Models that contain the Current : I CAN

(Calcium Activated Nonspecific cation channel)
Re-display model names without descriptions
    Models   Description
1.  A model of ventral Hippocampal CA1 pyramidal neurons of Tg2576 AD mice (Spoleti et al. 2021)
Gradual decline in cognitive and non-cognitive functions are considered clinical hallmarks of Alzheimer's Disease (AD). Post-mortem autoptic analysis shows the presence of amyloid ß deposits, neuroinflammation and severe brain atrophy. However, brain circuit alterations and cellular derailments, assessed in very early stages of AD, still remain elusive. The understanding of these early alterations is crucial to tackle defective mechanisms. In a previous study we proved that the Tg2576 mouse model of AD displays functional deficits in the dorsal hippocampus and relevant behavioural AD-related alterations. We had shown that these deficits in Tg2576 mice correlate with the precocious degeneration of dopamine (DA) neurons in the Ventral Tegmental Area (VTA) and can be restored by L-DOPA treatment. Due to the distinct functionality and connectivity of dorsal versus ventral hippocampus, here we investigated neuronal excitability and synaptic functionality in the ventral CA1 hippocampal sub-region of Tg2576 mice. We found an age-dependent alteration of cell excitability and firing in pyramidal neurons starting at 3 months of age, that correlates with reduced levels in the ventral CA1 of tyrosine hydroxylase – the rate-limiting enzyme of DA synthesis. Additionally, at odds with the dorsal hippocampus, we found no alterations in basal glutamatergic transmission and long-term plasticity of ventral neurons in 8-month old Tg2576 mice compared to age-matched controls. Last, we used computational analysis to model the early derailments of firing properties observed and hypothesize that the neuronal alterations found could depend on dysfunctional sodium and potassium conductances, leading to anticipated depolarization-block of action potential firing. The present study depicts that impairment of cell excitability and homeostatic control of firing in ventral CA1 pyramidal neurons is a prodromal feature in Tg2576 AD mice.
2.  A modified Morris-Lecar with TRPC4 & GIRK (Tian et al. 2022)
Simulates differential activation of TRPC4 and GIRK channel to reproduce various spiking patterns underlying Gq/11–Gi/o coincidence signals. The attached code reproduces Fig.5B-F in Tian et al. 2022. Please see readme.txt to get started.
3.  A multi-compartment model for interneurons in the dLGN (Halnes et al. 2011)
This model for dLGN interneurons is presented in two parameterizations (P1 & P2), which were fitted to current-clamp data from two different interneurons (IN1 & IN2). The model qualitatively reproduces the responses in IN1 & IN2 under 8 different experimental condition, and quantitatively reproduces the I/O-relations (#spikes elicited as a function of injected current).
4.  A network of AOB mitral cells that produces infra-slow bursting (Zylbertal et al. 2017)
Infra-slow rhythmic neuronal activity with very long (> 10 s) period duration was described in many brain areas but little is known about the role of this activity and the mechanisms that produce it. Here we combine experimental and computational methods to show that synchronous infra-slow bursting activity in mitral cells of the mouse accessory olfactory bulb (AOB) emerges from interplay between intracellular dynamics and network connectivity. In this novel mechanism, slow intracellular Na+ dynamics endow AOB mitral cells with a weak tendency to burst, which is further enhanced and stabilized by chemical and electrical synapses between them. Combined with the unique topology of the AOB network, infra-slow bursting enables integration and binding of multiple chemosensory stimuli over prolonged time scale. The example protocol simulates a two-glomeruli network with a single shared cell. Although each glomerulus is stimulated at a different time point, the activity of the entire population becomes synchronous (see paper Fig. 8)
5.  A synapse model for developing somatosensory cortex (Manninen et al 2020)
We developed a model for an L4-L2/3 synapse in somatosensory cortex to study the role of astrocytes in modulation of t-LTD. Our model includes the one-compartmental presynaptic L4 spiny stellate cell, two-compartmental (soma and dendrite) postsynaptic L2/3 pyramidal cell, and one-compartmental fine astrocyte process.
6.  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.
7.  A unified thalamic model of multiple distinct oscillations (Li, Henriquez and Fröhlich 2017)
We present a unified model of the thalamus that is capable of independently generating multiple distinct oscillations (delta, spindle, alpha and gamma oscillations) under different levels of acetylcholine (ACh) and norepinephrine (NE) modulation corresponding to different physiological conditions (deep sleep, light sleep, relaxed wakefulness and attention). The model also shows that entrainment of thalamic oscillations is state-dependent.
