Araki T, Kato H, Liu X H, Itoyama Y, Kogure K, Kato K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Neurosci Lett. 1994 Jul 18;176(1):17-20. doi: 10.1016/0304-3940(94)90860-5.
Immunohistochemical changes of striatal interneurons in the gerbil were investigated 1 h-7 days after 10 min cerebral ischemia. Marked reduction of parvalbumin-immunoreactive interneurons was seen in the striatum from 24 h after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity markedly decreased in striatal neurons 5 h after ischemia but was unaffected in interneurons. Thereafter, a severe loss of MAP2 immunoreactivity in the interneurons was found 48 h and 7 days after ischemia. The results demonstrate that transient cerebral ischemia can cause a loss of parvalbumin and MAP2 immunoreactivity in interneurons in the dorsolateral striatum in a delayed fashion as compared with a rapid loss of striatal neurons.
在沙土鼠大脑缺血10分钟后1小时至7天，对其纹状体中间神经元的免疫组化变化进行了研究。缺血24小时后，纹状体中可见小白蛋白免疫反应性中间神经元显著减少。微管相关蛋白2（MAP2）免疫反应性在缺血5小时后在纹状体神经元中显著降低，但在中间神经元中未受影响。此后，在缺血48小时和7天后发现中间神经元中MAP2免疫反应性严重丧失。结果表明，与纹状体神经元的快速丧失相比，短暂性脑缺血可导致背外侧纹状体中间神经元中小白蛋白和MAP2免疫反应性的延迟丧失。
