摘要
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。
The influence of somatostatin(SOM),enkephalin(ENK)and proenkephalin (PENK) mRNA in hippocampus to seizure episodes induced by pretreatment of kainic acid(KA)were investigatcd by immunohistochemistry (ICC) and in situ hybridization (In Situ).ICC revealed a great loss of SOM interneurons in the hilus,while a great increase of ENK in hippocampal mossy fibers was also seen in the same area.During the period of induction of enhanced seizurc susceptibility,some ENK neurons were found in hippocampus.In situ hybridization demonstrated an elevation of PENK mRNA in hippocampal dentate gyrus granule cells(DGCs) and the expression of PENK mRNA reached the peak on the first day.These results suggest that the net effect is a shift of the balance between excitation and inhibition in hippocampus ,which maybe relates to induction of enhanced seizure susceptibility.
出处
《大连医科大学学报》
CAS
2000年第4期245-248,共4页
Journal of Dalian Medical University