目的通过进一步研究慢性铝暴露引起大鼠海马细胞内[Ca^2+]i和钙调蛋白激酶激酶Ⅱ(CaM Ⅱ)蛋白表达的变化,来探讨铝损害学习记忆的作用机制。方法选择断乳后Wistar大鼠,以含有不同浓度AlCl3的水进行饲养。3个月后,取海马测定细胞内[Ca^2+]i,用Western blotting方法检测CaMK Ⅱ的蛋白表达。结果(1)各染铝组的[Ca^2+]i与对照组比较明显降低,差异有统计学意义(P〈0.01),但各染铝组间差异无统计学意义;(2)各染铝组CaMKⅡ蛋白表达与对照组比较也显著降低,并成剂量关系,差异有统计学意义(P〈0.01)。结论铝能够降低大鼠海马细胞内的[Ca^2+]i浓度并造成CaMKⅡ的蛋白表达降低,从而损伤学习记忆功能。
Objective To go deep into the mechanism for chronic aluminum-induced impairments to learning and memory by studying the change of [ Ca^2+ ]i and concentration of calcium ( [ Ca^2+ ]i ) calciurrdcalmodulin-dependent kinase Ⅱ ( CaMK Ⅱ ). Methods The ablactated Wistar rats were used to establish the chrenic-aluminium exposed models by the garages of aluminum chloride ( AlCl3 ) of different concentrations in the drinking water and measured the [ Ca^2+ ]i in hippocampi of the rats. Western Blot was used to determine CaMK II contents in hippocampi. Results (1) [ Ca^2+ ]i in AlCl3 exposed groups was obviously lower than that in control group ( P 〈 0.01 ) but there was no significant difference among aluminum treated groups. (2)The content of CaMK II in hippocampus of AlCl3-exposed groups fell down in a dose-dependent manner comparing with that of control group ( P 〈 0.01 ). Conclusion Chronic aluminum exposure can affect [ Ca^2+ ]i and CaMKⅡ content, which play most important roles in learning and memory, and impair the ability of learning and memory.