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作 者:宗志红[1] 陈井阳[1] 孟晓娜[1] 王彪[1] 时利德[2] 邢伟[1]
机构地区:[1]中国医科大学基础医学院生物化学与分子生物学教研室,辽宁沈阳110001 [2]中国医科大学生理学教研室
出 处:《中国医科大学学报》2007年第6期636-637,共2页Journal of China Medical University
基 金:国家自然科学基金资助项目(30371229)
摘 要:目的:探讨慢性铝暴露对海马CA1区长时程增强(LTP)及钙调素依赖性蛋白激酶Ⅱ(α-CaMKⅡ)活性的影响。方法:选择断乳后Wistar大鼠,分别以含有0.2%、0.4%、0.6%(W/V)的氯化铝(AlCl3)蒸馏水饲养。3个月后,测定脑铝、血铝的含量;用电极刺激海马的CA1区,记录单脉冲刺激引起的峰电位(PS),观察高频刺激前后各组的变化;用Westernblot方法,检测α-CaMKⅡ活性。结果:高频刺激后,铝暴露组PS幅值明显低于对照组(P<0.01);铝暴露组α-CaMKⅡ的活性和对照组相比明显降低(P<0.01)。结论:慢性铝暴露抑制大鼠CA1区LTP的形成,这种抑制可能与其抑制α-CaMKⅡ的活性有关。Objective:To investigate the effect of chronic aluminum exposure on Long term potentiation(LTP) in area CA1 and α-Ca2+/calmodulin-dependent protein kinase II(α-CaM KⅡ) activity in vivo.Methods:A stimulus bipolar electrode was placed in the CA3 area,with extra cellar microelectrode recording the population spike(PS) in CA1,and we observed the changes of PS amplitude before and after the high frequency stimulation(HFS) of lower,mid and higher level aluminum exposure groups and the control group,respectively.The α-CaMKⅡ activity was determined with Western blot by using phosphorylated antibody.Results:PS amplitude after HFS of the aluminum treated groups are significantly lower than that of control group(P 〈 0.01).The activity of CaMKⅡ in the aluminum-exposed groups is significantly lower than that in the control group(P 〈 0.01).Conclusion:Chronic aluminum exposure can inhibit the formation of LTP in vivo,and the decreased α-CaMKⅡ activity may play important role in this inhibition.
关 键 词:铝 钙调素依赖性蛋白激酶Ⅱ 长时程增强 学习记忆
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