Macdonald R L, Kelly K M
Department of Neurology, University of Michigan Medical Center, Ann Arbor.
Epilepsia. 1993;34 Suppl 5:S1-8. doi: 10.1111/j.1528-1157.1993.tb05918.x.
Clinically used antiepileptic drugs (AEDs) decrease membrane excitability by interacting with ion channels or neurotransmitter receptors. Currently available AEDs appear to act on sodium channels, GABAA receptors, or calcium channels. Phenytoin, carbamazepine, and possibly valproate (VPA) decrease high-frequency repetitive firing of action potentials by enhancing sodium channel inactivation. Benzodiazepines and barbiturates enhance GABAA receptor-mediated inhibition. Ethosuximide and possibly VPA reduce a low-threshold calcium current. The mechanisms of action of AEDs currently under development are less clear. Lamotrigine may decrease sustained high-frequency repetitive firing. The mechanisms of action of felbamate are unknown. Gabapentin (GBP) appears to bind to a specific binding site in the central nervous system with a restricted regional distribution, but the identity of the binding site and the mechanism of action of GBP remain uncertain.
临床使用的抗癫痫药物（AEDs）通过与离子通道或神经递质受体相互作用来降低膜兴奋性。目前可用的AEDs似乎作用于钠通道、GABAA受体或钙通道。苯妥英、卡马西平以及可能的丙戊酸（VPA）通过增强钠通道失活来减少动作电位的高频重复发放。苯二氮䓬类和巴比妥类药物增强GABAA受体介导的抑制作用。乙琥胺以及可能的VPA降低低阈值钙电流。目前正在研发的AEDs的作用机制尚不清楚。拉莫三嗪可能减少持续的高频重复发放。非氨酯的作用机制尚不清楚。加巴喷丁（GBP）似乎与中枢神经系统中一个区域分布受限的特定结合位点结合，但其结合位点的身份以及GBP的作用机制仍不确定。