8.  AOB mitral cell: persistent activity without feedback (Zylbertal et al., 2015)
Persistent activity has been reported in many brain areas and is hypothesized to mediate working memory and emotional brain states and to rely upon network or biophysical feedback. Here we demonstrate a novel mechanism by which persistent neuronal activity can be generated without feedback, relying instead on the slow removal of Na+ from neurons following bursts of activity. This is a realistic conductance-based model that was constructed using the detailed morphology of a single typical accessory olfactory bulb (AOB) mitral cell for which the electrophysiological properties were characterized.
9.  Ca+/HCN channel-dependent persistent activity in multiscale model of neocortex (Neymotin et al 2016)
"Neuronal persistent activity has been primarily assessed in terms of electrical mechanisms, without attention to the complex array of molecular events that also control cell excitability. We developed a multiscale neocortical model proceeding from the molecular to the network level to assess the contributions of calcium regulation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in providing additional and complementary support of continuing activation in the network. ..."
10.  CA1 network model: interneuron contributions to epileptic deficits (Shuman et al 2019)
Temporal lobe epilepsy causes significant cognitive deficits in both humans and rodents, yet the specific circuit mechanisms underlying these deficits remain unknown. There are profound and selective interneuron death and axonal reorganization within the hippocampus of both humans and animal models of temporal lobe epilepsy. To assess the specific contribution of these mechanisms on spatial coding, we developed a biophysically constrained network model of the CA1 region that consists of different subtypes of interneurons. More specifically, our network consists of 150 cells, 130 excitatory pyramidal cells and 20 interneurons (Fig. 1A). To simulate place cell formation in the network model, we generated grid cell and place cell inputs from the Entorhinal Cortex (ECLIII) and CA3 regions, respectively, activated in a realistic manner as observed when an animal transverses a linear track. Realistic place fields emerged in a subpopulation of pyramidal cells (40-50%), in which similar EC and CA3 grid cell inputs converged onto distal/proximal apical and basal dendrites. The tuning properties of these cells are very similar to the ones observed experimentally in awake, behaving animals To examine the role of interneuron death and axonal reorganization in the formation and/or tuning properties of place fields we selectively varied the contribution of each interneuron type and desynchronized the two excitatory inputs. We found that desynchronized inputs were critical in reproducing the experimental data, namely the profound reduction in place cell numbers, stability and information content. These results demonstrate that the desynchronized firing of hippocampal neuronal populations contributes to poor spatial processing in epileptic mice, during behavior. Given the lack of experimental data on the selective contributions of interneuron death and axonal reorganization in spatial memory, our model findings predict the mechanistic effects of these alterations at the cellular and network levels.
11.  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).
12.  Ca2+-activated I_CAN and synaptic depression promotes network-dependent oscil. (Rubin et al. 2009)
"... the preBotzinger complex... we present and analyze a mathematical model demonstrating an unconventional mechanism of rhythm generation in which glutamatergic synapses and the short-term depression of excitatory transmission play key rhythmogenic roles. Recurrent synaptic excitation triggers postsynaptic Ca2+- activated nonspecific cation current (ICAN) to initiate a network-wide burst. Robust depolarization due to ICAN also causes voltage-dependent spike inactivation, which diminishes recurrent excitation and thus attenuates postsynaptic Ca2+ accumulation. ..."
13.  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.
14.  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.
15.  Calcium response prediction in the striatal spines depending on input timing (Nakano et al. 2013)
We construct an electric compartment model of the striatal medium spiny neuron with a realistic morphology and predict the calcium responses in the synaptic spines with variable timings of the glutamatergic and dopaminergic inputs and the postsynaptic action potentials. The model was validated by reproducing the responses to current inputs and could predict the electric and calcium responses to glutamatergic inputs and back-propagating action potential in the proximal and distal synaptic spines during up and down states.
16.  Channel density variability among CA1 neurons (Migliore et al. 2018)
The peak conductance of many ion channel types measured in any given animal is highly variable across neurons, both within and between neuronal populations. The current view is that this occurs because a neuron needs to adapt its intrinsic electrophysiological properties either to maintain the same operative range in the presence of abnormal inputs or to compensate for the effects of pathological conditions. Limited experimental and modeling evidence suggests this might be implemented via the correlation and/or degeneracy in the function of multiple types of conductances. To study this mechanism in hippocampal CA1 neurons and interneurons, we systematically generated a set of morphologically and biophysically accurate models. We then analyzed the ensembles of peak conductance obtained for each model neuron. The results suggest that the set of conductances expressed in the various neuron types may be divided into two groups: one group is responsible for the major characteristics of the firing behavior in each population and the other more involved with degeneracy. These models provide experimentally testable predictions on the combination and relative proportion of the different conductance types that should be present in hippocampal CA1 pyramidal cells and interneurons.
