Objective To study the effects of mild hypothermia on cognitive function , synapsinⅠexpression and synaptic ultrastructure of hippocampus in epileptic rats induced by global cerebral ischemia. Methods Forty-eight male SD rats were randomly divided into control (NC) group, sham-operated (Sham) group, normothermic epilepsy (NT) group and mild hypothermic epilepsy (HT) group. The model of postischemic audio-genetic seizure was established by chest compression. Hypothermia intervention was given to HT group. Immunocytochemistry was conducted to detect the expressions of synapsin I in hippocampus at days 1 , 3, 14. the synaptic ultrastructure and cognitive function were respectively observed by electron microscope and Morris water maze. Results Compared with NC and Sham group, the expression of synapsinI in NT group was decreased, the escape latency was prolonged and across platform number decreased (P < 0.05). The synapses were decreased in number, and mitochondria was viewed swelling, synaptic membranes unclear, myelin fractured. Compared with NT group, the expression of synapsinⅠin HT group had no obvious change in 24 h but was significantly increased in days 3 and 14 (P < 0.01); The escape latency was decreased and the number of cross platform increased (P < 0.01); Synaptic structure was clear, with interface growing and postsynaptic density thickened. Conclusion Mild hypothermia may improve the cognitive function of the epileptic rats induced by global cerebral ischemia by upregulating the expression of synapsinⅠand alleviating the damage of synaptic structure.%目的:探讨亚低温对全脑缺血性癫痫大鼠认知功能和海马synapsinⅠ表达及突触超微结构的影响.方法:48只SD大鼠随机分为对照组(NC)、假手术组(Sham)、常温癫痫组(NT)和亚低温癫痫组(HT). 采用胸部挤压法建立全脑缺血声源性癫痫模型,HT组在NT组的基础上给予亚低温干预.免疫组化观察癫痫后24 h、3 d和14 d海马synapsinⅠ的表达,分别用Morris水迷宫实验和电镜观察大鼠的认知功能和突触超微结构. 结果:与NC和Sham组比较,NT组大鼠的synapsinⅠ表达降低,逃避潜伏期延长,穿过平台数减少(P<0.05);突触减少,线粒体肿胀,前后膜不清,髓鞘断裂. 与NT组比较,HT组synapsinⅠ表达在24 h无差异,3 d和14 d增加(P<0.01),逃避潜伏期降低、穿过平台数增加(P<0.01);突触结构转清,界面增长,突触后致密物质增厚.结论:亚低温可上调synapsinⅠ表达并减轻突触结构损伤,改善全脑缺血性癫痫大鼠的认知功能.
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