Effects of mild hypothermia on cognitive function and synapsin iexpression , synaptic ultrastructure of hippocampus in epileptic rats induced by global cerebral ischemia
10.3969/j.issn.1006-5725.2015.14.007
- VernacularTitle: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
- Author:
Guoshuai YANG
;
Xiaoyan ZHOU
;
Zhiping ZHOU
;
Xuefang AN
;
Dan YU
- Publication Type:Journal Article
- Keywords:
Epilepsy;
Mild hypothermia;
Cognitive function;
SynapsinⅠ;
Synaptic ultrastructure
- From:
The Journal of Practical Medicine
2015;31(14):2261-2264
- CountryChina
- Language:Chinese
-
Abstract:
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.
