Referenced in: none

Automatically associated channels: Nav1.1 , Nav1.2 , Nav1.7 , Slo1

Title: Voltage-gated sodium channels: pharmaceutical targets via anticonvulsants to treat epileptic syndromes.

Authors: Mena Abdelsayed, Stanislav Sokolov

Journal, date & volume: Channels (Austin), 2013 May-Jun , 7, 146-52

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/23531742

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.