论文部分内容阅读
目的探讨急性麦芽酚铝[Al(mal)3]染毒对大鼠海马CA1区长时程增强(LTP)影响。方法对照组及低、中、高染铝组大鼠通过侧脑室给药方式分别一次性注射生理盐水、2.43、12.15、60.75μg Al(mal)3,给药容积为5μL,5 min内缓慢匀速注入;采用在体海马CA1区LTP记录技术,记录兴奋性突触后电位(fEPSP)。结果高剂量染铝组大鼠在给药前和给药后30 min时fEPSP分别为(109±4)%和(111±7)%,差异无统计学意义(P>0.05);在高频刺激后60 min时,低、中、高染铝组fEPSP分别为(157±8)%、(140±13)%、(110±7)%,均低于对照组的(190±27)%,而相同剂量下的Al(mal)3对双脉冲易化(PPF)无影响。结论 Al(mal)3剂量依赖性抑制大鼠海马CA1区的LTP诱导和维持,其作用机制可能与突触前机制无关,而与突触后机制有关。
Objective To investigate the effect of acute maltol aluminum [Al (mal) 3] on long-term potentiation (LTP) in rat hippocampal CA1 region. Methods Rats in control group and low, medium and high aluminum groups were injected with saline, 2.43,12.15 and 60.75μg Al (mal) 3 respectively through intracerebroventricular injection. The volume of administration was 5μL, The excitatory postsynaptic potential (fEPSP) was recorded using LTP recording technique in the hippocampal CA1 region. Results The fEPSP was (109 ± 4)% and (111 ± 7)% in the high dose aluminum exposure group before administration and 30 min after administration, respectively, with no significant difference (P> 0.05) The fEPSP was (157 ± 8)%, (140 ± 13)% and (110 ± 7)% in the low, middle and high aluminum groups at 60 min after stimulation, both of which were lower than that of the control group (190 ± 27)% , While Al (mal) 3 at the same dosage had no effect on PPF. Conclusion Al (mal) 3 dose-dependently inhibits the induction and maintenance of LTP in the hippocampal CA1 region of rats. The mechanism may be related to the presynaptic mechanism but not to the presynaptic mechanism.