Glutamate and epilepsy
Glutamate and epilepsy
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DOI：
10.1093/jn/130.4.1043s
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发表时间：
2000-04-01
影响因子：
4.2
通讯作者：
Chapman, AG
中科院分区：
文献类型：
--
作者：
Chapman, AG
癫痫综合征有非常不同的主要原因，这可能是遗传，发育或获得。在啮齿动物模型中，通过敲除或敲低程序改变谷氨酸受体或谷氨酸转运蛋白表达可以诱导或抑制癫痫发作。不管主要原因是什么，作用于离子型和代谢型受体的突触释放的谷氨酸似乎在癫痫发作活动的启动和扩散中起主要作用。在获得性癫痫的啮齿动物模型和人类颞叶癫痫中，有证据表明离子型N-甲基-D-天冬氨酸（NMDA）和代谢型（I组）受体的功能功效增强。在癫痫动物模型中，作用于NMDA受体或I组代谢型受体的拮抗剂具有强效抗惊厥作用。
Epileptic syndromes have very diverse primary causes, which may be genetic, developmental or acquired. In rodent models, altering glutamate receptor or glutamate transporter expression by knockout or knockdown procedures can induce or suppress epileptic seizures. Regardless of the primary cause, synaptically released glutamate acting on ionotropic and metabotropic receptors appears to play a major role in the initiation and spread of seizure activity. In rodent models of acquired epilepsy and in human temporal lobe epilepsy, there is evidence for enhanced functional efficacy of ionotropic N-methyl-D-aspartate (NMDA) and metabotropic (Group I) receptors. In animal models of epilepsy, antagonists acting at NMDA receptors or at Group I metabotropic receptors have potent anticonvulsant actions.