ANTIEPILEPTIC DRUG MECHANISMS OF ACTION

被引：106

作者：

MACDONALD, RL ^{[1
]}

KELLY, KM ^{[1
]}

机构：

[1] UNIV MICHIGAN, MED CTR, DEPT PHYSIOL, ANN ARBOR, MI 48109 USA

来源：

EPILEPSIA | 1993年 / 34卷

关键词：

ANTICONVULSANTS; NEUROPHARMACOLOGY; NEUROTRANSMITTERS; GABA; PHENYTOIN; CARBAMAZEPINE; ETHOSUXIMIDE; TRIMETHADIONE; BENZODIAZEPINES; BARBITURATES; VALPROATE; FELBAMATE; GABAPENTIN; LAMOTRIGINE; NEURAL INHIBITION; SODIUM; CALCIUM;

D O I：

10.1111/j.1528-1157.1993.tb05918.x

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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, GABA(A) 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 GABA(A) 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.

引用

页码：S1 / S8

页数：8

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