摘要
目的 探讨短暂脑缺血再灌流后突触传递功能的改变和神经系统的可塑性。方法 采用线栓法建立大鼠大脑中动脉闭塞 (MCAO)模型 ,应用免疫组织化学的方法于缺血 10min后再灌流 1h、3h、6h、12h、2 4h和 72h分别观察尾壳核区 (caudateputamen ,CPU)及额顶叶皮质区 (frontparietalcortex,FPC)突触蛋白I(synapsinI)及磷酸化突触蛋白I(P synapsinI)表达的动态变化。结果 缺血 10min后再灌流 12h内CPU区和FPC区synapsinI的表达无明显变化 ,再灌流 2 4h后降低 ,至 72h恢复至对照组水平。而缺血 10min再灌流后synapsinI的磷酸化一直处于低下水平。结论 短暂脑缺血再灌流后存在失神经及其后的神经再获现象 ,同时还存在着突触传递阻断的现象。
Objective To investigate the synaptic transmission function and neural plasticity after transient ischemia followed by repufusion. Methods Rats were subjected to 10 minutes of middle cerebral artery occlusion (MCAO). At the time point of 1, 3, 6, 12,24 and 72 hours after reperfusion,expression of synapsin I and phosphosynapsin I in the area of caudate putamen and frontparietal cortex was observed by immunohistochemistry. Results No obvious changes in synapsin I immunoreactivity were detected within 12 hours of reperfusion. At the time point of 24 hours after reperfusion,a considerable reduction in synapsin I immunoreactivity of the two areas was observed (t=6.59 and 7.28,P< 0.01). After that the synapsin I immunoreactivity recovered to control level at the 72nd hour after reperfusion. However,the phosphorylation of synapsin I had been remaining low during the whole reperfusion process(t=3.27～9.86,P< 0.05). Conclusion It seems that denervation and following reinervation occur after transient ischemia followed by reperfusion. In addition,the synaptic transmission may be blocked,which is likely to be responsible for the cerebral stunning phenomenon after transient ischemia.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2004年第3期196-198,共3页
Journal of Apoplexy and Nervous Diseases
基金
国家自然科学基金面上项目 ( 3 0 0 70 82 5 )
