Markov models of SCN1A (NaV1.1) applied to abnormal gating and epilepsy (Clancy and Kass 2004)

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Accession:87278
"Recently, some forms of idiopathic epilepsy have been causally related to genetic mutations in neuronal ion channels. To understand disease mechanisms, it is crucial to understand how a gene defect can disrupt channel gating, which in turn can affect complex cellular dynamic processes. We develop a theoretical Markovian model of the neuronal Na+ channel NaV1.1 to explore and explain gating mechanisms underlying cellular excitability and physiological and pathophysiological mechanisms of abnormal neuronal excitability in the context of epilepsy. ..."
Reference:
1 . Clancy CE, Kass RS (2004) Theoretical investigation of the neuronal Na+ channel SCN1A: abnormal gating and epilepsy. Biophys J 86:2606-14 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Channel/Receptor;
Brain Region(s)/Organism:
Cell Type(s):
Channel(s): I Na,t;
Gap Junctions:
Receptor(s):
Gene(s): Nav1.1 SCN1A;
Transmitter(s):
Simulation Environment: C or C++ program;
Model Concept(s): Ion Channel Kinetics; Epilepsy; Markov-type model;
Implementer(s): Clancy, Colleen E [ceclancy at ucdavis.edu];
Search NeuronDB for information about:  I Na,t;
 
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clancykass04
readme.txt
SCN1A_global_function.h
WT_SCN1A_function.cc
                            
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