17.  Circadian rhythmicity shapes astrocyte morphology and neuronal function in CA1 (McCauley et al 2020)
Most animal species operate according to a 24-hour period set by the suprachiasmatic nucleus (SCN) of the hypothalamus. The rhythmic activity of the SCN modulates hippocampal-dependent memory, but the molecular and cellular mechanisms that account for this effect remain largely unknown. In McCauley et al. 2020 [1], we identify cell-type specific structural and functional changes that occur with circadian rhythmicity in neurons and astrocytes in hippocampal area CA1. Pyramidal neurons change the surface expression of NMDA receptors. Astrocytes change their proximity clustered excitatory synaptic inputs, ultimately shaping hippocampal-dependent learning in vivo. We identify to synapses. Together, these phenomena alter glutamate clearance, receptor activation and integration of temporally corticosterone as a key contributor to changes in synaptic strength. These findings highlight important mechanisms through which neurons and astrocytes modify the molecular composition and structure of the synaptic environment, contribute to the local storage of information in the hippocampus and alter the temporal dynamics of cognitive processing. [1] "Circadian modulation of neurons and astrocytes controls synaptic plasticity in hippocampal area CA1" by J.P. McCauley, M.A. Petroccione, L.Y. D’Brant, G.C. Todd, N. Affinnih, J.J. Wisnoski, S. Zahid, S. Shree, A.A. Sousa, R.M. De Guzman, R. Migliore, A. Brazhe, R.D. Leapman, A. Khmaladze, A. Semyanov, D.G. Zuloaga, M. Migliore and A. Scimemi. Cell Reports (2020),
18.  Computer model of clonazepam's effect in thalamic slice (Lytton 1997)
Demonstration of the effect of a minor pharmacological synaptic change at the network level. Clonazepam, a benzodiazepine, enhances inhibition but is paradoxically useful for certain types of seizures. This simulation shows how inhibition of inhibitory cells (the RE cells) produces this counter-intuitive effect.
19.  Conductance based model for short term plasticity at CA3-CA1 synapses (Mukunda & Narayanan 2017)
We develop a new biophysically rooted, physiologically constrained conductance-based synaptic model to mechanistically account for short-term facilitation and depression, respectively through residual calcium and transmitter depletion kinetics. The model exhibits different synaptic filtering profiles upon changing certain parameters in the base model. We show degenercy in achieving similar plasticity profiles with different presynaptic parameters. Finally, by virtually knocking out certain conductances, we show the differential contribution of conductances.
20.  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. ..."
21.  Hippocampal Mossy Fiber bouton: presynaptic KV7 channel function (Martinello et al 2019)
22.  Intrinsic sensory neurons of the gut (Chambers et al. 2014)
A conductance base model of intrinsic neurons neurons in the gastrointestinal tract. The model contains all the major voltage-gated and calcium-gated currents observed in these neurons. This model can reproduce physiological observations such as the response to multiple brief depolarizing currents, prolonged depolarizing currents and hyperpolarizing currents. This model can be used to predict how different currents influence the excitability of intrinsic sensory neurons in the gut.
23.  Ionic mechanisms of dendritic spikes (Almog and Korngreen 2014)
We used a combined experimental and numerical parameter peeling procedure was implemented to optimize a detailed ionic mechanism for the generation and propagation of dendritic spikes in neocortical L5 pyramidal neurons. Run the cc_run.hoc to get a demo for dendritic calcium spike generated by coincidence of a back-propagating AP and distal synaptic input.
24.  KV1 channel governs cerebellar output to thalamus (Ovsepian et al. 2013)
The output of the cerebellum to the motor axis of the central nervous system is orchestrated mainly by synaptic inputs and intrinsic pacemaker activity of deep cerebellar nuclear (DCN) projection neurons. Herein, we demonstrate that the soma of these cells is enriched with KV1 channels produced by mandatory multi-merization of KV1.1, 1.2 alpha andKV beta2 subunits. Being constitutively active, the K+ current (IKV1) mediated by these channels stabilizes the rate and regulates the temporal precision of self-sustained firing of these neurons. ... Through the use of multi-compartmental modelling and ... the physiological significance of the described functions for processing and communication of information from the lateral DCN to thalamic relay nuclei is established.
25.  L5 PFC microcircuit used to study persistent activity (Papoutsi et al. 2014, 2013)
Using a heavily constrained biophysical model of a L5 PFC microcircuit we investigate the mechanisms that underlie persistent activity emergence (ON) and termination (OFF) and search for the minimum network size required for expressing these states within physiological regimes.
