Transient focal cerebral ischemia down-regulates glutamate transporters GLT-1 and EAAC1 expression in rat brain

被引：0

作者：

Rao, VLR

Bowen, KK

Dempsey, RJ

机构：

[1] Univ Wisconsin, Dept Neurol Surg, Madison, WI 53792 USA

[2] Univ Wisconsin, Cardiovasc Res Ctr, Madison, WI USA

[3] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA

来源：

NEUROCHEMICAL RESEARCH | 2001年 / 26卷 / 05期

关键词：

EAAC1; focal cerebral ischemia; gene expressions; GLT-1; glutamate transporters; stroke;

D O I：

暂无

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Transient focal cerebral ischemia leads to extensive excitotoxic neuronal damage in rat cerebral cortex. Efficient reuptake of the released glutamate is essential for preventing glutamate receptor over-stimulation and neuronal death. Present study evaluated the expression of the glial (GLT-1 and GLAST) and neuronal (EAAC1) subtypes of glutamate transporters after transient middle cerebral artery occlusion (MCAO) induced focal cerebral ischemia in rats. Between 24h to 72h of reperfusion after transient MCAO, GLT-1 and EAAC1 protein levels decreased significantly (by 36% to 56%, p < 0.05) in the ipsilateral cortex compared with the contralateral cortex or sham control. GLT-1 and EAAC1 mRNA expression also decreased in the ipsilateral cortex of ischemic rats at both 24h and 72h of reperfusion, compared with the contralateral cortex or sham control. Glutamate transporter down-regulation may disrupt the normal clearance of the synaptically-released glutamate and may contribute to the ischemic neuronal death.

引用

页码：497 / 502

页数：6