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(Includes BK, IK, SK, and I AHP currents; K current activated by increases in [Ca2+]i; voltage dependence varies)
| Models | Description |
| A Fast Rhythmic Bursting Cell: in vivo cell modeling (Lee 2007) | |
| One of the cellular mechanisms underlying the generation of gamma oscillations is a type of cortical pyramidal neuron named fast rhythmic bursting (FRB) cells. After cells from cats' primary visual cortices were filled with Neurobiotin, the brains were cut, and the cells were photographed. One FRB cell was chosen to be confocaled, reconstructed with Neurolucida software, and generated a detailed multi-compartmental model in the NEURON program. We explore firing properties of FRB cells and the role of enhanced Na+ conductance. | |
| A Model of Multiple Spike Initiation Zones in the Leech C-interneuron (Crisp 2009) | |
| The leech C-interneuron and its electrical synapse with the S-interneuron exhibit unusual properties: an asymmetric delay when impulses travel from one soma to the other, and graded C-interneuron impulse amplitudes under elevated divalent cation concentrations. These properties have been simulated using a SNNAP model in which the C-interneuron has multiple, independent spike initiation zones associated with individual electrical junctions with the C-interneuron. | |
| A Moth MGC Model-A HH network with quantitative rate reduction (Buckley & Nowotny 2011) | |
| We provide the model used in Buckley & Nowotny (2011). It consists of a network of Hodgkin Huxley neurons coupled by slow GABA_B synapses which is run alongside a quantitative reduction described in the associated paper. | |
| A model for pituitary GH(3) lactotroph (Wu and Chang 2005) | |
| The ATP-sensitive K(+) (K(ATP)) channels are composed of sulfonylurea receptor and inwardly rectifying K(+) channel (Kir6.2) subunit. These channels are regulated by intracellular ADP/ATP ratio and play a role in cellular metabolism. ... The objective of this study was to determine whether Diethyl pyrocarbonate (DEPC) modifies K(ATP)-channel activity in pituitary GH(3) cells. ... Simulation studies also demonstrated that the increased conductance of K(ATP)-channels used to mimic DEPC actions reduced the frequency of spontaneous action potentials and fluctuation of intracellular Ca(2+). The results indicate that chemical modification with DEPC enhances K(ATP)-channel activity and influences functional activities of pituitary GH(3) cells. See paper for more and details. | |
| A set of reduced models of layer 5 pyramidal neurons (Bahl et al. 2012) | |
| These are the NEURON files for 10 different models of a reduced L5 pyramidal neuron. The parameters were obtained by automatically fitting the models to experimental data using a multi objective evolutionary search strategy. Details on the algorithm can be found at www.g-node.org/emoo and in Bahl et al. (2012). | |
| A simplified cerebellar Purkinje neuron (the PPR model) (Brown et al. 2010) | |
| These models were implemented in NEURON by Sherry-Ann Brown in the laboratory of Leslie M. Loew. The files reproduce Figures 2c-f from Brown et al, 2010 "Virtual NEURON: a Strategy For Merged Biochemical and Electrophysiological Modeling". | |
| A simplified model of NMDA oscillations in lamprey locomotor neurons (Huss et al. 2008) | |
| Using experiments in conjunction with this simplified model, we sought to understand the basic mechanisms behind NMDA-induced oscillations in lamprey locomotor neurons, specifically (a) how the oscillation frequency depends on NMDA concentration and why, and (b) what the minimal number of components for generating NMDA oscillations is (in vitro and in the model). | |
| 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. | |
| 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. | |
| AP back-prop. explains threshold variability and rapid rise (McCormick et al. 2007, Yu et al. 2008) | |
| This simple axon-soma model explained how the rapid rising phase in the somatic spike is derived from the propagated axon initiated spike, and how the somatic spike threshold variance is affected by spike propagation. | |
| AP shape and parameter constraints in optimization of compartment models (Weaver and Wearne 2006) | |
| "... We construct an objective function that includes both time-aligned action potential shape error and errors in firing rate and firing regularity. We then implement a variant of simulated annealing that introduces a recentering algorithm to handle infeasible points outside the boundary constraints. We show how our objective function captures essential features of neuronal firing patterns, and why our boundary management technique is superior to previous approaches." | |
| Action Potential initiation and backpropagation in Neocortical L5 Pyramidal Neuron (Hu et al. 2009) | |
| "...Previous computational studies have yielded conflicting conclusions about the role of Na+ channel density and biophysical properties in action potential initiation as a result of inconsistent estimates of channel density. Our modeling studies integrated the immunostaining and electrophysiological results and showed that the lowest threshold for action potential initiation at the distal AIS was largely determined by the density of low-threshold Nav1.6 channels ... Distinct from the function of Nav1.6 channel, the Nav1.2 channel may control action potential backpropagation because of its high density at the proximal AIS and high threshold. ... In conclusion, distal AIS accumulation of Nav1.6 channels determines the low threshold for action potential initiation; whereas proximal AIS accumulation of Nav1.2 channels sets the threshold for the generation of somatodendritic potentials and ensures action potential backpropagation to the soma and dendrites. Thus, Nav1.6 and Nav1.2 channels serve distinct functions in action potential initiation and backpropagation." | |
| Activity dependent conductances in a neuron model (Liu et al. 1998) | |
| "... We present a model of a stomatogastric ganglion (STG) neuron in which several Ca2+-dependent pathways are used to regulate the maximal conductances of membrane currents in an activity-dependent manner. Unlike previous models of this type, the regulation and modification of maximal conductances by electrical activity is unconstrained. The model has seven voltage-dependent membrane currents and uses three Ca2+ sensors acting on different time scales. ... The model suggests that neurons may regulate their conductances to maintain fixed patterns of electrical activity, rather than fixed maximal conductances, and that the regulation process requires feedback systems capable of reacting to changes of electrical activity on a number of different time scales." | |
| Afferent Integration in the NAcb MSP Cell (Wolf et al. 2005) | |
| "We describe a computational model of the principal cell in the nucleus accumbens (NAcb), the medium spiny projection (MSP) neuron. The model neuron, constructed in NEURON, includes all of the known ionic currents in these cells and receives synaptic input from simulated spike trains via NMDA, AMPA, and GABAA receptors. ... results suggest that afferent information integration by the NAcb MSP cell may be compromised by pathology in which the NMDA current is altered or modulated, as has been proposed in both schizophrenia and addiction." | |
| Allosteric gating of K channels (Horrigan et al 1999) | |
| Calcium sensitive large-conductance K channel conductance is controlled by both cytoplasmic calcium and membrane potential. Experimental data obtained by the inside out patch method can be understood in terms of a gating scheme where a central transition between a closed and an open conformation is allosterically regulated by the state of four independent and identical voltage sensors. See paper for more and details. | |
| Axonal NaV1.6 Sodium Channels in AP Initiation of CA1 Pyramidal Neurons (Royeck et al. 2008) | |
| "... We show that the Na+ channel NaV1.6 displays a striking aggregation at the AIS of cortical neurons. ... In combination with simulations using a realistic computer model of a CA1 pyramidal cell, our results imply that a hyperpolarized voltage-dependence of activation of AIS NaV1.6 channels is important both in determining spike threshold and localizing spike initiation to the AIS. ... These results suggest that NaV1.6 subunits at the AIS contribute significantly to its role as spike trigger zone and shape repetitive discharge properties of CA1 neurons." | |
| Axonal Projection and Interneuron Types (Helmstaedter et al. 2008) | |
| "Interneurons in layer 2/3 (L2/3) of the somatosensory cortex show 4 types of axonal projection patterns with reference to the laminae and borders of columns in rat barrel cortex (Helmstaedter et al. 2008a). Here, we analyzed the dendritic geometry and electrical excitability of these interneurons. ... We conclude that 1) dendritic polarity is correlated to intrinsic electrical excitability, and 2) the axonal projection pattern represents an independent classifier of interneurons. " | |
| Axonal gap junctions produce fast oscillations in cerebellar Purkinje cells (Traub et al. 2008) | |
| Examines how electrical coupling between proximal axons produces fast oscillations in cerebellar Purkinje cells. Traub RD, Middleton SJ, Knopfel T, Whittington MA (2008) Model of very fast (>75 Hz) network oscillations generated by electrical coupling between the proximal axons of cerebellar Purkinje cells. European Journal of Neuroscience in press. | |
| Basal ganglia-thalamic network model for deep brain stimulation (So et al. 2011) | |
| This is a model of the basal ganglia-thalamic network, modified from the Rubin and Terman model (High frequency stimulation of the Subthalamic Nucleus, Rubin and Terman 2004). We subsequently used this model to investigate the effectiveness of STN and GPi DBS as well as lesion when various proportions of local cells and fibers of passage were activated or silenced. The BG network exhibited characteristics consistent with published experimental data, both on the level of single cells and on the network level. Perhaps most notably, and in contrast to the original RT model, the changes in the thalamic error index with changes in the DBS frequency matched well the changes in clinical symptoms with changes in DBS frequency. | |
| Bursting and resonance in cerebellar granule cells (D'Angelo et al 2001) | |
