Voltage-gated sodium channels Pharmaceutical targets via anticonvulsants to treat epileptic syndromes

被引：38
作者：
Abdelsayed, Mena [1 ]
Sokolov, Stanislav [1 ]
机构：
[1] Simon Fraser Univ, Dept Biomed Physiol & Kinesiol, Burnaby, BC V5A 1S6, Canada
来源：
CHANNELS | 2013年 / 7卷 / 03期
关键词：
VGSC; epilepsy; anticonvulsants; AEDs; hyperexcitability; steady-state slow inactivation; steady-state fast inactivation; ANTIEPILEPTIC DRUGS; NA+ CHANNELS; NEUROLOGICAL DISORDERS; MOLECULAR DETERMINANTS; THERAPEUTIC TARGETS; CRYSTAL-STRUCTURE; CARBAMAZEPINE; RANOLAZINE; MUTATION; INACTIVATION;
D O I：
10.4161/chan.24380
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：146 / 152
页数：7
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