"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. ..."
Model Type: Channel/Receptor
Currents: I Na,t
Genes: Nav1.1 SCN1A
Model Concept(s): Ion Channel Kinetics; Epilepsy; Markov-type model
Simulation Environment: C or C++ program
Implementer(s): Clancy, Colleen E [ceclancy at ucdavis.edu]
References:
Clancy CE, Kass RS. (2004). Theoretical investigation of the neuronal Na+ channel SCN1A: abnormal gating and epilepsy. Biophysical journal. 86 [PubMed]