| In this study we report theta-frequency (3–12 Hz) bursting and resonance in rat cerebellar granule cells and show that these neurons express a previously unidentified slow repolarizing K1 current (IK-slow ). Our experimental and modeling results indicate that IK-slow was necessary for both bursting and resonance. See paper for more. | |
| 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. | |
| CA1 pyramidal neuron to study INaP properties and repetitive firing (Uebachs et al. 2010) | |
| A model of a CA1 pyramidal neuron containing a biophysically realistic morphology and 15 distributed voltage and Ca2+-dependent conductances. Repetitive firing is modulated by maximal conductance and the voltage dependence of the persistent Na+ current (INaP). | |
| CA1 pyramidal neuron: as a 2-layer NN and subthreshold synaptic summation (Poirazi et al 2003) | |
| We developed a CA1 pyramidal cell model calibrated with a broad spectrum of in vitro data. Using simultaneous dendritic and somatic recordings, and combining results for two different response measures (peak vs. mean EPSP), two different stimulus formats (single shock vs. 50 Hz trains), and two different spatial integration conditions (within vs. between-branch summation), we found the cell's subthreshold responses to paired inputs are best described as a sum of nonlinear subunit responses, where the subunits correspond to different dendritic branches. In addition to suggesting a new type of experiment and providing testable predictions, our model shows how conclusions regarding synaptic arithmetic can be influenced by an array of seemingly innocuous experimental design choices. | |
| CA1 pyramidal neuron: depolarization block (Bianchi et al. 2012) | |
| NEURON files from the paper: On the mechanisms underlying the depolarization block in the spiking dynamics of CA1 pyramidal neurons by D.Bianchi, A. Marasco, A.Limongiello, C.Marchetti, H.Marie,B.Tirozzi, M.Migliore (2012). J Comput. Neurosci. In press. DOI: 10.1007/s10827-012-0383-y. Experimental findings shown that under sustained input current of increasing strength neurons eventually stop firing, entering a depolarization block. We analyze the spiking dynamics of CA1 pyramidal neuron models using the same set of ionic currents on both an accurate morphological reconstruction and on its reduction to a single-compartment. The results show the specic ion channel properties and kinetics that are needed to reproduce the experimental findings, and how their interplay can drastically modulate the neuronal dynamics and the input current range leading to depolarization block. | |
| CA1 pyramidal: Stochastic amplification of KCa in Ca2+ microdomains (Stanley et al. 2011) | |
| This minimal model investigates stochastic amplification of calcium-activated potassium (KCa) currents. Amplification results from calcium being released in short high amplitude pulses associated with the stochastic gating of calcium channels in microdomains. This model predicts that such pulsed release of calcium significantly increases subthreshold SK2 currents above what would be produced by standard deterministic models. However, there is little effect on a simple sAHP current kinetic scheme. This suggests that calcium stochasticity and microdomains should be considered when modeling certain KCa currents near subthreshold conditions. | |
| CA3 Pyramidal Neuron (Migliore et al 1995) | |
| Model files from the paper: M. Migliore, E. Cook, D.B. Jaffe, D.A. Turner and D. Johnston, Computer simulations of morphologically reconstructed CA3 hippocampal neurons, J. Neurophysiol. 73, 1157-1168 (1995). Demonstrates how the same cell could be bursting or non bursting according to the Ca-independent conductance densities. Includes calculation of intracellular Calcium. Instructions are provided in the below README file. Contact michele.migliore@pa.ibf.cnr.it if you have any questions about the implementation of the model. | |
| CA3 pyramidal cell: rhythmogenesis in a reduced Traub model (Pinsky, Rinzel 1994) | |
| Fig. 2A and 3 are reproduced in this simulation of Pinsky PF, Rinzel J (1994). | |
| CA3 pyramidal neuron (Lazarewicz et al 2002) | |
| The model shows how using a CA1-like distribution of active dendritic conductances in a CA3 morphology results in dendritic initiation of spikes during a burst. | |
| CA3 pyramidal neuron: firing properties (Hemond et al. 2008) | |
| In the paper, this model was used to identify how relative differences in K+ conductances, specifically KC, KM, & KD, between cells contribute to the different characteristics of the three types of firing patterns observed experimentally. | |
| Ca-dependent K Channel: kinetics from rat muscle (Moczydlowski, Latorre 1983) NEURON | |
| Macroscopic channel model based on Moczydlowski, E. and Latorre, R. (1983). Gating kinetics of Ca++ activated K+ channels from rat muscle incorporated into planar lipid bilayers. J. Gen. Physiol. 82: 511-542 See README file for more information. | |
| Ca-dependent K Channel: kinetics from rat muscle (Moczydlowski, Latorre 1983) XPP | |
| This is an XPP version of the classic KCa channel from Moczydlowski and Latorre 1983. | |
| Cerebellar Golgi cell (Solinas et al. 2007a, 2007b) | |
| "... Our results suggest that a complex complement of ionic mechanisms is needed to fine-tune separate aspects of the neuronal response dynamics. Simulations also suggest that the Golgi cell may exploit these mechanisms to obtain a fine regulation of timing of incoming mossy fiber responses and granular layer circuit oscillation and bursting." | |
| Cerebellar Purkinje Cell: resurgent Na current and high frequency firing (Khaliq et al 2003) | |
| These mod files supplied by Dr Raman are for the below two references. ... we modeled action potential firing by simulating eight currents directly recorded from Purkinje cells in both wild-type and (mutant) med mice. Regular, high-frequency firing was slowed in med Purkinje neurons. In addition to disrupted sodium currents, med neurons had small but significant changes in potassium and leak currents. Simulations indicated that these modified non-sodium currents could not account for the reduced excitability of med cells but instead slightly facilitated spiking. The loss of NaV1.6-specific kinetics, however, slowed simulated spontaneous activity. Together, the data suggest that across a range of conditions, sodium currents with a resurgent component promote and accelerate firing. See papers for more and details. | |
| Cerebellar purkinje cell (De Schutter and Bower 1994) | |
| Tutorial simulation of a cerebellar Purkinje cell. This tutorial is based upon a GENESIS simulation of a cerebellar Purkinje cell, modeled and fine-tuned by Erik de Schutter. The tutorial assumes that you have a basic knowledge of the Purkinje cell and its synaptic inputs. It gives visual insight in how different properties as concentrations and channel conductances vary and interact within a real Purkinje cell. | |
| Cerebellar purkinje cell: K and Ca channels regulate APs (Miyasho et al 2001) | |
| We adopted De Schutter and Bower's model as the starting point, then modified the descriptions of several ion channels, such as the P-type Ca channel and the delayed rectifier K channel, and added class-E Ca channels and D-type K channels to the model. Our new model reproduces most of our experimental results and supports the conclusions of our experimental study that class-E Ca channels and D-type K channels are present and functioning in the dendrites of Purkinje neurons. | |
| Cerebellar purkinje cell: interacting Kv3 and Na currents influence firing (Akemann, Knopfel 2006) | |
| Purkinje neurons spontaneously generate action potentials in the absence of synaptic drive and thereby exert a tonic, yet plastic, input to their target cells in the deep cerebellar nuclei. Purkinje neurons express two ionic currents with biophysical properties that are specialized for high-frequency firing: resurgent sodium currents and potassium currents mediated by Kv3.3. … Numerical simulations indicated that Kv3.3 increases the spontaneous firing rate via cooperation with resurgent sodium currents. We conclude that the rate of spontaneous action potential firing of Purkinje neurons is controlled by the interaction of Kv3.3 potassium currents and resurgent sodium currents. See paper for more and details. | |
| Comparison of full and reduced globus pallidus models (Hendrickson 2010) | |
| In this paper, we studied what features of realistic full model activity patterns can and cannot be preserved by morphologically reduced models. To this end, we reduced the morphological complexity of a full globus pallidus neuron model possessing active dendrites and compared its spontaneous and driven responses to those of the reduced models. | |
| Complex CA1-neuron to study AP initiation (Wimmer et al. 2010) | |
| Complex model of a pyramidal CA1-neuron, adapted from Royeck, M., et al. Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons. Journal of neurophysiology 100, 2361-2380 (2008). It contains a biophysically realistic morphology comprising 265 compartments (829 segments) and 15 different distributed Ca2+- and/or voltage-dependent conductances. | |
| Computer simulations of neuron-glia interactions mediated by ion flux (Somjen et al. 2008) | |
| "... To examine the effect of glial K+ uptake, we used a model neuron equipped with Na+, K+, Ca2+ and Cl− conductances, ion pumps and ion exchangers, surrounded by interstitial space and glia. The glial membrane was either “passive”, incorporating only leak channels and an ion exchange pump, or it had rectifying K+ channels. We computed ion fluxes, concentration changes and osmotic volume changes. ... We conclude that voltage gated K+ currents can boost the effectiveness of the glial “potassium buffer” and that this buffer function is important even at moderate or low levels of excitation, but especially so in pathological states." | |
| Contrast invariance by LGN synaptic depression (Banitt et al. 2007) | |
| "Simple cells in layer 4 of the primary visual cortex of the cat show contrast-invariant orientation tuning, in which the amplitude of the peak response is proportional to the stimulus contrast but the width of the tuning curve hardly changes with contrast. This study uses a detailed model of spiny stellate cells (SSCs) from cat area 17 to explain this property. The model integrates our experimental data, including morphological and intrinsic membrane properties and the number and spatial distribution of four major synaptic input sources of the SSC: the dorsal lateral geniculate nucleus (dLGN) and three cortical sources. ... The model response is in close agreement with experimental results, in terms of both output spikes and membrane voltage (amplitude and fluctuations), with reasonable exceptions given that recurrent connections were not incorporated." | |
