Anderson K J, Nellgård B, Wieloch T
Department of Physiological Sciences, University of Florida, Gainesville 32610-0144.
Brain Res. 1993 Sep 17;622(1-2):93-8. doi: 10.1016/0006-8993(93)90806-x.
The response of excitatory amino acid transporter binding sites in the rat brain to 10 min of cerebral ischemia induced by bilateral common carotid occlusion combined with hypotension was examined. We observed a transient increase in the density of transporter binding sites that was first noticeable at 5 min post-recovery and persisted for 48 h. The increase in binding sites was found throughout the brain, but was most prevalent in hippocampus and other cortical regions. We conclude that delayed neuronal death following transient cerebral ischemia may not be due to a decrease in the number of excitatory amino acid transport sites.
研究了大鼠大脑中兴奋性氨基酸转运体结合位点对双侧颈总动脉闭塞合并低血压诱导的10分钟脑缺血的反应。我们观察到转运体结合位点密度出现短暂增加，在恢复后5分钟时首次明显，持续48小时。结合位点增加在全脑均有发现，但在海马体和其他皮质区域最为普遍。我们得出结论，短暂性脑缺血后延迟性神经元死亡可能并非由于兴奋性氨基酸转运位点数量减少所致。
