大鼠杏仁核电刺激癫痫模型海马JNK的磷酸化改变
Change of JNK phosphorylation in the hippocampus of amygdala-kindled rats
目的 研究大鼠杏仁核电点燃癫痫模型海马中JNK的磷酸化改变,探讨JNK磷酸化与癫痫发生发展的关系.方法 建立大鼠杏仁核电点燃癫痫模型.设立空白对照组、手术对照组、点燃组,癫痫点燃成功后取脑,分别采用Western blot和免疫荧光方法 检测海马中JNK的表达变化,采用TUNEL染色和GFAP免疫组化染色观察海马形态学改变.结果 36只大鼠在12-20 d成功点燃.Western blot显示点燃组磷酸化JNK水平较手术对照组和空白对照组高(P<0.05).形态学检测显示点燃组海马区神经元缺失及神经胶质细胞增生(P<0.05).结论 电刺激诱发大鼠癫痫发作后,海马组织JNK磷酸化水平升高,该信号通路的激活可能参与颞叶内侧癫痫海马硬化的发生过程.
更多Objective To investigate the change of phosphorylation of JNK in the hippocampus of epilepsy rats kindled by chronic electrical stimulation in the basolateral nucleus of the amygdala. Method Eighty male Wistar rats were randomly divided into 3 groups:15 in blank control group,15 in sharn group and 50 in kindling group.The amygdala of the rats in the kindling group was stimulated with constant pulse current. Rats'seizures and electroencephalogram were recorded throughout the stimulation process.JNK phosphorylation level in the rat hippocampus was detected by Western blot. TUNEL staining and immunohistochemical staining of GFAP were performed to evaluate the neuronal death and gliosis in the hippocampus. Results Thirty-six rats were kindled successfully 12 to 20 days after the kindling began.The level of JNK phosphorylafion in the hippocmnpns was significantly higher in kindled rats(2.39±0.14)than those in other two groups(1.13±0.06 in the sham group,1.11±0.77in control group)(P<0.05).There was no significant difference in JNK phosphorylation between the sham group and the control group(P>0.05).Expression of GFAP in the hippocampus of kindled rats was significantly stronger than those in the blank control group and in the sham group(P<0.05).TUNEL staining positive cells in the hippocampus of kindled rats were significantly more than those in the blank control group and in the sham group(P<0.05).Conclusions The level of JNK phosphorylation in the hippocampns increases in the amygdala kindled rats.JNK signal transductiou pathway may be involved in the process of hippocampal sclerosis in the mesial temporal lobe epilepsy.
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