| Controlling KCa channels with different Ca2+ buffering models in Purkinje cell (Anwar et al. 2010) | |
| In this work, we compare the dynamics of different buffering models during generation of a dendritic Ca2+ spike in a single compartment model of a Purkinje cell dendrite. The Ca2+ buffering models used are 1) a single Ca2+ pool, 2) two Ca2+ pools respectively for the fast and slow transients, 3) a detailed calcium model with buffers, pump (Schmidt et al., 2003), and diffusion and 4) a calcium model with buffers, pump and diffusion compensation. The parameters of single pool and double pool are tuned, using Neurofitter (Van Geit et al., 2007), to approximate the behavior of detailed calcium dynamics over range of 0.5 µM to 8 µM of intracellular calcium. The diffusion compensation is modeled using a buffer-like mechanism called DCM. To use DCM robustly for different diameter compartments, its parameters are estimated, using Neurofitter (Van Geit et al., 2007), as a function of compartment diameter (0.8 µm-20 µm). | |
| D2 dopamine receptor modulation of interneuronal activity (Maurice et al. 2004) | |
| "... Using a combination of electrophysiological, molecular, and computational approaches, the studies reported here show that D2 dopamine receptor modulation of Na+ currents underlying autonomous spiking contributes to a slowing of discharge rate, such as that seen in vivo. Four lines of evidence support this conclusion. ... Fourth, simulation of cholinergic interneuron pacemaking revealed that a modest increase in the entry of Na+ channels into the slow-inactivated state was sufficient to account for the slowing of pacemaker discharge. These studies establish a cellular mechanism linking dopamine and the reduction in striatal cholinergic interneuron activity seen in the initial stages of associative learning." See paper for more and details. | |
| Data-driven, HH-type model of the lateral pyloric (LP) cell in the STG (Nowotny et al. 2008) | |
| This model was developed using voltage clamp data and existing LP models to assemble an initial set of currents which were then adjusted by extensive fitting to a long data set of an isolated LP neuron. The main points of the work are a) automatic fitting is difficult but works when the method is carefully adjusted to the problem (and the initial guess is good enough). b) The resulting model (in this case) made reasonable predictions for manipulations not included in the original data set, e.g., blocking some of the ionic currents. c) The model is reasonably robust against changes in parameters but the different parameters vary a lot in this respect. d) The model is suitable for use in a network and has been used for this purpose (Ivanchenko et al. 2008) | |
| Dendritica (Vetter et al 2001) | |
| Dendritica is a collection of programs for relating dendritic geometry and signal propagation. The programs are based on those used for the simulations described in: Vetter, P., Roth, A. & Hausser, M. (2001) For reprint requests and additional information please contact Dr. M. Hausser, email address: m.hausser@ucl.ac.uk | |
| Dentate gyrus granule cell: calcium and calcium-dependent conductances (Aradi and Holmes 1999) | |
| We have constructed a detailed model of a hippocampal dentate granule (DG) cell that includes nine different channel types. Channel densities and distributions were chosen to reproduce reported physiological responses observed in normal solution and when blockers were applied. The model was used to explore the contribution of each channel type to spiking behavior with particular emphasis on the mechanisms underlying postspike events. ... The model was used to predict changes in channel densities that could lead to epileptogenic burst discharges and to predict the effect of altered buffering capacity on firing behavior. We conclude that the clustered spatial distributions of calcium related channels, the presence of slow delayed rectifier potassium currents in dendrites, and calcium buffering properties, together, might explain the resistance of DG cells to the development of epileptogenic burst discharges. | |
| 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. | |
| Differences between type A and B photoreceptors (Blackwell 2006) | |
| In Hermissenda crassicornis, the memory of light associated with turbulence is stored as changes in intrinsic and synaptic currents in both type A and type B photoreceptors. These photoreceptor types exhibit qualitatively different responses to light and current injection, and these differences shape the spatiotemporal firing patterns that control behavior. Thus the objective of the study was to identify the mechanisms underlying these differences. The approach was to develop a type B model that reproduced characteristics of type B photoreceptors recorded in vitro, and then to create a type A model by modifying a select number of ionic currents. Comparison of type A models with characteristics of type A photoreceptors recorded in vitro revealed that type A and type B photoreceptors have five main differences, three that have been characterized experimentally and two that constitute hypotheses to be tested with experiments in the future. See paper for more and details. | |
| Differential modulation of pattern and rate in a dopamine neuron model (Canavier and Landry 2006) | |
| "A stylized, symmetric, compartmental model of a dopamine neuron in vivo shows how rate and pattern can be modulated either concurrently or differentially. If two or more parameters in the model are varied concurrently, the baseline firing rate and the extent of bursting become decorrelated, which provides an explanation for the lack of a tight correlation in vivo and is consistent with some independence of the mechanisms that generate baseline firing rates versus bursting. ..." See paper for more and details. | |
| Dopaminergic cell bursting model (Kuznetsov et al 2006) | |
| Dopaminergic neurons of the midbrain fire spontaneously at rates <10/s and ordinarily will not exceed this range even when driven with somatic current injection. During spontaneous bursting of dopaminergic neurons in vivo, bursts related to reward expectation in behaving animals, and bursts generated by dendritic application of N-methyl-D-aspartate (NMDA) agonists, transient firing attains rates well above this range. We suggest a way such highfrequency firing may occur in response to dendritic NMDA receptor activation. We have extended the coupled oscillator model of the dopaminergic neuron, which represents the soma and dendrites as electrically coupled compartments with different natural spiking frequencies, by addition of dendritic AMPA (voltage-independent) or NMDA (voltage-dependent) synaptic conductance. Both soma and dendrites contain a simplified version of the calcium-potassium mechanism known to be the mechanism for slow spontaneous oscillation and background firing in dopaminergic cells. We show that because of its voltage dependence, NMDA receptor activation acts to amplify the effect on the soma of the high-frequency oscillation of the dendrites, which is normally too weak to exert a large influence on the overall oscillation frequency of the neuron. | |
| Dynamical model of olfactory bulb mitral cell (Rubin, Cleland 2006) | |
| This four-compartment mitral cell exhibits endogenous subthreshold oscillations, phase resetting, and evoked spike phasing properties as described in electrophysiological studies of mitral cells. It is derived from the prior work of Davison et al (2000) and Bhalla and Bower (1993). See readme.txt for details. | |
| ERG current in repolarizing plateau potentials in dopamine neurons (Canavier et al 2007) | |
| "Blocking the small-conductance (SK) calcium-activated potassium channel promotes burst firing in dopamine neurons both in vivo and in vitro. ... We focus on the underlying plateau potential oscillation generated in the presence of both apamin and TTX, so that action potentials are not considered. We find that although the plateau potentials are mediated by a voltage-gated Ca2+ current, they do not depend on the accumulation of cytosolic Ca2+, then use a computational model to test the hypothesis that the slowly voltage-activated ether-a-go-go–related gene (ERG) potassium current repolarizes the plateaus. The model, which includes a material balance on calcium, is able to reproduce the time course of both membrane potential and somatic calcium concentration, and can also mimic the induction of plateau potentials by the calcium chelator BAPTA." See paper for more. | |
| Effect of riluzole on action potential in cultured human skeletal muscle cells (Wang YJ et al. 2008) | |
| Simulation studies also unraveled that both decreased conductance of I(Na) and increased conductance of I(K(Ca)) utilized to mimic riluzole actions in skeletal muscle cells could combine to decrease the amplitude of action potentials and increase the repolarization of action potentials. | |
| Effect of voltage sensitive fluorescent proteins on neuronal excitability (Akemann et al. 2009) | |
| "Fluorescent protein voltage sensors are recombinant proteins that are designed as genetically encoded cellular probes of membrane potential using mechanisms of voltage-dependent modulation of fluorescence. Several such proteins, including VSFP2.3 and VSFP3.1, were recently reported with reliable function in mammalian cells. ... Expression of these proteins in cell membranes is accompanied by additional dynamic membrane capacitance, ... We used recordings of sensing currents and fluorescence responses of VSFP2.3 and of VSFP3.1 to derive kinetic models of the voltage-dependent signaling of these proteins. Using computational neuron simulations, we quantitatively investigated the perturbing effects of sensing capacitance on the input/output relationship in two central neuron models, a cerebellar Purkinje and a layer 5 pyramidal neuron. ... ". The Purkinje cell model is included in ModelDB. | |
| Effects of Acetyl-L-carnitine on neural transmission (Lombardo et al 2004) | |
