Long-Term Inactivation of Na+ Channels as a Mech of Adaptation in CA1 Pyr Cells (Upchurch et al '22)

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"... Ramps were applied to CA1 pyramidal neurons from male rats in vitro (slice electrophysiology) and in silico (multi-compartmental NEURON model). Under control conditions, CA1 neurons fired more action potentials at higher frequencies on the up-ramp versus the down-ramp. This effect was more pronounced for dendritic compared to somatic ramps. We incorporated a four-state Markov scheme for NaV1.6 channels into our model and calibrated the spatial dependence of long-term inactivation according to the literature; this spatial dependence was sufficient to explain the difference in dendritic versus somatic ramps. Long-term inactivation reduced the firing frequency by decreasing open-state occupancy, and reduced spike amplitude during trains by decreasing occupancy in closed states, which comprise the available pool..."
1 . Upchurch CM, Combe CL, C Knowlton, V Rousseau, Gasparini S, Canavier CC (2021) Long-Term Inactivation of Sodium Channels as a Mechanism of Adaptation in CA1 Pyramidal Cells J Neuroscience [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I K,Ca; I Calcium; I L high threshold; I R; I T low threshold; I h; I_KD; I K; I M; I Potassium; I Sodium;
Gap Junctions:
Receptor(s): NMDA;
Gene(s): Nav1.6 SCN8A;
Simulation Environment: NEURON;
Model Concept(s): Place cell/field;
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; NMDA; I L high threshold; I T low threshold; I K; I M; I h; I K,Ca; I Sodium; I Calcium; I Potassium; I R; I_KD;
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