Circuits 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.	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).
2.	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.
3.	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. ..."
4.	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.
5.	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.
6.	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.
7.	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.
8.	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. …”
9.	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.
10.	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)
11.	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.
12.	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.
13.	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.
14.	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.
15.	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.
16.	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.
17.	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. ..."
18.	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. ..."
19.	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.
20.	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. ..."
21.	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.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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. ..."
28.	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. ..."
29.	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.
30.	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."
31.	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.
32.	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
33.	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.
34.	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.
35.	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.
36.	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
37.	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.
38.	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
39.	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."
40.	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).
41.	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.
42.	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.
43.	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. "
44.	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. ...
45.	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).
46.	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.
47.	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).
48.	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.
49.	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.
50.	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. ..."
51.	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. ... "
52.	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. ..."
53.	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.
54.	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. ..."
55.	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."
56.	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.
57.	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.
58.	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.
59.	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). ..."
60.	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.
61.	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.
62.	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.
63.	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.
64.	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."
65.	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.
66.	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
67.	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.
68.	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.
69.	Hopfield and Brody model (Hopfield, Brody 2000) (NEURON+python)
		Demonstration of Hopfield-Brody snychronization using artificial cells in NEURON+python.
70.	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.
71.	Human layer 2/3 cortical microcircuits in health and depression (Yao et al, 2022)
72.	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. ..."
73.	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"
74.	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.
75.	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.
76.	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.
77.	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.
78.	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
79.	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. ..."
80.	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...."
81.	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.
82.	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).
83.	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.
84.	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).
85.	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.
86.	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..."
87.	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."
88.	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. "
89.	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.
90.	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."
91.	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. ..."
92.	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. ..."
93.	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.
94.	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. ..."
95.	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. …”
96.	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."
97.	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 ..."
98.	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.
99.	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. ..."
100.	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.
101.	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.
102.	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. ..."
103.	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).
104.	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
105.	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."
106.	Olfactory bulb cluster formation (Migliore et al. 2010)
		Functional roles of distributed synaptic clusters in the mitral-granule cell network of the olfactory bulb.
107.	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.
108.	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.
109.	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.
110.	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.
111.	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.
112.	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.
113.	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."
114.	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.
115.	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. [...]"
116.	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, ..."
117.	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.
118.	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.
119.	Phase response theory in sparsely + strongly connected inhibitory NNs (Tikidji-Hamburyan et al 2019)
120.	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. ..."
121.	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.
122.	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. "
123.	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.
124.	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. ..."
125.	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.
126.	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
127.	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
128.	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. ..."
129.	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.
130.	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.
131.	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. ..."
132.	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. ... "
133.	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.
134.	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. ..."
135.	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.
136.	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. ..."
137.	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.
138.	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. ..."
139.	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.
140.	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.
141.	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.
142.	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.
143.	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..."
144.	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. ... "
145.	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.
146.	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."
147.	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.
148.	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.
149.	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."
150.	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).
151.	Thalamic Reticular Network (Destexhe et al 1994)
		Demo for simulating networks of thalamic reticular neurons (reproduces figures from Destexhe A et al 1994)
152.	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)
153.	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.
154.	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. ..."
155.	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."
156.	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.
157.	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.

Re-display model names without descriptions