| Acetyl-L-carnitine is known to improve many aspects of the neural activity even if its exact role in neurotransmission is still unknown. This study investigates the effects of acetyl-L-carnitine in T segmental sensory neurons of the leech Hirudo medicinalis. These neurons are involved in some forms of neural plasticity associated with learning processes. Their physiological firing is accompanied by a large afterhyperpolarization that is mainly due to the Na+/K+ ATPase activity and partially to a Ca2+-dependent K+ current. A clear-cut hyperpolarization and a significant increase of the afterhyperpolarization have been recorded in T neurons of leeches injected with 2 mM acetyl-L-carnitine some days before. Acute treatments of 50 mM acetyl-L-carnitine induced similar effects in T cells of naive animals. Moreover, in these cells, widely arborized, the afterhyperpolarization seems to play an important role in determining the action potential transmission at neuritic bifurcations. A computational model of a T cell has been previously developed considering detailed data for geometry and the modulation of the pump current. Herein, we showed that to a larger afterhyperpolarization, due to the acetyl-L-carnitine-induced effects, corresponds a decrement in the number of action potentials reaching synaptic terminals. | |
| Effects of KIR current inactivation in NAc Medium Spiny Neurons (Steephen and Manchanda 2009) | |
| "Inward rectifying potassium (KIR) currents in medium spiny (MS) neurons of nucleus accumbens inactivate significantly in ~40% of the neurons but not in the rest, which may lead to differences in input processing by these two groups. Using a 189-compartment computational model of the MS neuron, we investigate the influence of this property using injected current as well as spatiotemporally distributed synaptic inputs. Our study demonstrates that KIR current inactivation facilitates depolarization, firing frequency and firing onset in these neurons. ..." | |
| 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. ..." | |
| 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. ..." | |
| Enhanced Excitability in Hermissenda: modulation by 5-HT (Cai et al 2003) | |
| Serotonin (5-HT) applied to the exposed but otherwise intact nervous system results in enhanced excitability of Hermissenda type-B photoreceptors. Several ion currents in the type-B photoreceptors are modulated by 5-HT, including the A-type K+ current (IK,A), sustained Ca2+ current (ICa,S), Ca-dependent K+ current (IK,Ca), and a hyperpolarization-activated inward rectifier current (Ih). In this study,we developed a computational model that reproduces physiological characteristics of type B photoreceptors, e.g. resting membrane potential, dark-adapted spike activity, spike width, and the amplitude difference between somatic and axonal spikes. We then used the model to investigate the contribution of different ion currents modulated by 5-HT to the magnitudes of enhanced excitability produced by 5-HT. See paper for results and more details. | |
| Fast oscillations in inhibitory networks (Maex, De Schutter 2003) | |
| We observed a new phenomenon of resonant synchronization in computer-simulated networks of inhibitory neurons in which the synaptic current has a delayed onset, reflecting finite spike propagation and synaptic transmission times. At the resonant level of network excitation, all neurons fire synchronously and rhythmically with a period approximately four times the mean delay of the onset of the inhibitory synaptic current. ... By varying the axonal delay of the inhibitory connections, networks with a realistic synaptic kinetics can be tuned to frequencies from 40 to >200 Hz. ... We conclude that the delay of the synaptic current is the primary parameter controlling the oscillation frequency of inhibitory networks and propose that delay-induced synchronization is a mechanism for fast brain rhythms that depend on intact inhibitory synaptic transmission. | |
| Frog second-order vestibular neuron models (Rössert et al. 2011) | |
| This implements spiking Hodgkin-Huxley type models of tonic and phasic second-order vestibular neurons. Models fitted to intracellular spike and membrane potential recordings from frog (Rana temporaria). The models can be stimulated by intracellular step current, frequency current (ZAP) or synaptic stimulation. | |
| Global structure, robustness, and modulation of neuronal models (Goldman et al. 2001) | |
| "The electrical characteristics of many neurons are remarkably robust in the face of changing internal and external conditions. At the same time, neurons can be highly sensitive to neuromodulators. We find correlates of this dual robustness and sensitivity in a global analysis of the structure of a conductance-based model neuron. ..." | |
| Globus pallidus multi-compartmental model neuron with realistic morphology (Gunay et al. 2008) | |
| "Globus pallidus (GP) neurons recorded in brain slices show significant variability in intrinsic electrophysiological properties. To investigate how this variability arises, we manipulated the biophysical properties of GP neurons using computer simulations. ... Our results indicated that most of the experimental variability could be matched by varying conductance densities, which we confirmed with additional partial block experiments. Further analysis resulted in two key observations: (1) each voltage-gated conductance had effects on multiple measures such as action potential waveform and spontaneous or stimulated spike rates; and (2) the effect of each conductance was highly dependent on the background context of other conductances present. In some cases, such interactions could reverse the effect of the density of one conductance on important excitability measures. ..." | |
| Globus pallidus neuron models with differing dendritic Na channel expression (Edgerton et al., 2010) | |
| A set of 9 multi-compartmental rat GP neuron models (585 compartments) differing only in their expression of dendritic fast sodium channels were compared in their synaptic integration properties. Dendritic fast sodium channels were found to increase the importance of distal synapses (both excitatory AND inhibitory), increase spike timing variability with in vivo-like synaptic input, and make the model neurons highly sensitive to clustered synchronous excitation. | |
| Hypocretin and Locus Coeruleus model neurons (Carter et al 2012) | |
| Conductance based model of the hypocretin neurons (HCRT) and another one of the Locus Coeruleus one (LC). The HCRT drive the LCs via the HCRT receptor on the LCs. The LCs lead to the awakening of the mice if the number of spikes raises over 10 spikes in 10 seconds window. | |
| Impact of dendritic atrophy on intrinsic and synaptic excitability (Narayanan & Chattarji, 2010) | |
| These simulations examined the atrophy induced changes in electrophysiological properties of CA3 pyramidal neurons. We found these neurons change from bursting to regular spiking as atrophy increases. Region-specific atrophy induced region-specific increases in synaptic excitability in a passive dendritic tree. All dendritic compartments of an atrophied neuron had greater synaptic excitability and a larger voltage transfer to the soma than the control neuron. | |
| Impact of dendritic size and topology on pyramidal cell burst firing (van Elburg and van Ooyen 2010) | |
| The code provided here was written to systematically investigate which of the
physical parameters controlled by dendritic morphology underlies the differences
in spiking behaviour observed in different realizations of the
'ping-pong'-model. Structurally varying dendritic topology and length in a
simplified model allows us to separate out the physical parameters derived from
morphology underlying burst firing. To perform the parameter scans we created a new NEURON tool the MultipleRunControl which can be used to easily set up a parameter scan and write the simulation results to file. Using this code we found that not input conductance but the arrival time of the return current, as measured provisionally by the average electrotonic path length, determines whether the pyramidal cell (with ping-pong model dynamics) will burst or fire single spikes. | |
| Intracortical synaptic potential modulation by presynaptic somatic potential (Shu et al. 2006, 2007) | |
| " ... Here we show that the voltage fluctuations associated with dendrosomatic synaptic activity propagate significant distances along the axon, and that modest changes in the somatic membrane potential of the presynaptic neuron modulate the amplitude and duration of axonal action potentials and, through a Ca21- dependent mechanism, the average amplitude of the postsynaptic potential evoked by these spikes. These results indicate that synaptic activity in the dendrite and soma controls not only the pattern of action potentials generated, but also the amplitude of the synaptic potentials that these action potentials initiate in local cortical circuits, resulting in synaptic transmission that is a mixture of triggered and graded (analogue) signals." | |
| Ionic mechanisms of bursting in CA3 pyramidal neurons (Xu and Clancy 2008) | |
| "... We present a single-compartment model of a CA3 hippocampal pyramidal neuron based on recent experimental data. We then use the model to determine the roles of primary depolarizing currents in burst generation. The single compartment model incorporates accurate representations of sodium (Na+) channels (NaV1.1) and T-type calcium (Ca2+) channel subtypes (CaV3.1, CaV3.2, and CaV3.3). Our simulations predict the importance of Na+ and T-type Ca2+ channels in hippocampal pyramidal cell bursting and reveal the distinct contribution of each subtype to burst morphology. We also performed fastslow analysis in a reduced comparable model, which shows that our model burst is generated as a result of the interaction of two slow variables, the T-type Ca2+ channel activation gate and the Ca2+-dependent potassium (K+) channel activation gate. The model reproduces a range of experimentally observed phenomena including afterdepolarizing potentials, spike widening at the end of the burst, and rebound. Finally, we use the model to simulate the effects of two epilepsy-linked mutations: R1648H in NaV1.1 and C456S in CaV3.2, both of which result in increased cellular excitability." | |
| 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. ..." | |
| L5b PC model constrained for BAC firing and perisomatic current step firing (Hay et al., 2011) | |
