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Ca_V1.2和钙调蛋白在自发性遗传性癫痫大鼠小脑中的异常表达
引用本文:马丽华,吕昕瞳,刘雅静,徐晓雪,闵冬雨,程晓茜,杨春宇,蔡际群,郭凤.Ca_V1.2和钙调蛋白在自发性遗传性癫痫大鼠小脑中的异常表达[J].解剖科学进展,2013,19(1):27-31.
作者姓名:马丽华  吕昕瞳  刘雅静  徐晓雪  闵冬雨  程晓茜  杨春宇  蔡际群  郭凤
作者单位:中国医科大学药学院药物毒理学教研室,辽宁沈阳,110001
基金项目:国家自然科学基金资助项目,辽宁省教育厅资助项目
摘    要:目的研究自发性遗传性癫痫大鼠(Tremor,TRM)小脑组织中CaV1.2与钙调蛋白(Calmodulin,CaM)蛋白表达与共定位情况。方法应用Westernblot技术检测CaV1.2与CaM蛋白表达,应用免疫荧光技术定位CaV1.2与CaM蛋白的分布,应用激光共聚焦显微镜检测Ca2+]。结果 TRM大鼠小脑内CaV1.2的蛋白表达低于正常iWistar大鼠(P<0.05),而CaM的蛋白表达高于正常Wistar大鼠(P<0.05);荧光定位显示CaV1.2与CaM共定位的阳性细胞比率较之正常组表达降低(P<0.01)。与正常的Wistar大鼠相比,急性分离的TRM大鼠小脑神经元中Ca2+]明显增强。结论 TRM大鼠小脑内CaV1.2和CaM蛋白表达异常可能是癫痫的发病机制之一。

关 键 词:钙调蛋白  遗传性癫痫  电压门控性钙通道  小脑  大鼠

Abnormal expressions of Cav1.2 and calmodulin in the cerebellum of genetic epileptic rats
MA Li-hua , LV Xin-tong , LIU Ya-jing , XU Xiao-xue , MIN Dong-yu , CHENG Xiao-xi , YANG Chun-yu , CAI Ji-qun , GUO Feng.Abnormal expressions of Cav1.2 and calmodulin in the cerebellum of genetic epileptic rats[J].Progress of Anatomical Sciences,2013,19(1):27-31.
Authors:MA Li-hua  LV Xin-tong  LIU Ya-jing  XU Xiao-xue  MIN Dong-yu  CHENG Xiao-xi  YANG Chun-yu  CAI Ji-qun  GUO Feng
Institution:(Department of Pharmaceutical Toxicology, School of Pharmaceutical Sciences, China Medical University, Shenyang 110001, China)
Abstract:Objective To investigate the expressions and distribution of CaV1.2 and calmodulin(CaM) proteins in cerebellum of Tremor rats(TRM). Methods The expressions of CaV1.2 and CaM proteins were detected by Western blot and the proteins distributions were detected by immunofluorescence, the concentration of Ca2+]i was measured in cerebellum by confocal laser scanning microscope. Results The expression level of CaV1.2 protein in cerebellum was significantly reduced ( P<0.05), but the expression level of CaM protein was significantly increased in TRM rats than in the normal control rats( P<0.05). In addition, the percentage of CaM and CaV1.2 double labled positive cells in Tremor rats cerebellum were decreased compared with the control group (P<0.01). Furthermore, intracellular calcium concentrations were increased in TRM rats than in the normal control rats (P< 0.01). Conclusion The abnormal expressions of CaV1.2 and CaM in TRM cerebellum may be related to the mechanism of TRM, which is likely to provide the potential therapeutic targets for genetic epilepsy.
Keywords:calmodulin  genetic epilepsy  voltage-gated calcium channels  cerebellum  rat
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