癫痫发病中突触机制的研究进展

Progress in synaptic mechanism in epileptogenesis

反复的癫痫发作可导致突触蛋白的表达异常、突触重塑和异常神经元网络的形成,这是难治性癫痫的病理生理学机制之一。近年来发现突触蛋白在原发性癫痫的发病机制中同样发挥重要的作用。多个突触调控蛋白以及突触后膜受体蛋白表达异常可导致癫痫发作。绝大多数的抗癫痫药物是以离子通道为作用靶点,但卡马西平及唑尼沙胺可通过影响突触融合蛋白及可溶性N-乙基马来酰亚胺敏感因子附着蛋白受体复合物的功能而发挥抗癫痫作用。突触囊泡蛋白2A是新型抗癫痫药物左乙拉西坦、布瓦西坦和seletracetam的作用靶点。

Recurrent seizures lead to abnormal expression of synaptic proteins, reorganization of synapse and formation of abnormal neuron network. Recently, it is identified that the synaptic proteins are involved in epileptogenesis. The abnormal expression of several synaptic regulatory proteins and postsynaptic membrane receptor proteins may result in epilepsy, The ion channels usually are the action target of most antiepileptic drugs. However, carbamazepine and zonisamide may interact with syntaxin and/or soluble N-ethylmaleimide-sensitive factor attachment protein receptor complex to exert its function of anti-epilepsy. The synaptic vesicle protein 2A is the action target for new anti-epileptic drugs, including levetiracetam, brivaracetam and seletracetam.