| "... L5b pyramidal cells have been the subject of extensive experimental and modeling studies, yet conductance-based models of these cells that faithfully reproduce both their perisomatic Na+-spiking behavior as well as key dendritic active properties, including Ca2+ spikes and back-propagating action potentials, are still lacking. Based on a large body of experimental recordings from both the soma and dendrites of L5b pyramidal cells in adult rats, we characterized key features of the somatic and dendritic firing and quantified their statistics. We used these features to constrain the density of a set of ion channels over the soma and dendritic surface via multi-objective optimization with an evolutionary algorithm, thus generating a set of detailed conductance-based models that faithfully replicate the back-propagating action potential activated Ca2+ spike firing and the perisomatic firing response to current steps, as well as the experimental variability of the properties. ... The models we present provide several experimentally-testable predictions and can serve as a powerful tool for theoretical investigations of the contribution of single-cell dynamics to network activity and its computational capabilities. " | |
| LGMD Variability and logarithmic compression in dendrites (Jones and Gabbiani, 2012, 2012B) | |
| A compartmental model of the LGMD with a simplified, rake shaped, excitatory dendrite. It receives spontaneous input and excitatory and inhibitory synaptic inputs triggered by visual stimuli. It generates realistic responses to looming through the velocity dependent scaling and delay of individual excitatory synaptic inputs, with variability. We use the model to show that the key determinants of output variability are spontaneous input and temporal jitter of the excitatory inputs, rather than variability in magnitude of individual inputs (2012B, J Neurophysiol). We also use the model to analyze the transformation of the excitatory signals through the visual pathway; concluding that the representation of stimulus velocity is transformed from an expansive relationship at the level of the LGMD inputs to a logarithmic one at the level of its membrane potential (2012, J Neurosci). | |
| Lamprey spinal CPG neuron (Huss et al. 2007) | |
| This is a model of a generic locomotor network neuron in the lamprey spinal cord. The given version is assumed to correspond to an interneuron; motoneurons can also be modelled by changing the dendritic tree morphology. | |
| 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. | |
| Layer V PFC pyramidal neuron used to study persistent activity (Sidiropoulou & Poirazi 2012) | |
| "... Here, we use a compartmental modeling approach to search for discriminatory features in the properties of incoming stimuli to a PFC pyramidal neuron and/or its response that signal which of these stimuli will result in persistent activity emergence. Furthermore, we use our modeling approach to study cell-type specific differences in persistent activity properties, via implementing a regular spiking (RS) and an intrinsic bursting (IB) model neuron. ... Collectively, our results pinpoint to specific features of the neuronal response to a given stimulus that code for its ability to induce persistent activity and predict differential roles of RS and IB neurons in persistent activity expression. " | |
| Leaky integrate-and-fire model of spike frequency adaptation in the LGMD (Gabbiani and Krapp 2006) | |
| This will reproduce Figure 9 of Gabbiani and Krapp (2006) J Neurophysiol 96:2951-2962. The figure simply shows that a leaky-integrate-and-fire model cannot reproduce spike frequency adaptation as it is seen experimentally in the LGMD neuron. | |
| Leech Mechanosensory Neurons: Synaptic Facilitation by Reflected APs (Baccus 1998) | |
| This model by Stephen Baccus explores the phenomena of action potential (AP) propagation at branch boints in axons. APs are sometimes transmitted down the efferent processes and sometimes are reflected back to the axon of AP origin or neither. See the paper for details. The model zip file contains a readme.txt which list introductory steps to follow to run the simulation. Stephen Baccus's email address: baccus@fas.harvard.edu | |
| Leech S Cell: Modulation of Excitability by Serotonin (Burrell and Crisp 2007) | |
| Serotonergic modulation of the afterhyperpolarization (AHP) contributes to the regulation of the excitability of the leech S cell, a neuron critical for sensitization of the shortening reflex. Pharmacological and physiological data suggest that three currents contribute to the S cell's afterhyperpolarization: a charybdotoxin-sensitive, fast calcium-dependent potassium current (fAHP); a tubocurare-sensitive, calcium-dependent potassium current (mAHP); and, a saxitoxin-sensitive, afterdepolarization current (ADP). This single-compartment model of the S cell is constructed using fAHP, mAHP and ADP currents, and shows that reduction of the conductances to mimic the effects of serotonin is sufficient to enhance excitability (repetitive firing). Burrell BD, Crisp KM (2007) Serotonergic modulation of afterhyperpolarization in a neuron that contributes to learning in the leech. J Neurophysiol, in press. | |
| Lobster STG pyloric network model with calcium sensor (Gunay & Prinz 2010) (Prinz et al. 2004) | |
| This pyloric network model simulator is a C/C++ program that saves 384 different calcium sensor values that are candidates for activity sensors (Gunay and Prinz, 2010). The simulator was used to scan all of the 20 million pyloric network models that were previously collected in a database (Prinz et al, 2004). | |
| Low dose of dopamine may stimulate prolactin secretion by increasing K currents (Tabak et al. 2006) | |
| ".. We considered the fast K+ currents flowing through large-conductance BK channels and through A-type channels. We developed a minimal lactotroph model to investigate the effects of these two currents. Both IBK and IA could transform the electrical pattern of activity from spiking to bursting, but through distinct mechanisms. IBK always increased the intracellular Ca2+ concentration, while IA could either increase or decrease it. Thus, the stimulatory effects of DA could be mediated by a fast K+ conductance which converts tonically spiking cells to bursters. In addition, the study illustrates that a heterogeneous distribution of fast K+ conductances could cause heterogeneous lactotroph firing patterns." | |
| 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." | |
| Mathematical model for windup (Aguiar et al. 2010) | |
| "Windup is characterized as a frequency-dependent increase in the number of evoked action potentials in dorsal horn neurons in response to electrical stimulation of afferent C-fibers. ... The approach presented here relies on mathematical and computational analysis to study the mechanism(s) underlying windup. From experimentally obtained windup profiles, we extract the time scale of the facilitation mechanisms that may support the characteristics of windup. Guided by these values and using simulations of a biologically realistic compartmental model of a wide dynamic range (WDR) neuron, we are able to assess the contribution of each mechanism for the generation of action potentials windup. ..." | |
| Mechanisms of fast rhythmic bursting in a layer 2/3 cortical neuron (Traub et al 2003) | |
| This simulation is based on the reference paper listed below.
This port was made by Roger D Traub and Maciej T Lazarewicz (mlazarew@seas.upenn.edu) Thanks to Ashlen P Reid for help with porting a morphology of the cell. | |
| Model of SK current`s influence on precision in Globus Pallidus Neurons (Deister et al. 2009) | |
| " ... In numerical simulations, the availability of both Na+ and A-type K+ channels during autonomous firing were reduced when SK channels were removed, and a nearly equal reduction in Na+ and K+ subthreshold-activated ion channel availability produced a large decrease in the neuron's slope conductance near threshold. This change made the neuron more sensitive to intrinsically generated noise. In vivo, this change would also enhance the sensitivity of GP (Globus Pallidus) neurons to small synaptic inputs." | |
| Modeling interactions in Aplysia neuron R15 (Yu et al 2004) | |
| "The biophysical properties of neuron R15 in Aplysia endow it with the ability to express multiple modes of oscillatory electrical activity, such as beating and bursting. Previous modeling studies examined the ways in which membrane conductances contribute to the electrical activity of R15 and the ways in which extrinsic modulatory inputs alter the membrane conductances by biochemical cascades and influence the electrical activity. The goals of the present study were to examine the ways in which electrical activity influences the biochemical cascades and what dynamical properties emerge from the ongoing interactions between electrical activity and these cascades." See paper for more and details. | |
| Modelling reduced excitability in aged CA1 neurons as a Ca-dependent process (Markaki et al. 2005) | |
| "We use a multi-compartmental model of a CA1 pyramidal cell to study changes in hippocampal excitability that result from aging-induced alterations in calcium-dependent membrane mechanisms. The model incorporates N- and L-type calcium channels which are respectively coupled to fast and slow afterhyperpolarization potassium channels. Model parameters are calibrated using physiological data. Computer simulations reproduce the decreased excitability of aged CA1 cells, which results from increased internal calcium accumulation, subsequently larger postburst slow afterhyperpolarization, and enhanced spike frequency adaptation. We find that aging-induced alterations in CA1 excitability can be modelled with simple coupling mechanisms that selectively link specific types of calcium channels to specific calcium-dependent potassium channels." | |
| Modulation of neuronal synchronization by D4 dopamine receptor-mediated phospholipid methylation | |
| "We describe a new molecular mechanism of dopamine-induced membrane protein modulation that can tune neuronal oscillation frequency to attention related gamma rhythm. This mechanism is based on the unique ability of D4 dopamine receptors (D4R) to carry out phospholipid methylation (PLM) that may affect the kinetics of ion channels. We show that by deceasing the inertia of the delayed rectifier potassium channel, a transition to 40 Hz oscillations can be achieved. ..." | |
| Modulation of septo-hippocampal theta activity by GABAA receptors (Hajos et al. 2004) | |