26.  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. "
27.  Linear vs non-linear integration in CA1 oblique dendrites (Gómez González et al. 2011)
The hippocampus in well known for its role in learning and memory processes. The CA1 region is the output of the hippocampal formation and pyramidal neurons in this region are the elementary units responsible for the processing and transfer of information to the cortex. Using this detailed single neuron model, it is investigated the conditions under which individual CA1 pyramidal neurons process incoming information in a complex (non-linear) as opposed to a passive (linear) manner. This detailed compartmental model of a CA1 pyramidal neuron is based on one described previously (Poirazi, 2003). The model was adapted to five different reconstructed morphologies for this study, and slightly modified to fit the experimental data of (Losonczy, 2006), and to incorporate evidence in pyramidal neurons for the non-saturation of NMDA receptor-mediated conductances by single glutamate pulses. We first replicate the main findings of (Losonczy, 2006), including the very brief window for nonlinear integration using single-pulse stimuli. We then show that double-pulse stimuli increase a CA1 pyramidal neuron’s tolerance for input asynchrony by at last an order of magnitude. Therefore, it is shown using this model, that the time window for nonlinear integration is extended by more than an order of magnitude when inputs are short bursts as opposed to single spikes.
28.  Membrane electrical properties of mouse CA1 pyramidal cells during strong inputs (Bianchi et al 22)
ABSTRACT: In this work we highlight an electrophysiological feature, often observed in recordings from mouse CA1 pyramidal cells, which has been so far ignored by experimentalists and modelers. It consists of a large and dynamic increase in the depolarization baseline (i.e. the minimum value of the membrane potential between successive action potentials during a sustained input) in response to strong somatic current injections. Such an increase can directly affect neurotransmitter release properties and, more generally, efficacy of synaptic transmission. However, it cannot be explained by any currently available conductance-based computational model. Here we present a model addressing this issue, demonstrating that experimental recordings can be reproduced by assuming that an input current modifies, in a time-dependent manner, the electrical and permeability properties of the neuron membrane by shifting the ionic reversal potentials and channel kinetics. For this reason, we propose that any detailed model of ion channel kinetics, for neurons exhibiting this characteristic, should be adapted to correctly represent the response and the synaptic integration process during strong and sustained inputs.
29.  Model of eupnea and sigh generation in respiratory network (Toporikova et al 2015)
Based on recent in vitro data obtained in the mouse embryo, we have built a computational model consisting of two compartments, interconnected through appropriate synapses. One compartment generates sighs and the other produces eupneic bursts. The model reproduces basic features of simultaneous sigh and eupnea generation (two types of bursts differing in terms of shape, amplitude, and frequency of occurrence) and mimics the effect of blocking glycinergic synapses
30.  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. ..."
31.  Multiscale simulation of the striatal medium spiny neuron (Mattioni & Le Novere 2013)
"… We present a new event-driven algorithm to synchronize different neuronal models, which decreases computational time and avoids superfluous synchronizations. The algorithm is implemented in the TimeScales framework. We demonstrate its use by simulating a new multiscale model of the Medium Spiny Neuron of the Neostriatum. The model comprises over a thousand dendritic spines, where the electrical model interacts with the respective instances of a biochemical model. Our results show that a multiscale model is able to exhibit changes of synaptic plasticity as a result of the interaction between electrical and biochemical signaling. …"
32.  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.
33.  Neuromusculoskeletal modeling with neural and finite element models (Volk et al, 2021)
"In this study, we present a predictive NMS model that uses an embedded neural architecture within a finite element (FE) framework to simulate muscle activation. A previously developed neuromuscular model of a motor neuron was embedded into a simple FE musculoskeletal model. Input stimulation profiles from literature were simulated in the FE NMS model to verify effective integration of the software platforms. Motor unit recruitment and rate coding capabilities of the model were evaluated. The integrated model reproduced previously published output muscle forces with an average error of 0.0435 N. The integrated model effectively demonstrated motor unit recruitment and rate coding in the physiological range based upon motor unit discharge rates and muscle force output."
