Ca2+ and KCA currents ... did not abolish the basic pattern of tonic firing, indicating that it was generated by voltage-gated Na+ and K+ currents. ... on the basis of present data, we created a model of TFN and showed that Na+ and KDR currents are sufficient to generate a basic pattern of tonic firing. It is concluded that the balanced contribution of all ionic conductances described here is important for generation and modulation of tonic firing in SG neurons. See paper for more and details.
728.	Tonic neuron in spinal lamina I: prolongation of subthreshold depol. (Prescott and De Koninck 2005)
		Model demonstrates mechanism whereby two kinetically distinct inward currents act synergistically to prolong subthreshold depolarization. The important currents are a persistent Na current (with fast kinetics) and a persistent Ca current (with slower kinetics). Model also includes a slow K current and transient Ca current, in addition to standard HH currents. Model parameters are set to values used in Fig. 8A. Simulation shows prolonged depolarizations in response to two brief stimuli.
729.	Tonic-clonic transitions in a seizure simulation (Lytton and Omurtag 2007)
		"... The authors have ... computationally manageable networks of moderate size consisting of 1,000 to 3,000 neurons with multiple intrinsic and synaptic properties. Experiments on these simulations demonstrated the presence of epileptiform behavior in the form of repetitive high-intensity population events (clonic behavior) or latch-up with near maximal activity (tonic behavior). ... Several simulations revealed the importance of random coincident inputs to shift a network from a low-activation to a high-activation epileptiform state. Finally, a simulated anticonvulsant acting on excitability tended to preferentially decrease tonic activity."
730.	Transfer properties of Neuronal Dendrites (Korogod et al 1998)
		The somatopetal current transfer was studied in mathematical models of a reconstructed brainstem motoneuron with tonically activated excitatory synaptic inputs uniformly distributed over the dendritic arborization. See paper and below readme.txt for more information.
731.	Translating network models to parallel hardware in NEURON (Hines and Carnevale 2008)
		Shows how to move a working network model written in NEURON from a serial processor to a parallel machine in such a way that the final result will produce numerically identical results on either serial or parallel hardware.
732.	TRPM8-dependent dynamic response in cold thermoreceptors (Olivares et al. 2015)
		This model reproduces the dynamic response of cold thermoreceptors, transiently changing the firing rate upon heating or cooling. It also displays the 'static' or adapted firing patterns observed in these receptors.
733.	TTX-R Na+ current effect on cell response (Herzog et al 2001)
		"Small dorsal root ganglion (DRG) neurons, which include nociceptors, express multiple voltage-gated sodium currents. In addition to a classical fast inactivating tetrodotoxin-sensitive (TTX-S) sodium current, many of these cells express a TTX-resistant (TTX-R) sodium current that activates near -70 mV and is persistent at negative potentials. To investigate the possible contributions of this TTX-R persistent (TTX-RP) current to neuronal excitability, we carried out computer simulations using the Neuron program with TTX-S and -RP currents, fit by the Hodgkin-Huxley model, that closely matched the currents recorded from small DRG neurons. ..." See paper for more and details.
734.	Two populations of excitatory neurons in the superficial retrosplenial cortex (Brennan et al 2020)
		Hyperexcitable neurons enable precise and persistent information encoding in the superficial retrosplenial cortex
735.	Updated Tritonia Swim CPG (Calin-Jagemann et al. 2007)
		Model of the 3-cell core CPG (DSI, C2, and VSI-B) mediating escape swimming in Tritonia diomedea. Cells use a hybrid integrate-and-fire scheme pioneered by Peter Getting. Each model cell is reconstructed from extensive physiological measurements to precisely mimic I-F curves, synaptic waveforms, and functional connectivity.
736.	Using NEURON for reaction-diffusion modeling of extracellular dynamics (Newton et al 2018)
		Development of credible clinically-relevant brain simulations has been slowed due to a focus on electrophysiology in computational neuroscience, neglecting the multiscale whole-tissue modeling approach used for simulation in most other organ systems. We have now begun to extend the NEURON simulation platform in this direction by adding extracellular modeling. NEURON's extracellular reaction-diffusion is supported by an intuitive Python-based where/who/what command sequence, derived from that used for intracellular reaction diffusion, to support coarse-grained macroscopic extracellular models. This simulation specification separates the expression of the conceptual model and parameters from the underlying numerical methods. In the volume-averaging approach used, the macroscopic model of tissue is characterized by free volume fraction—the proportion of space in which species are able to diffuse, and tortuosity—the average increase in path length due to obstacles. These tissue characteristics can be defined within particular spatial regions, enabling the modeler to account for regional differences, due either to intrinsic organization, particularly gray vs. white matter, or to pathology such as edema. We illustrate simulation development using spreading depression, a pathological phenomenon thought to play roles in migraine, epilepsy and stroke.
737.	Using Strahler's analysis to reduce realistic models (Marasco et al, 2013)
		Building on our previous work (Marasco et al., (2012)), we present a general reduction method based on Strahler's analysis of neuron morphologies. We show that, without any fitting or tuning procedures, it is possible to map any morphologically and biophysically accurate neuron model into an equivalent reduced version. Using this method for Purkinje cells, we demonstrate how run times can be reduced up to 200-fold, while accurately taking into account the effects of arbitrarily located and activated synaptic inputs.
