title: Voltage-gated sodium channels: pharmaceutical targets via anticonvulsants to treat epileptic syndromes.
abstract: Epilepsy is a brain disorder characterized by seizures and convulsions. The basis of epilepsy is an increase in neuronal excitability that, in some cases, may be caused by functional defects in neuronal voltage gated sodium channels, Nav1.1 and Nav1.2. The effects of antiepileptic drugs (AEDs) as effective therapies for epilepsy have been characterized by extensive research. Most of the classic AEDs targeting Nav share a common mechanism of action by stabilizing the channel's fast-inactivated state. In contrast, novel AEDs, such as lacosamide, stabilize the slow-inactivated state in neuronal Nav1.1 and Nav1.7 isoforms. This paper reviews the different mechanisms by which this stabilization occurs to determine new methods for treatment.
authors.affiliation: Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, BC, Canada. mabdelsa@sfu.ca
authors.forename: Mena
authors.initials: M
authors.lastname: Abdelsayed
authors.forename: Stanislav
authors.initials: S
authors.lastname: Sokolov
mesh_terms: D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology* / Q000627:therapeutic use*; D004827:Epilepsy / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D013577:Syndrome; D061567:Voltage-Gated Sodium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use; D061566:Voltage-Gated Sodium Channels / Q000378:metabolism*
chemical_list: D000927:Anticonvulsants; D061567:Voltage-Gated Sodium Channel Blockers; D061566:Voltage-Gated Sodium Channels
keywords: AEDs; VGSC; anticonvulsants; epilepsy; hyperexcitability; steady-state fast inactivation; steady-state slow inactivation