大鼠脑缺血对癫痫敏感性和脑内胶质原纤维酸性蛋白免疫反应的影响

本实验采用改良栓线法制备大鼠右侧大脑中动脉 (Middlecerebralartery ,MCA)缺血再灌注模型 ,腹腔注射阈下剂量 (35mg/kg·2d)戊四唑 (pentylenetetrazol,PTZ)制备慢性癫痫点燃模型。通过观察大鼠的行为 ,来检测其癫痫敏感性的改变。分别用硫堇染色、免疫细胞化学方法观察PTZ点燃脑缺血大鼠的相应脑区的神经病理学改变及脑内胶质原纤维酸性蛋白 (gliafibrillaryacidicprotein ,GFAP)免疫反应活性 (immunoreactivity,IR)的变化。结果显示 :脑缺血后大鼠癫痫敏感性明显增强 (P <0 0 5 )。右背侧海马CA1、CA3 区锥体细胞、额叶皮质神经元不同程度的脱失 (P <0 0 5 )并出现大量GFAP免疫反应阳性的星形胶质细胞 ,且细胞体积变大 ,突起变长变粗 ,免疫染色强度明显增强 (P <0 0 5 ) ,提示脑缺血大鼠癫痫敏感性增强 ,可能与海马及额叶皮质的神经元脱失及星形胶质细胞活化增生有关。

Effects of cerebral ischemia on the susceptibility to seizure and immunoreacitivity of GFAP in rats

The rat model was established by a modified intraluminal thread method of occlusion and reperfusion in right middle cerebral artery and followed by chronically induced seizure with sub dosage of Pentylenetetrazol(PTZ, 35mg/kg,i.p.). Behaviors were recorded in rat model to evaluate the changes in susceptibility to seizure, then the changes in neuropathology and immunoreactivity of GFAP in sub regions of rat brain were studied by Thionine staining and immunocytochemistry. The results demonstrated that, loss of pyramidal cells of CA 1 and CA 3 occurred on right side of dorsal hippocampus as well as neurons in frontal cortex( P <0.05). Meanwhile, GFAP immunoreacitive astrocytes showed bigger cell bodies, thicker and deeper protrusions and deeper staining( P <0.05). It was suggested that the enhancement in susceptibility to seizure in rats with cerebral ischemia was closely related to the sclerosis of hippocampus, loss of neurons in frontal cortex and proliferation of astrocytes.