| θ Frequency oscillation of the septo-hippocampal system has been considered as a prominent activity associated with cognitive function and affective processes. ... In the present experiments we applied a combination of computational and physiological techniques to explore the functional role of GABAA receptors in θ oscillation. ... In parallel to these experimental observations, a computational model has been constructed by implementing a septal GABA neuron model with a CA1 hippocampal model containing three types of neurons (including oriens and basket interneurons and pyramidal cells; latter modeled by multicompartmental techniques; for detailed model description with network parameters see online addendum: http://geza.kzoo.edu/theta). This connectivity made the network capable of simulating the responses of the septo-hippocampal circuitry to the modulation of GABAA transmission, and the presently described computational model proved suitable to reveal several aspects of pharmacological modulation of GABAA receptors. In addition, computational findings indicated different roles of distinctively located GABAA receptors in θ generation. | |
| Motoneuron model of self-sustained firing after spinal cord injury (Kurian et al. 2011) | |
| " ... During the acute-stage of spinal cord injury (SCI), the endogenous ability to generate plateaus is lost; however, during the chronic-stage of SCI, plateau potentials reappear with prolonged self-sustained firing that has been implicated in the development of spasticity. In this work, we extend previous modeling studies to systematically investigate the mechanisms underlying the generation of plateau potentials in motoneurons, including the influences of specific ionic currents, the morphological characteristics of the soma and dendrite, and the interactions between persistent inward currents and synaptic input. ..." | |
| Multicompartmental cerebellar granule cell model (Diwakar et al. 2009) | |
| A detailed multicompartmental model was used to study neuronal electroresponsiveness of cerebellar granule cells in rats. Here we show that, in cerebellar granule cells, Na+ channels are enriched in the axon, especially in the hillock, but almost absent from soma and dendrites. Numerical simulations indicated that granule cells have a compact electrotonic structure allowing EPSPs to diffuse with little attenuation from dendrites to axon. The spike arose almost simultaneously along the whole axonal ascending branch and invaded the hillock, whose activation promoted spike back-propagation with marginal delay (<200 micros) and attenuation (<20 mV) into the somato-dendritic compartment. For details check the cited article. | |
| Multiscale interactions between chemical and electric signaling in LTP (Bhalla 2011) | |
| "Synaptic plasticity leads to long-term changes in excitability, whereas cellular homeostasis maintains excitability. Both these processes involve interactions between molecular events, electrical events, and network activity. Here I explore these intersections with a multilevel model that embeds molecular events following synaptic calcium influx into a multicompartmental electrical model of a CA1 hippocampal neuron. ..." | |
| MyFirstNEURON (Houweling, Sejnowski 1997) | |
| MyFirstNEURON is a NEURON demo by Arthur Houweling and Terry Sejnowski. Perform experiments from the book 'Electrophysiology of the Neuron, A Companion to Shepherd's Neurobiology, An Interactive Tutorial' by John Huguenard & David McCormick, Oxford University Press 1997, or design your own one or two cell simulation. For more information see http://www.cnl.salk.edu/Simulations. Salk Institute, Computational Neurobiology Lab, 10010 North Torrey Pines Rd., La Jolla CA 092037. Email: arthur@salk.edu | |
| NMDA subunit effects on Calcium and STDP (Evans et al. 2012) | |
| Effect of NMDA subunit on spike timing dependent plasticity. | |
| Na channel mutations in the dentate gyrus (Thomas et al. 2009) | |
| These are source files to generate the data in Figure 6 from "Mossy fiber sprouting interacts with sodium channel mutations to increase dentate gyrus excitability" Thomas EA, Reid CA, Petrou S, Epilepsia (2009) | |
| Nav1.6 sodium channel model in globus pallidus neurons (Mercer et al. 2007) | |
| Model files for the paper Mercer JN, Chan CS, Tkatch T, Held J, Surmeier DJ. Nav1.6 sodium channels are critical to pacemaking and fast spiking in globus pallidus neurons.,J Neurosci. 2007 Dec 5;27(49):13552-66. | |
| Network model of the granular layer of the cerebellar cortex (Maex, De Schutter 1998) | |
| We computed the steady-state activity of a large-scale model of the granular layer of the rat cerebellum. Within a few tens of milliseconds after the start of random mossy fiber input, the populations of Golgi and granule cells became entrained in a single synchronous oscillation, the basic frequency of which ranged from 10 to 40 Hz depending on the average rate of firing in the mossy fiber population. ... The synchronous, rhythmic firing pattern was robust over a broad range of biologically realistic parameter values and to parameter randomization. Three conditions, however, made the oscillations more transient and could desynchronize the entire network in the end: a very low mossy fiber activity, a very dominant excitation of Golgi cells through mossy fiber synapses (rather than through parallel fiber synapses), and a tonic activation of granule cell GABAA receptors (with an almost complete absence of synaptically induced inhibitory postsynaptic currents). The model predicts that, under conditions of strong mossy fiber input to the cerebellum, Golgi cells do not only control the strength of parallel fiber activity but also the timing of the individual spikes. Provided that their parallel fiber synapses constitute an important source of excitation, Golgi cells fire rhythmically and synchronized with granule cells over large distances along the parallel fiber axis. See paper for more and details. | |
| Network model with neocortical architecture (Anderson et al. 2011 plus under review paper) | |
| Architecturally realistic neocortical model using seven classes of excitatory and inhibitory single compartment Hodgkin-Huxley cells. This is an addendum to ModelDB Accession # 98902, Studies of stimulus parameters for seizure disruption (Anderson et al. 2007). Wiring is adapted from the minicolumn hypothesis and incorporates visual and neocortical wiring data. Simulation demonstrates spontaneous bursting onset and cessation. This activity can be induced by random fluctuations in the surrounding background input (Manuscript in preparation). | |
| Nodose sensory neuron (Schild et al. 1994, Schild and Kunze 1997) | |
| This is a simulink implementation of the model described in Schild et al. 1994, and Schild and Kunze 1997 papers on Nodose sensory neurons. These papers describe the sensitivity these models have to their parameters and the match of the models to experimental data. | |
| O-LM interneuron model (Lawrence et al. 2006) | |
| Exploring the kinetics and distribution of the muscarinic potassium channel, IM, in 2 O-LM interneuron morphologies. Modulation of the ion channel by drugs such as XE991 (antagonist) and retigabine (agonist) are simulated in the models to examine the role of IM in spiking properties. | |
| 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. | |
| Olfactory Mitral Cell (Bhalla, Bower 1993) | |
| This is a conversion to NEURON of the mitral cell model described in Bhalla and Bower (1993). The original model was written in GENESIS and is available by joining BABEL, the GENESIS users' group. | |
| Olfactory Mitral Cell (Davison et al 2000) | |
| A four-compartment model of a mammalian olfactory bulb mitral cell, reduced from the complex 286-compartment model described by Bhalla and Bower (1993). The compartments are soma/axon, secondary dendrites, primary dendrite shaft and primary dendrite tuft. The reduced model runs 75 or more times faster than the full model, making its use in large, realistic network models of the olfactory bulb practical. | |
| 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. | |
| Paired turbulence and light effect on calcium increase in Hermissenda (Blackwell 2004) | |
| The sea slug Hermissenda learns to associate light and hair cell stimulation, but not when the stimuli are temporally uncorrelated...These issues were addressed using a multi-compartmental computer model of phototransduction, calcium dynamics, and ionic currents of the Hermissenda photoreceptor...simulations show that a potassium leak channel, which closes with an increase in calcium, is required to produce both the untrained LLD and the enhanced LLD due to the decrease in voltage dependent potassium currents. | |
| Paradoxical GABA-mediated excitation (Lewin et al. 2012) | |
| "GABA is the key inhibitory neurotransmitter in the adult central nervous system, but in some circumstances can lead to a paradoxical excitation that has been causally implicated in diverse pathologies from endocrine stress responses to diseases of excitability including neuropathic pain and temporal lobe epilepsy. We undertook a computational modeling approach to determine plausible ionic mechanisms of GABAA-dependent excitation in isolated post-synaptic CA1 hippocampal neurons because it may constitute a trigger for pathological synchronous epileptiform discharge. In particular, the interplay intracellular chloride accumulation via the GABAA receptor and extracellular potassium accumulation via the K/Cl co-transporter KCC2 in promoting GABAA-mediated excitation is complex. ..." | |
| 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. | |
| Phase response curve of a globus pallidal neuron (Fujita et al. 2011) | |
| We investigated how changes in ionic conductances alter the phase response curve (PRC) of a globus pallidal (GP) neuron and stability of a synchronous activity of a GP network, using a single-compartmental conductance-based neuron model. The results showed the PRC and the stability were influenced by changes in the persistent sodium current, the Kv3 potassium, the M-type potassium and the calcium-dependent potassium current. | |
| Pyramidal Neuron Deep, Superficial; Aspiny, Stellate (Mainen and Sejnowski 1996) | |
