摘要
目的通过研究海人酸致痫大鼠海马NMDAR2B及ERK1/2蛋白表达的变化,为进一步探明癫痫脑损伤的机制奠定基础。方法采用在立体定位仪下,将海人酸注射至大鼠杏仁核的方法制备癫痫模型。将大鼠随机分为正常对照组,假手术组及致痫组,分别于不同时间取材,应用免疫组化的方法观察脑组织NMDAR2B蛋白及ERK1/2蛋白表达的变化。结果正常海马各区均有极少量的NMDAR2B阳性细胞分布,海人酸致痫组后2h大鼠海马各区NMDAR2B表达迅速增加,6h达高峰,并持续至至癫痫后24h(P<0.01),ERK1/2蛋白致痫后半小时表达开始增高,3h达高峰,后开始下降,6h后恢复到致<痫前的水平(P<0.01)。结论NMDAR2B参与了癫痫发生和癫痫脑的长时程的兴奋过程,ERK1/2短时程参与了癫痫的发生过程。
Objective To observe the protein expression＇of NMDAR2B and ERK1/2 in hippocampus of epilepsy rats. Methods Epilepsy rat models were made by injecting kainic acid into amygdale under stereotactic instrument. 70 male Wistar rats were divided randomly into 7 groups：（ 1 ） the control group;（2）the pseudo operation group;（3 - 7） epilepsy group,the protein expression of NMDAR2B and ERK1/2 in the rat brain was tested with the method of immunohisto- chemistry. Results In the 1,2 group, NMDAR2B and ERK1/2 positive cells distributed rarely in hippocampus, the protein expression of NMDAR2B increased until 24h after kindling and the protein expression of ERK1/2 increased 3h, then returned to normal level. Conclusion NMDAR2 B and ERK1/2 are involved in the process of temporal epilepsy and the brain injury.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2008年第2期149-151,共3页
Journal of Apoplexy and Nervous Diseases
基金
2007年吉林省科技厅科研基金(No.200705159)