738.	Ventromedial Thalamocortical Neuron (Bichler et al 2021)
		"Biophysical computer modeling of a thalamic neuron demonstrated that an increase in rebound spiking can also be accounted for by a decrease in the M-type potassium current. Modeling also showed that an increase in sag with hyperpolarizing steps found after 6-OHDA treatment could in part but not fully be accounted for by the decrease in M-type current. These findings support the hypothesis that homeostatic changes in BGMT neural properties following 6-OHDA treatment likely influence the signal processing taking place in the BG thalamocortical network in Parkinson's disease."
739.	Vertical system (VS) fly cells with biophysics (Dan et al 2018)
		"The fly visual system offers a unique opportunity to explore computations performed by single neurons. Two previous studies characterized, in vivo, the receptive field (RF) of the vertical system (VS) cells of the blowfly (calliphora vicina), both intracellularly in the axon, and, independently using Ca2+ imaging, in hundreds of distal dendritic branchlets. We integrated this information into detailed passive cable and compartmental models of 3D reconstructed VS cells. Within a given VS cell type, the transfer resistance (TR) from different branchlets to the axon differs substantially, suggesting that they contribute unequally to the shaping of the axonal RF. ..."
740.	Visual Cortex Neurons: Dendritic computations (Archie, Mel 2000)
		Neuron and C program files from Archie, K.A. and Mel, B.W. A model of intradendritic computation of binocular disparity. Nature Neuroscience 3:54-63, 2000 The original files for this model are located at the web site http://www-lnc.usc.edu/~karchie/synmap
741.	Visual Cortex Neurons: Dendritic study (Anderson et al 1999)
		Neuron mod and hoc files for the paper: Anderson, J.C. Binzegger, T., Kahana, O., Segev, I., and Martin, K.A.C Dendritic asymmetry cannot account for directional responses in visual cortex. Nature Neuroscience 2:820:824, 1999
742.	Voltage and light-sensitive Channelrhodopsin-2 model (ChR2-H134R) (Williams et al. 2013) (NEURON)
		" ... Focusing on one of the most widely used ChR2 mutants (H134R) with enhanced current, we collected a comprehensive experimental data set of the response of this ion channel to different irradiances and voltages, and used these data to develop a model of ChR2 with empirically-derived voltage- and irradiance- dependence, where parameters were fine-tuned via simulated annealing optimization. This ChR2 model offers: 1) accurate inward rectification in the current-voltage response across irradiances; 2) empirically-derived voltage- and light-dependent kinetics (activation, deactivation and recovery from inactivation); and 3) accurate amplitude and morphology of the response across voltage and irradiance settings. Temperature-scaling factors (Q10) were derived and model kinetics was adjusted to physiological temperatures. ... "
743.	Voltage- and Branch-specific Climbing Fiber Responses in Purkinje Cells (Zang et al 2018)
		"Climbing fibers (CFs) provide instructive signals driving cerebellar learning, but mechanisms causing the variable CF responses in Purkinje cells (PCs) are not fully understood. Using a new experimentally validated PC model, we unveil the ionic mechanisms underlying CF-evoked distinct spike waveforms on different parts of the PC. We demonstrate that voltage can gate both the amplitude and the spatial range of CF-evoked Ca2+ influx by the availability of K+ currents. ... The voltage- and branch-specific CF responses can increase dendritic computational capacity and enable PCs to actively integrate CF signals."
744.	Voltage-based STDP synapse (Clopath et al. 2010)
		Implementation of the STDP rule by Clopath et al., Nat. Neurosci. 13(3):344-352,2010 STDP mechanism added to the AlphaSynapse in NEURON.
745.	Vomeronasal sensory neuron (Shimazaki et al 2006)
		NEURON model files from the papers: Shimazaki et al, Chem. Senses, epub ahead of print (2006) Electrophysiological properties and modeling of murine vomeronasal sensory neurons in acute slice preparations. The model reproduces quantitatively the experimentally observed firing rates of these neurons under a wide range of input currents.
746.	VTA neurons: Morphofunctional alterations in acute opiates withdrawal (Enrico et al. 2016)
		" ... Here we present a biophysical model of a DA VTA neuron based on 3D morphological reconstruction and electrophysiological data, showing how opiates withdrawal-driven morphological and electrophysiological changes could affect the firing rate and discharge pattern...."
747.	Xenopus Myelinated Neuron (Frankenhaeuser, Huxley 1964)
		Frankenhaeuser, B. and Huxley, A. F. (1964), The action potential in the myelinated nerve fiber of Xenopus Laevis as computed on the basis of voltage clamp data. J. Physiol. 171: 302-315. See README file for more information.
748.	Zebrafish Mauthner-cell model (Watanabe et al 2017)
		The NEURON model files encode the channel generator and firing simulator for simulating development and differentiation of the Mauthner cell (M-cell) excitability in zebrafish. The channel generator enables us to generate arbitrary Na+ and K+ channels by changing parameters of a Hodgkin-Huxley model under emulation of two-electrode voltage-clamp recordings in Xenopus oocyte system. The firing simulator simulates current-clamp recordings to generate firing patterns of the model M-cell, which are implemented with arbitrary-generated basic Na+ and K+ conductances and low-threshold K+ channels Kv7.4/KCNQ4 and sole Kv1.1 or Kv1.1 coexpressed with Kvbeta2.

Re-display model names without descriptions