| This package contains compartmental models of four reconstructed neocortical neurons (layer 3 Aspiny, layer 4 Stellate, layer 3 and layer 5 Pyramidal neurons) with active dendritic currents using NEURON. Running this simulation demonstrates that an entire spectrum of firing patterns can be reproduced in this set of model neurons which share a common distribution of ion channels and differ only in their dendritic geometry. The reference paper is: Z. F. Mainen and T. J. Sejnowski (1996) Influence of dendritic structure on firing pattern in model neocortical neurons. Nature 382: 363-366. See also http://www.cnl.salk.edu/~zach/methods.html and http://www.cnl.salk.edu/~zach/ More info in readme.txt file below made visible by clicking on the patdemo folder and then on the readme.txt file. | |
| Pyramidal Neuron Deep: Constrained by experiment (Dyhrfjeld-Johnsen et al. 2005) | |
| "... As a practical demonstration of the use of CoCoDat we constructed a detailed computer model of an intrinsically bursting (IB) layer V pyramidal neuron from the rat barrel cortex supplementing experimental data (Schubert et al., 2001) with information extracted from the database. The pyramidal neuron morphology (Fig. 10B) was reconstructed from histological sections of a biocytin-stained IB neuron using the NeuroLucida software package..." | |
| Pyramidal neuron coincidence detection tuned by dendritic branching pattern (Schaefer et al 2006) | |
| "... We examined the relationship between dendritic arborization and the coupling between somatic and dendritic action potential (AP) initiation sites in layer 5 (L5) neocortical pyramidal neurons. Coupling was defined as the relative reduction in threshold for initiation of a dendritic calcium AP due to a coincident back-propagating AP. Simulations based on reconstructions of biocytin-filled cells showed that addition of oblique branches of the main apical dendrite in close proximity to the soma (d < 140 um) increases the coupling between the apical and axosomatic AP initiation zones, whereas incorporation of distal branches decreases coupling. ... We conclude that variation in dendritic arborization may be a key determinant of variability in coupling (49+-17%; range 19-83%; n = 37) and is likely to outweigh the contribution made by variations in active membrane properties. Thus coincidence detection of inputs arriving from different cortical layers is strongly regulated by differences in dendritic arborization." | |
| Rapid desynchronization of an electrically coupled Golgi cell network (Vervaeke et al. 2010) | |
| Electrical synapses between interneurons contribute to synchronized firing and network oscillations in the brain. However, little is known about how such networks respond to excitatory synaptic input. In addition to detailed electrophysiological recordings and histological investigations of electrically coupled Golgi cells in the cerebellum, a detailed network model of these cells was created. The cell models are based on reconstructed Golgi cell morphologies and the active conductances are taken from an earlier abstract Golgi cell model (Solinas et al 2007, accession no. 112685). Our results show that gap junction coupling can sometimes be inhibitory and either promote network synchronization or trigger rapid network desynchronization depending on the synaptic input. The model is available as a neuroConstruct project and can executable scripts can be generated for the NEURON simulator. | |
| Rat phrenic motor neuron (Amini et al 2004) | |
| We have developed a model for the rat phrenic motor neuron (PMN) that robustly replicates many experimentally observed behaviors of PMNs in response to pharmacological, ionic, and electrical perturbations using a single set of parameters. | |
| Rat subthalamic projection neuron (Gillies and Willshaw 2006) | |
| A computational model of the rat subthalamic nucleus projection neuron is constructed using electrophysiological and morphological data and a restricted set of channel specifications. The model cell exhibits a wide range of electrophysiological behaviors characteristic of rat subthalamic neurons. It reveals that a key set of three channels play a primary role in distinguishing behaviors: a high-voltage-activated calcium channel (Cav 1.2.-1.3), a low-voltage-activated calcium channel (Cav 3.-), and a small current calcium-activated potassium channel (KCa 2.1-2.3). See paper for more and details. | |
| Reciprocal regulation of rod and cone synapse by NO (Kourennyi et al 2004) | |
| We constructed models of rod and cone photoreceptors using NEURON software to predict how changes in Ca channels would affect the light response in these cells and in postsynaptic horizontal cells. | |
| Reconstructing cerebellar granule layer evoked LFP using convolution (ReConv) (Diwakar et al. 2011) | |
| The model allows reconstruction of evoked local field potentials as seen in the cerebellar granular layer. The approach uses a detailed model of cerebellar granule neuron to generate data traces and then uses a "ReConv" or jittered repetitive convolution technique to reproduce post-synaptic local field potentials in the granular layer. The algorithm was used to generate both in vitro and in vivo evoked LFP and reflected the changes seen during LTP and LTD, when such changes were induced in the underlying neurons by modulating release probability of synapses and sodium channel regulated intrinsic excitability of the cells. | |
| Regulation of firing frequency in a midbrain dopaminergic neuron model (Kuznetsova et al. 2010) | |
| A dopaminergic (DA) neuron model with a morphologicaly realistic dendritic architecture. The model captures several salient features of DA neurons under different pharmacological manipulations and exhibits depolarization block for sufficiently high current pulses applied to the soma. | |
| Regulation of the firing pattern in dopamine neurons (Komendantov et al 2004) | |
| Midbrain dopaminergic (DA) neurons in vivo exhibit two major firing patterns: single-spike firing and burst firing. The firing pattern expressed is dependent on both the intrinsic properties of the neurons and their excitatory and inhibitory synaptic inputs. Experimental data suggest that the activation of NMDA and GABAA receptors is crucial contributor to the initiation and suppression of burst firing, respectively, and that blocking calcium-activated potassium channels can facilitate burst firing. This multi-compartmental model of a DA neuron with a branching structure was developed and calibrated based on in vitro experimental data to explore the effects of different levels of activation of NMDA and GABAA receptors as well as the modulation of the SK current on the firing activity. | |
| Rejuvenation model of dopamine neuron (Chan et al. 2007) | |
| Model files for the paper C. Savio Chan, et al. 'Rejuvenation' protects neurons in mouse models of Parkinson's disease, Nature 447, 1081-1086(28 June 2007). | |
| Rod photoreceptor (Barnes and Hille 1989, Publio et al. 2006, Kourennyi and Liu et al. 2004) | |
| This a conductance-based model of a rod photoreceptor cell based on other modeling works (Barnes and Hille 1989 and Publio et al. 2006 and Kourennyi and Liu et al. 2004 ). In this model four types of ionic channels identified in the inner segment of the rod: nonselective cation channel (h), delayed rectifying potassium channel (Kv), noninactivating potassium channel (Kx) and calcium channel (Ca) was used. The model accurately reproduces the rod response when stimulated with a simulated photocurrent signal. We can show the effect of nonselective cation channel. The absence of this channel cause increasing the peak amplitude and the time to reach the peak of voltage response and absence of transient mode in this response. | |
| Role of Ih in firing patterns of cold thermoreceptors (Orio et al., 2012) | |
| " ... Here we investigated the role of Ih in cold-sensitive (CS) nerve endings, where cold sensory transduction actually takes place. Corneal CS nerve endings in mice show a rhythmic spiking activity at neutral skin temperature that switches to bursting mode when the temperature is lowered. ... Mathematical modeling shows that the firing phenotype of CS nerve endings from HCN1−/− mice can be reproduced by replacing HCN1 channels with the slower HCN2 channels rather than by abolishing Ih. We propose that Ih carried by HCN1 channels helps tune the frequency of the oscillation and the length of bursts underlying regular spiking in cold thermoreceptors, having important implications for neural coding of cold sensation. " | |
| STD-dependent and independent encoding of Input irregularity as spike rate (Luthman et al. 2011) | |
| "... We use a conductance-based model of a CN neuron to study the effect of the regularity of Purkinje cell spiking on CN neuron activity. We find that increasing the irregularity of Purkinje cell activity accelerates the CN neuron spike rate and that the mechanism of this recoding of input irregularity as output spike rate depends on the number of Purkinje cells converging onto a CN neuron. ..." | |
| STDP depends on dendritic synapse location (Letzkus et al. 2006) | |
| This model was published in Letzkus, Kampa & Stuart (2006) J Neurosci 26(41):10420-9. The simulation creates several plots showing voltage and NMDA current and conductance changes at different apical dendritic locations in layer 5 pyramidal neurons during STDP induction protocols. Created by B. Kampa (2006). | |
| Salamander retinal ganglian cells: morphology influences firing (Sheasby, Fohlmeister 1999) | |
| Nerve impulse entrainment and other excitation and passive phenomena are analyzed for a morphologically diverse and exhaustive data set (n=57) of realistic (3-dimensional computer traced) soma-dendritic tree structures of ganglion cells in the tiger salamander (Ambystoma tigrinum) retina. | |
| Salamander retinal ganglion cell: ion channels (Fohlmeister, Miller 1997) | |
| A realistic five (5) channel spiking model reproduces the bursting behavior of tiger salamander ganglion cells in the retina. Please see the readme for more information. | |
| Serotonergic modulation of Aplysia sensory neurons (Baxter et al 1999) | |
