脑缺血选择性海马CA1区神经元损害的实验研究

采用Ｐｕｌｓｉｎｅｌｉ－Ｂｒｉｅｒｌｅｙ４血管阻塞脑缺血模型观察了大鼠全脑缺血２０ｍｉｎ再灌流８ｈ，ｃ－ｆｏｓ基因表达及再灌流７ｄ海马ＣＡ１区迟发性神经元损害。在缺血再灌流早期（８ｈ）海马ＣＡ１区极少ｃ－ｆｏｓ表达，而齿状回、海马ＣＡ３区、杏仁核大量ｃ－ｆｏｓ表达。缺血再灌流晚期（７ｄ）镀银染色显示海马ＣＡ１区神经元及其突触终末带呈黑色溃变相，而齿状回、海马ＣＡ３区、杏仁核呈金黄色正常相。相邻切片ＨＥ染色示缺血组海马ＣＡ１区核完整的锥体细胞数（５±２．６个／２００μｍ）与对照组（４０±２．９个／μｍ）比较差异有显著意义（Ｐ＜０．０１）。脑缺血诱导的ｃ－ｆｏｓ基因表达对于缺血易损海马ＣＡ１区迟发性神经元坏死可能起直接的调控作用。

The neuronal damage in the CA 1 region of hippocampus after cerebral ischemia

The four vessal occulsion model as described previously by Pulsinelli Brierley was used. C fos protein induction in the early(8 hours) and delayed neuronal death in the CA 1 region of hippocampus in the late(7 days) were observed after being ischemia for 20 min and reperfused. C fos protein induction largely confined to the dentate gyrus, CA 3 region of hippocampus and amygdaloid nucleus 8 hours after ischemia and reperfusion. Little C fos protein like immunoreativity was seen in the CA 1 field. The silver impregnation of Gallyas et al results showed that neurons and their neuropil of the CA 1 region of hippocampus appeared to be dark gray or black which was degenerative staining 7 days after ischemia and reperfusion. But the dentate gyrus,CA 3 region of hippocampus and amygdaloid nucleus showed normal light yellow brown staining.The next slide in the silver impregnation procedure stained by the Hematoxylin Eosin showed that the CA 1 region of hippocampus had significant quantitative pyramidal cell loss(P<0.01). In conclusion,C fos activation after cerebral ischemia may have regulated the delayed neuronal death in the CA 1 region of hippocampus.