摘要
目的观察创伤后应激障碍(PTSD)样行为异常大鼠杏仁核神经元CaM依赖性蛋白激酶IIα(CaMKIIα)及磷酸化CaM依赖性蛋白激酶IIα(pCaMKIIα)表达变化。方法采用国际认定的SPS方法刺激建立大鼠PTSD模型,取成年健康雄性Wistar大鼠75只,随机分为SPS模型的12h、1d、4d、7d组及正常对照组,采用免疫组织化学、免疫印迹法检测大鼠杏仁核CaMKIIα及pCaMKIIα的表达变化。结果SPS刺激后大鼠杏仁核神经元细胞内CaMKIIα于12h开始减少,1d表达最少,4d开始逐渐增多,至7d时基本恢复正常;pCaMKIIα的表达则于SPS12h开始增多,1d时表达最多,4d时开始减少,至7d时基本恢复正常。CaMKIIα阳性细胞在SPS各组模型均出现,1d表达最少。结论杏仁核CaMKIIα及pCaMKIIα的表达变化,可能是PTSD大鼠情感行为异常的重要病理生理基础之一。
Objective To observe the changes of CaMKII α and pCaMKII α expression in the amygdala neurons of posttraumatic stress disorder（PTSD） rats to explore the pathogensis of PTSD. Methods The SPS-method was used to set up the rat PTSD models. A total of 75 male Wistar rats were randomly divided into12h, 1d, 4d, 7d groups of single prolonged stress（SPS） and normal control group. The expression of CaMKIIα and pCaMKIIα as detected using immunohistochemistry and western blotting. Results The expression of CaMKII α in the amygdala of rats was decreased 12h after SPS stimulation, and reached the lowest at ld after SPS, began to recover 4 days and to normal 7 days. However, the expression of pCaMKII α was increased 12h after SPS stimulation, and peaked at ld after SPS, and began to decrease 4 days and to normal level after SPS stimulation. The CaMKII α positive cells were detected in each SPS models and reached the lowest at ld after SPS. Conclusion The changes of expression of CaMKII α and pCaMKII α in the amygdala of PTSD rats may be related to the pathogenesis of PTSD.
出处
《解剖科学进展》
CAS
2009年第4期396-399,共4页
Progress of Anatomical Sciences
基金
国家自然科学基金资助项目(NO.30600341)
