红藻氨酸诱导慢性颞叶癫痫鼠脑海马胶质细胞增生和突触重建的研究

目的 探讨红藻氨酸诱导的慢性颞叶癫痫鼠脑海马突触重建及胶质增生与颞叶癫痫发病机制的关系。方法 采用Neo-Timm银染观察苔藓纤维出芽及突触重建；免疫组织化学染色观察质原纤维酸性蛋白（GFAP）和神经细胞粘附分子（NCAM）表达水平。结果 鼠脑海马注入红藻氨酸后，双侧海马区均出现神经元脱失、突触重建及胶质细胞增生，注射侧以CA3区、门区明显，CA1区受累较轻；对侧CA1区、门区明显，CA3区相对较轻，其程度随存活时间延长而加重。结论 鼠脑海马内注射红藻氨酸引起的神经元脱失、反应性胶质细胞增生和神经元可塑性改变，可能与形成异常神经元放电环路，最终诱发癫痫发作有关。

Experimental study of gliosis and synaptic reorganization in the hippocampus of chronic temporal lobe epilepsy rats induced by kainic acid

Objective To investigate the relationship between gliosis, synaptic reorganization and the mechanism of chronic temporal lobe epilepsy induced by kainic acid. Methods The mossy fibers sprouting, synaptic reorganization and gliosis were observed by Neo-Timm staining and immunohistochemical staining respectively. Results The injected (ipslateral) side was injured predominantly in the CA 3 subfield and hilus, whereas the CA 1 subfield was injured mildlyThe contralateral side showed pathological changes mainly in the CA 1 subfield and hilus, and moderately in the CA 3 subfieldThe longer the rats survived, the more obvious changes were observed in the hippocampuses. Conclusion The injection of kainic acid in hippocampus can cause neuronal loss, reactive gliosis and plasticity of neurons, probably form the abnormal neuronal discharge circuit, finally induce the seizures