34.  Neuronal dendrite calcium wave model (Neymotin et al, 2015)
"... We developed a reaction-diffusion model of an apical dendrite with diffusible inositol triphosphate (IP3 ), diffusible Ca2+, IP3 receptors (IP3 Rs), endoplasmic reticulum (ER) Ca2+ leak, and ER pump (SERCA) on ER. ... At least two modes of Ca2+ wave spread have been suggested: a continuous mode based on presumed relative homogeneity of ER within the cell; and a pseudo-saltatory model where Ca2+ regeneration occurs at discrete points with diffusion between them. We compared the effects of three patterns of hypothesized IP3 R distribution: 1. continuous homogeneous ER, 2. hotspots with increased IP3R density (IP3 R hotspots), 3. areas of increased ER density (ER stacks). All three modes produced Ca2+ waves with velocities similar to those measured in vitro (~50 - 90µm /sec). ... The measures were sensitive to changes in density and spacing of IP3 R hotspots and stacks. ... An extended electrochemical model, including voltage gated calcium channels and AMPA synapses, demonstrated that membrane priming via AMPA stimulation enhances subsequent Ca2+ wave amplitude and duration. Our modeling suggests that pharmacological targeting of IP3 Rs and SERCA could allow modulation of Ca2+ wave propagation in diseases where Ca2+ dysregulation has been implicated. "
35.  Persistent Spiking in ACC Neurons (Ratte et al 2018)
"Neurons use action potentials, or spikes, to encode information. Some neurons can store information for short periods (seconds to minutes) by continuing to spike after a stimulus ends, thus enabling working memory. This so-called “persistent” spiking occurs in many brain areas and has been linked to activation of canonical transient receptor potential (TRPC) channels. However, TRPC activation alone is insufficient to explain many aspects of persistent spiking such as resumption of spiking after periods of imposed quiescence. Using experiments and simulations, we show that calcium influx caused by spiking is necessary and sufficient to activate TRPC channels and that the ensuing positive feedback interaction between intracellular calcium and TRPC channel activation can account for many hitherto unexplained aspects of persistent spiking."
36.  PreBotzinger Complex inspiratory neuron with NaP and CAN currents (Park and Rubin 2013)
We have built on earlier models to develop a single-compartment Hodgkin-Huxley type model incorporating NaP and CAN currents, both of which can play important roles in bursting of inspiratory neurons in the PreBotzinger Complex of the mammalian respiratory brain stem. The model tracks the evolution of membrane potential, related (in)activation variables, calcium concentration, and available fraction of IP3 channels. The model can produce several types of bursting, presented and analyzed from a dynamical systems perspective in our paper.
37.  Reduced-morphology model of CA1 pyramidal cells optimized + validated w/ HippoUnit (Tomko et al '21)
Here we employ the HippoUnit tests to optimize and validate our new compartmental model with reduced morphology. We show that our model is able to account for the following six well-established characteristic anatomical and physiological properties of CA1 pyramidal cells: (1) The reduced dendritic morphology contains all major dendritic branch classes. In addition to anatomy, the model reproduces also 5 key physiological features, including (2) somatic electrophysiological responses, (3) depolarization block, (4) EPSP attenuation (5) action potential (AP) backpropagation, and (6) synaptic integration at oblique dendrites.
38.  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.
39.  Striatal D1R medium spiny neuron, including a subcellular DA cascade (Lindroos et al 2018)
We are investigating how dopaminergic modulation of single channels can be combined to make the D1R possitive MSN more excitable. We also connect multiple channels to substrates of a dopamine induced subcellular cascade to highlight that the classical pathway is too slow to explain DA induced kinetics in the subsecond range (Howe and Dombeck, 2016. doi: 10.1038/nature18942)
40.  Striatal Spiny Projection Neuron, inhibition enhances spatial specificity (Dorman et al 2018)
We use a computational model of a striatal spiny projection neuron to investigate dendritic spine calcium dynamics in response to spatiotemporal patterns of synaptic inputs. We show that spine calcium elevation is stimulus-specific, with supralinear calcium elevation in cooperatively stimulated spines. Intermediate calcium elevation occurs in neighboring non-stimulated dendritic spines, predicting heterosynaptic effects. Inhibitory synaptic inputs enhance the difference between peak calcium in stimulated spines, and peak calcium in non-stimulated spines, thereby enhancing stimulus specificity.
41.  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
42.  Thalamic Reticular Network (Destexhe et al 1994)
Demo for simulating networks of thalamic reticular neurons (reproduces figures from Destexhe A et al 1994)
43.  The subcellular distribution of T-type Ca2+ channels in LGN interneurons (Allken et al. 2014)
" ...To study the relationship between the (Ca2+ channel) T-distribution and several (LGN interneuron) IN response properties, we here run a series of simulations where we vary the T-distribution in a multicompartmental IN model with a realistic morphology. We find that the somatic response to somatic current injection is facilitated by a high T-channel density in the soma-region. Conversely, a high T-channel density in the distal dendritic region is found to facilitate dendritic signalling in both the outward direction (increases the response in distal dendrites to somatic input) and the inward direction (the soma responds stronger to distal synaptic input). ..."

Re-display model names without descriptions