| The present study investigated how the modulation of these currents altered the spike duration and excitability of sensory neurons and examined the relative contributions of PKA- and PKC-mediated effects to the actions of 5-HT. A Hodgkin-Huxley type model was developed that described the ionic conductances in the somata of sensory neurons. The descriptions of these currents and their modulation were based largely on voltageclamp data from sensory neurons. Simulations were preformed with the program SNNAP (Simulator for Neural Networks and Action Potentials). The model was sufficient to replicate empirical data that describes the membrane currents, action potential waveform and excitability as well as their modulation by application of 5-HT, increased levels of adenosine cyclic monophosphate or application of active phorbol esters. The results provide several predictions that warrant additional experimental investigation and illustrate the importance of considering indirect as well as direct effects of modulatory agents on the modulation of membrane currents. See paper for more details. | |
| Shaping of action potentials by different types of BK channels (Jaffe et al., 2011) | |
| Dentate gyrus granule cells highly express the beta4 accessory subunit which confer BK channels with type II properties. The properties of heterologously-expressed BK channels (with and without the beta4 subunit) were used to construct channel models. These were then used to study how they affect single action potentials and trains of spikes in a model dentate gyrus granule cells (based on Aradi and Holmes, 1999). | |
| Simulated light response in rod photoreceptors (Liu and Kourennyi 2004) | |
| We developed a complete computer model of the rod, which accurately reproduced the main features of the light response and allowed us to demonstrate that it was suppression of Kx channels that was essential for slowing SLR and increasing excitability of rods. The results reported in this work further establish the importance of Kx channels in rod photoreceptor function. | |
| Sleep-wake transitions in corticothalamic system (Bazhenov et al 2002) | |
| The authors investigate the transition between sleep and awake states with intracellular recordings in cats and computational models. The model describes many essential features of slow wave sleep and activated states as well as the transition between them. | |
| Spike frequency adaptation in the LGMD (Peron and Gabbiani 2009) | |
| This model is used in the referenced paper to demonstrate that a model of an SK-like calcium-sensitive potassium (KCa) conductance can replicate the spike frequency adaptation (SFA) of the locust lobula giant movement detector (LGMD) neuron. The model simulates current injection experiments with and without KCa block in the LGMD, as well as visual stimulation experiments with and without KCa block. | |
| Spine fusion and branching effects synaptic response (Rusakov et al 1996, 1997) | |
| This compartmental model of a hippocampal granule cell has spinous synapses placed on the second-order dendrites. Changes in shape and connectivity of the spines usually does not effect the synaptic response of the cell unless active conductances are incorporated into the spine membrane (e.g. voltage-dependent Ca2+ channels). With active conductances, spines can generate spike-like events. We showed that changes like fusion and branching, or in fact any increase in the equivalent spine neck resistance, could trigger a dramatic increase in the spine's influence on the dendritic shaft potential. | |
| Studies of stimulus parameters for seizure disruption using NN simulations (Anderson et al. 2007) | |
| Architecturally realistic neocortical model using seven classes of excitatory and inhibitory single compartment Hodgkin-Huxley cells. Wiring is adapted to minicolumn hypothesis and incorporates visual and neocortical data. Simulation demonstrates spontaneous bursting onset and cessation, and activity can be altered with external electric field. | |
| Synaptic integration in a model of granule cells (Gabbiani et al 1994) | |
| We have developed a compartmental model of a turtle cerebellar granule cell consisting of 13 compartments that represent the soma and 4 dendrites. We used this model to investigate the synaptic integration of mossy fiber inputs in granule cells. See reference or abstract at PubMed link below for more information. | |
| Synaptic integration in tuft dendrites of layer 5 pyramidal neurons (Larkum et al. 2009) | |
| Simulations used in the paper. Voltage responses to current injections in different tuft locations; NMDA and calcium spike generation. Summation of multiple input distribution. | |
| Thalamic Reticular Network (Destexhe et al 1994) | |
| Demo for simulating networks of thalamic reticular neurons (reproduces figures from Destexhe A et al 1994) | |
| Thalamic interneuron multicompartment model (Zhu et al. 1999) | |
| this is an attempt to recreate a set of simulations originally performed in 1994 under NEURON version 3 and last tested in 1999. When I ran it now it did not behave exactly the same as previously which I suspect is due to some minor mod file changes on my side rather than due to any differences among versions. After playing around with the parameters a little bit I was able to get something that looks generally like a physiological trace in J Neurophysiol, 81:702--711, 1999, fig. 8b top trace. This sad preface is simply offered in order to encourage anyone who is interested in this model to make and post fixes. I'm happy to help out. Simulation by JJ Zhu To run nrnivmodl nrngui.hoc | |
| 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. | |
| Theta phase precession in a model CA3 place cell (Baker and Olds 2007) | |
| "... The present study concerns a neurobiologically based computational model of the emergence of theta phase precession in which the responses of a single model CA3 pyramidal cell are examined in the context of stimulation by realistic afferent spike trains including those of place cells in entorhinal cortex, dentate gyrus, and other CA3 pyramidal cells. Spike-timing dependent plasticity in the model CA3 pyramidal cell leads to a spatially correlated associational synaptic drive that subsequently creates a spatially asymmetric expansion of the model cell’s place field. ... Through selective manipulations of the model it is possible to decompose theta phase precession in CA3 into the separate contributing factors of inheritance from upstream afferents in the dentate gyrus and entorhinal cortex, the interaction of synaptically controlled increasing afferent drive with phasic inhibition, and the theta phase difference between dentate gyrus granule cell and CA3 pyramidal cell activity." | |
| Tonic neuron in spinal lamina I: prolongation of subthreshold depol. (Prescott and De Koninck 2005) | |
| Model demonstrates mechanism whereby two kinetically distinct inward currents act synergistically to prolong subthreshold depolarization. The important currents are a persistent Na current (with fast kinetics) and a persistent Ca current (with slower kinetics). Model also includes a slow K current and transient Ca current, in addition to standard HH currents. Model parameters are set to values used in Fig. 8A. Simulation shows prolonged depolarizations in response to two brief stimuli. | |
| Touch Sensory Cells (T Cells) of the Leech (Cataldo et al. 2004) (Scuri et al. 2007) | |
| Bursts of spikes in leech T cells produce an AHP, which results from activation of a Na+/K+ pump and a Ca2+-dependent K+ current. Activity-dependent increases in the AHP are believed to induce conduction block of spikes in several regions of the neuron, which in turn, may decrease presynaptic invasion of spikes and thereby decrease transmitter release. To explore this possibility, we used the neurosimulator SNNAP to develop a multi-compartmental model of the T cell. Each compartment was modeled as an equivalent electrical circuit, in which some currents were regulated by intracellular Ca2+ and Na+. The membrane model consisted of a membrane capacitance (Cm), for which we used the value 1 uF/cm2, in parallel with two inward currents (Na+ and Ca2+), two K+ currents, a leak current and pump current. The model incorporated empirical data that describe the geometry of the cell and activity-dependent changes of the AHP (see paper for details). Simulations indicated that at some branching points, activity-dependent increases of the AHP reduced the number of spikes transmitted from the minor receptive field to the soma and beyond. These results suggest that the AHP can regulate spike conduction within the presynaptic arborizations of the cell and could in principle contribute to the synaptic depression that is correlated with increases in the AHP. | |
| Turtle visual cortex model (Nenadic et al. 2003, Wang et al. 2005, Wang et al. 2006) | |
| This is a model of the visual cortex of freshwater turtles that is based upon the known anatomy and physiology of individual neurons. The model was published in three papers (Nenadic et al., 2003; Wang et al., 2005; Wang et al., 2006), which should be consulted for full details on its construction. The model has also been used in several papers (Robbins and Senseman, 2004; Du et al., 2005; Du et al., 2006). It is implemented in GENESIS (Bower and Beeman, 1998). | |
| Zonisamide-induced inhibition of the firing of APs in hippocampal neurons (Huang et al. 2007) | |
| Zonisamide (ZNS), a synthetic benzisoxazole derivative, has been used as an alternative choice in the treatment of epilepsy with a better efficacy and safety profile. However, little is known regarding the mechanism of ZNS actions on ion currents in neurons. We thus investigated its effect on ion currents in differentiated hippocampal 19-7 cells. The ZNS (30 ƒÝM) reversibly increased the amplitude of K+ outward currents and paxilline (1 ƒÝM) was effective in suppressing ZNS-induced increase of K+ outward currents. In inside-out configuration, ZNS (30 ƒÝM) applied to the intracellular face of the membrane did not alter single-channel conductance; however, it did enhance the activity of large-conductance Ca2+-activated K+ (BKCa) channels primarily by decreasing mean closed time. The EC50 value for ZNS-stimulated BKCa channels was 34 ƒÝM. This drug caused a left shift in the activation curve of BKCa channels with no change in the gating charge of these channels. ZNS at a concentration greater than 100 ƒÝM also reduced the amplitude of A-type K+ current in these cells. A simulation modeling based on hippocampal CA3 pyramidal neurons (Pinsky-Rinzel model) was also analyzed to investigate the inhibitory effect of ZNS on the firing of simulated action potentials. Taken together, this study suggests that in hippocampal neurons, during the exposure to ZNS, the ZNS-mediated effects on BKCa channels and IA could be one of the ionic mechanisms through which it affects neuronal excitability. | |
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