Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1
Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1
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DOI：
10.1126/science.276.5319.1699
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发表时间：
1997-06-13
期刊：
影响因子：
56.9
通讯作者：
Wada, K
中科院分区：
文献类型：
--
作者：
Tanaka, K;Watase, K;Wada, K
神经系统中兴奋性神经递质谷氨酸的细胞外水平由主动从细胞外空间去除谷氨酸的转运蛋白维持。GLT-1（一种广泛分布的星形胶质细胞谷氨酸转运蛋白）缺陷的纯合子小鼠表现出致命的自发性癫痫发作和对急性皮质损伤的易感性增加。这些效应可归因于这些小鼠脑中残留谷氨酸水平升高。
Extracellular levels of the excitatory neurotransmitter glutamate in the nervous system are maintained by transporters that actively remove glutamate from the extracellular space. Homozygous mice deficient in GLT-1, a widely distributed astrocytic glutamate transporter, show lethal spontaneous seizures and increased susceptibility to acute cortical injury. These effects can be attributed to elevated levels of residual glutamate in the brains of these mice.