Rao V L, Bowen K K, Dempsey R J
Department of Neurological Surgery, Cardiovascular Research Center, University of Wisconsin-Madison, 53792, USA.
Neurochem Res. 2001 May;26(5):497-502. doi: 10.1023/a:1010956711295.
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.
短暂性局灶性脑缺血会导致大鼠大脑皮层广泛的兴奋性毒性神经元损伤。有效重新摄取释放的谷氨酸对于防止谷氨酸受体过度刺激和神经元死亡至关重要。本研究评估了短暂性大脑中动脉闭塞（MCAO）诱导大鼠局灶性脑缺血后，谷氨酸转运体的胶质细胞亚型（GLT-1和GLAST）和神经元亚型（EAAC1）的表达。在短暂性MCAO后的再灌注24小时至72小时之间，与对侧皮层或假手术对照组相比，同侧皮层中GLT-1和EAAC1蛋白水平显著降低（降低36%至56%，p<0.05）。与对侧皮层或假手术对照组相比，在再灌注24小时和72小时时，缺血大鼠同侧皮层中GLT-1和EAAC1 mRNA表达也降低。谷氨酸转运体下调可能会破坏突触释放谷氨酸的正常清除，并可能导致缺血性神经元死亡。
