摘要
目的研究慢性铝暴露引起大鼠海马蛋白激酶C(PKC)、有丝分裂激活蛋白激酶(MAPK)活力的变化,对海马齿状回(CAI区)产生长时程增强(LTP)幅值改变的调节作用,探讨铝暴露对学习记忆功能的影响。方法选择断乳后Wistar大鼠,随机分4组(1个对照组,3个染毒组),每组20只,染毒组大鼠分别喂食质量浓度为0.2%、0.4%和0.6%氯化铝的水,饲养3个月后,测量大鼠海马LTP,用改良的Takai法测定PKC、MAPK活力的变化。结果3个浓度的染铝,PKC的活力均依浓度依赖方式被抑制,细胞浆比活力的倍数分别为:4.95±0.76、5.31±0.90、5.50±1.46(P<0.01);细胞膜为9.84±3.84、8.35±2.327、.56±2.06(P<0.01)。MAPK活力依浓度依赖方式被抑制,比活力的倍数分别为:3.43±0.91、2.53±1.21和2.64±0.55(P<0.05)。结论慢性铝暴露引起PKC及ERK活力降低,导致大鼠海马LTP幅值下降。
Objective In this research, we have observed changes of the activities of PKC and MAPK, and their regulatory roles in changing the amplitude value of LTP due to aluminium exposure so that we can discuss the impact on the learning and memory that caused by the changed activities of PKC and MAPK due to chronic aluminium exposure. Methods 80 Delactosed wistar rats were divided into 4 groups. The rats drank water containing different doses of aluminium chloride（AlCl3 ）（0,2,4,6 g/L respectively） for 3 m. Measured the LTP in hippocampus and determined the activities of PKC ＆ MAPK with improved Takai method. Results AlCl3 exposure could inhibit both PKC and MAPK in dose-dependent manner. For MAPK, the multiple of specific activity for each group was respectively 3.43 ± 0.91, 2.53 ± 1.21 and 2.64 ± 0.55（ P 〈 0.05） ; For PKC in cytoplasm, the multiple of specific activity for each group was respectively 4.95 ± 0.76, 5.31 ± 0.90 and 5.50 ± 1.46 （ P 〈 0.01） ; For PKC in cytolemma, the multiple of specific activity for each group was separately 9.84 ± 3.84, 8.35 ± 2.32 and 7.56 ± 2.06 （ P 〈 0.01 ）. Conclusions Chronic aluminium exposure can reduce the amplitude value of LTP in hippocampus of rats and adjust the activities of PKC and ERK downwards.
出处
《毒理学杂志》
CAS
CSCD
北大核心
2007年第2期102-104,共3页
Journal of Toxicology
基金
国家自然科学基金项目(30371229)
