Models that contain the Current : I Na, slow inactivation

(Voltage gated Na channel with prolonged inactivation)
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    Models   Description
1.  Computational model of bladder small DRG neuron soma (Mandge & Manchanda 2018)
Bladder small DRG neurons, which are putative nociceptors pivotal to urinary bladder function, express more than a dozen different ionic membrane mechanisms: ion channels, pumps and exchangers. Small-conductance Ca2+-activated K+ (SKCa) channels which were earlier thought to be gated solely by intracellular Ca2+ concentration ([Ca]i ) have recently been shown to exhibit inward rectification with respect to membrane potential. The effect of SKCa inward rectification on the excitability of these neurons is unknown. Furthermore, studies on the role of KCa channels in repetitive firing and their contributions to different types of afterhyperpolarization (AHP) in these neurons are lacking. In order to study these phenomena, we first constructed and validated a biophysically detailed single compartment model of bladder small DRG soma constrained by physiological data. The model includes twenty-two major known membrane mechanisms along with intracellular Ca2+ dynamics comprising Ca2+ diffusion, cytoplasmic buffering, and endoplasmic reticulum (ER) and mitochondrial mechanisms. Using modelling studies, we show that inward rectification of SKCa is an important parameter regulating neuronal repetitive firing and that its absence reduces action potential (AP) firing frequency. We also show that SKCa is more potent in reducing AP spiking than the large-conductance KCa channel (BKCa) in these neurons. Moreover, BKCa was found to contribute to the fast AHP (fAHP) and SKCa to the medium-duration (mAHP) and slow AHP (sAHP). We also report that the slow inactivating A-type K+ channel (slow KA) current in these neurons is composed of 2 components: an initial fast inactivating (time constant ~ 25-100 ms) and a slow inactivating (time constant ~ 200-800 ms) current. We discuss the implications of our findings, and how our detailed model can help further our understanding of the role of C-fibre afferents in the physiology of urinary bladder as well as in certain disorders.
2.  Distance-dependent synaptic strength in CA1 pyramidal neurons (Menon et al. 2013)
Menon et al. (2013) describes the experimentally-observed variation in synaptic AMPA and NMDA conductance as a function of distance from the soma. This model explores the effect of this variation on somatic EPSPs and dendritic spike initiation, as compared to the case of uniform AMPA and NMDA conductance.
3.  Dynamics of ramping bursts in a respiratory pre-Botzinger Complex model (Abdulla et al, accepted)
This single-neuron model is, to the authors' knowledge, the first to capture the pre-inspiratory ramping aspects of preBotzinger Complex inspiratory neurons' activity patterns, in which relatively slow tonic spiking gradually progresses to faster spiking and a full-blown burst, with a corresponding gradual development of an underlying plateau potential. The key to this pattern is the incorporation of the dynamics of the extracellular potassium ion concentration, which is here integrated into an existing model for pre-BotC neuron bursting along with some parameter adjustments. Using fast-slow decomposition, this activity can be shown to be a form of parabolic bursting, but with burst termination at a homoclinic bifurcation rather than at a SNIC bifurcation.
4.  Hippocampal CA1 pyramidal cell demonstrating dynamic mode switching (Berteau & Bullock 2020)
A simulated proposed single-cell mechanism for CA1’s behavior as an associative mismatch detector. Shifts in spiking mode (accomplished via KCNQ interaction with chloride leak currents) signal matches vs. mismatches.
5.  Hippocampus CA1 pyramidal model with Na channel exhibiting slow inactivation (Menon et al. 2009)
These NEURON simulations show the effect of prolonged inactivation of sodium channels on attenuation of trains of backpropagating action potentials (bAPs). The new sodium channel model is a Markov model derived using a state-mutating genetic algorithm, as described in the paper.
6.  Maximal firing rate in midbrain dopamine neurons (Knowlton et al., accepted)
7.  Striatum D1 Striosome and Matrix Upstates (Prager et al., 2020)
"...We show that dopamine oppositely shapes responses to convergent excitatory inputs in mouse striosome and matrix striatal spiny projection neurons (SPNs). Activation of postsynaptic D1 dopamine receptors promoted the generation of long-lasting synaptically evoked 'up-states' in matrix SPNs but opposed it in striosomes, which were more excitable under basal conditions. Differences in dopaminergic modulation were mediated, in part, by dendritic voltage-gated calcium channels (VGCCs): pharmacological manipulation of L-type VGCCs reversed compartment-specific responses to D1 receptor activation..."

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