Talwar D
University Pediatric Epilepsy Program, University of Minnesota Hospital and Clinic, Minneapolis 55455.
Pediatr Neurol. 1990 Sep-Oct;6(5):289-95. doi: 10.1016/0887-8994(90)90019-w.
Animal seizure models, in vitro preparations of cell cultures and tissue slices, and an unravelling of some of the basic mechanisms underlying epileptogenesis and epilepsy have furthered the understanding of mechanisms of action of antiepileptic drugs at the cellular and subcellular levels. Nevertheless, the mechanism of action of most antiepileptic drugs in clinical use is incompletely understood. Multiple physiologic mechanisms are altered by antiepileptic drugs. Some of these drugs, such as phenytoin and carbamazepine, decrease sustained repetitive firing and post-tetanic potentiation through their blocking effects on the sodium channel. Benzodiazepines and barbiturates enhance GABA-mediated inhibition. Many antiepileptic drugs inhibit calcium influx and calcium-mediated secondary effects at supratherapeutic concentrations. Newer drugs that inhibit excitatory receptors or enhance various forms of inhibition are presently under investigation.
动物癫痫模型、细胞培养物和组织切片的体外制备，以及对癫痫发生和癫痫背后一些基本机制的阐明，进一步加深了我们在细胞和亚细胞水平上对抗癫痫药物作用机制的理解。然而，目前临床上大多数抗癫痫药物的作用机制仍未被完全理解。抗癫痫药物会改变多种生理机制。其中一些药物，如苯妥英和卡马西平，通过对钠通道的阻断作用，减少持续性重复放电和强直后增强。苯二氮䓬类药物和巴比妥类药物增强γ-氨基丁酸（GABA）介导的抑制作用。许多抗癫痫药物在超治疗浓度下会抑制钙内流和钙介导的继发效应。目前正在研究抑制兴奋性受体或增强各种抑制形式的新型药物。
