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用惊厥剂量 ( 10mg/kg)的红藻氨酸 (Kainicacid ,KA)诱发SD大鼠出现癫痫发作后 ,观察癫痫发作对海马结构内、海马门部位含生长抑素 (SOM)的抑制性中间神经元以及海马齿状回颗粒细胞 (DGCs)部位的脑啡肽及脑啡肽原mRNA表达的影响。免疫组化结果显示 ,在癫痫发作敏感性形成期 (KA后 5～ 7d)出现前 ,海马门区含SOM抑制性中间神经元进行性脱失 ,而海马苔状纤维 (MF)部位的具有兴奋和致癫痫作用的ENK免疫反应阳性纤维明显增多 ;KA后 2d在海马的DGCs部位开始出现脑啡肽免疫反应阳性神经元。原位杂交技术显示 ,KA后海马DGCs部位脑啡肽原mRNA亦明显增加 ,其峰值出现在KA后 1d (P <0 0 1)。结果提示KA后海马结构内兴奋和抑制过程失衡 ,这很可能与KA后癫痫发作敏感性增强的形成有关。
Epileptic seizures were induced in seizures induced by seizures (Kainicacid, KA) at a dose of 10 mg / kg in seizures, and the inhibitory effects of seizures on the inhibitory mesocortensis of somatostatin (SOM) in the hippocampus And enkephalin and enkephalin mRNA expression in the hippocampal dentate gyrus granulosa cells (DGCs). Immunohistochemical results showed that, before the onset of seizure susceptibility (5-7 days after KA), the SOM-containing inhibitory interneurons gradually degenerated while the hippocampal moss-like fibers (MF) were excited And induced epilepsy ENK immunoreactive fibers increased significantly; 2d after KA in hippocampus DGCs began enkephalin-immunoreactive neurons. In situ hybridization showed that the level of enkephalin mRNA in hippocampal DGCs was also significantly increased after KA, with peak at 1 day after KA (P <0.01). The results suggest that there is an imbalance between the excitatory and inhibitory processes in the hippocampal formation after KA, which is probably related to the increased sensitivity of post-KA seizures.