NMDA受体在癫痫发病机制中的作用  

NMDA receptor in the pathogenesis of epilepsy

作　　者：彭毓棻[1] 宋治[1] 

机构地区：[1]中南大学湘雅三医院神经内科,湖南长沙410013

出　　处：《中国病理生理杂志》2011年第6期1230-1233,1239,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30971534)

摘　　要：癫痫是慢性反复发作短暂脑功能失调综合征,是神经科常见疾病之一。目前有关癫痫的发病机制尚未阐明。研究表明,癫痫的发生与兴奋性神经递质和抑制性神经递质的失衡有关[1]。Epilepsy is a chronic recurrent transient brain dysfunction syndrome.Seizure is correlated with the enhancement of glutamate responses mediated by N-methyl-D-aspartate（NMDA） receptor.NMDA receptor-mediated signal transduction is critical for synaptic plasticity,learning and memory.When epilepsy occurs,the NMDA receptors are up-regulated and the corresponding ion channels are kept open so that the neurons discharge continuously.At the same time,increased intracellular calcium causes the disorder of calcium homeostasis,resulting in neuron death.Postsynaptic density protein-95（PSD-95）,localized to NMDA receptor,may be involved in the pathophysiological process of seizure.As a selective NMDA receptor antagonist,the NR2B subunit selective antagonist has broad clinical application prospects in acute and chronic seizures.

关 键 词：受体 N-甲基-D-天冬氨酸 癫痫 

分 类 号：R363[医药卫生—病理学]