Models that contain the Gene Name : Cav3.1 CACNA1G

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    Models   Description
1.  A detailed Purkinje cell model (Masoli et al 2015)
The Purkinje cell is one of the most complex type of neuron in the central nervous system and is well known for its massive dendritic tree. The initiation of the action potential was theorized to be due to the high calcium channels presence in the dendritic tree but, in the last years, this idea was revised. In fact, the Axon Initial Segment, the first section of the axon was seen to be critical for the spontaneous generation of action potentials. The model reproduces the behaviours linked to the presence of this fundamental sections and the interplay with the other parts of the neuron.
2.  Availability of low-threshold Ca2+ current in retinal ganglion cells (Lee SC et al. 2003)
"... we measured T-type current of isolated goldfish retinal ganglion cells with perforated-patch voltageclamp methods in solutions containing a normal extracellular Ca2+ concentration. The voltage sensitivities and rates of current activation, inactivation, deactivation, and recovery from inactivation were similar to those of expressed +1G (CaV3.1) Ca2+ channel clones, except that the rate of deactivation was significantly faster. We reproduced the amplitude and kinetics of measured T currents with a numerical simulation based on a kinetic model developed for an +1G Ca2+ channel. Finally, we show that this model predicts the increase of T-type current made available between resting potential and spike threshold by repetitive hyperpolarizations presented at rates that are within the bandwidth of signals processed in situ by these neurons."
3.  Biophysically detailed model of the mouse sino-atrial node cell (Kharche et al. 2011)
This model is developed to study the role of various electrophysiological mechanisms in generating cardiac pacemaking action potentials (APs).The model incorporates membrane ionic currents and intracellular mechanisms contributing to spontaneous mouse SAN APs. The model was validated by testing the functional roles of individual membrane currents in one and multiple parameter analyses.The roles of intracellular Ca2+-handling mechanisms on cardiac pacemaking were also investigated in the model.
4.  CA1 pyramidal neuron dendritic spine with plasticity (O`Donnell et al. 2011)
Biophysical model of a dendritic spine and adjacent dendrite with synapse. Model parameters adjusted to fit CA3-CA1 Shaffer collateral synapse data from literature. Model includes both electrical and Ca2+ dynamics, including AMPARs, NMDARs, 4 types of CaV channel, and leak conductance. Spine and synapse are plastic according to Ca2+ dependent rule. The aim of the model is to explore the effects of dendritic spine structural plasticity on the rules of synaptic plasticity.
5.  Calcium dynamics depend on dendritic diameters (Anwar et al. 2014)
"... in dendrites there is a strong contribution of morphology because the peak calcium levels are strongly determined by the surface to volume ratio (SVR) of each branch, which is inversely related to branch diameter. In this study we explore the predicted variance of dendritic calcium concentrations due to local changes in dendrite diameter and how this is affected by the modeling approach used. We investigate this in a model of dendritic calcium spiking in different reconstructions of cerebellar Purkinje cells and in morphological analysis of neocortical and hippocampal pyramidal neurons. ..."
6.  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."
7.  Learning intrinsic excitability in Medium Spiny Neurons (Scheler 2014)
"We present an unsupervised, local activation-dependent learning rule for intrinsic plasticity (IP) which affects the composition of ion channel conductances for single neurons in a use-dependent way. We use a single-compartment conductance-based model for medium spiny striatal neurons in order to show the effects of parameterization of individual ion channels on the neuronal membrane potential-curent relationship (activation function). We show that parameter changes within the physiological ranges are sufficient to create an ensemble of neurons with significantly different activation functions. ... "
8.  Stochastic calcium mechanisms cause dendritic calcium spike variability (Anwar et al. 2013)
" ... In single Purkinje cells, spontaneous and synaptically evoked dendritic calcium bursts come in a variety of shapes with a variable number of spikes. The mechanisms causing this variability have never been investigated thoroughly. In this study, a detailed computational model employing novel simulation routines is applied to identify the roles that stochastic ion channels, spatial arrangements of ion channels and stochastic intracellular calcium have towards producing calcium burst variability. … Our findings suggest that stochastic intracellular calcium mechanisms play a crucial role in dendritic calcium spike generation and are, therefore, an essential consideration in studies of neuronal excitability and plasticity."
9.  T-type Calcium currents (McRory et al 2001)
NEURON mod files for CaT currents from the paper McRory et al., J.Biol.Chem. 276:3999 (2001). In this paper, three members (alpha-1G, -1H, and -1I) of the LVA calcium channels family were studied. Kinetic parameters were derived from functional expression in transfected cells.

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