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目的观察大鼠癫发作后海马区囊泡锚定蛋白Ⅰ(synapsinⅠ)的表达和突触超微结构的变化,探讨突触功能、形态可塑性与癫的关系。方法用锂匹罗卡品制作癫疒间大鼠模型,应用免疫组化法观察致疒间后急性期、静止期和慢性期synapsinⅠ在海马的表达;应用电镜和图像处理软件观察海马突触超微结构。结果癫疒间组大鼠海马区synapsinⅠ的表达于致疒间后3h减弱;6h和12h达高峰,与对照组比较差异有显著性(P<0.05～0.01);24h恢复正常并持续到60d。致疒间后3h突触后致密物质厚度(PSD)和突触数密度(Nv)无显著改变;6hPSD增高,Nv降低;7d、30dPSD恢复正常,Nv增高。结论synapsinⅠ的高表达和PSD的增高可能与急性期癫疒间持续状态的维持有关;synapsinⅠ的正常表达和PSD的正常可能是静止期内癫疒间不发作的原因之一;慢性期Nv的增加是自发性发作出现的物质基础。
Objective To observe the changes of synapsin Ⅰ and synapse ultrastructure in the hippocampus after epileptic seizure in rats and to explore the relationship between synaptic function, morphological plasticity and epilepsy. Methods Epilepsy model rats were made by lithium pilocarpine. The expression of synapsin Ⅰ in acute, quiescent and chronic phases of the pterygium was observed by immunohistochemistry. The ultrastructure of hippocampal synaptic ultrastructure was observed by electron microscope and image processing software microstructure. Results The expression of synapsin Ⅰ in hippocampus of rats in epileptic group decreased 3 h after rehmannia, reached the peak at 6 h and 12 h, and the difference was significant compared with that in control group (P <0.05-0.01). There was no significant change of PSD and Nv after 3h. The PSD of 6hPSD increased and Nv decreased. On the 7d, 30d, PSD returned to normal and Nv increased. Conclusions The high expression of synapsin Ⅰ and the increase of PSD may be related to the maintenance of persistent status in acute epilepsy. The normal expressions of synapsin Ⅰ and normal PSD may be one of the reasons for the non-seizures of epilepsy in quiescent period. The increase of chronic Nv Is the material basis for spontaneous seizures.