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宋静, 张慧芳, 刘莹, 牛侨. 麦芽酚铝对大鼠在体海马长时程增强影响[J]. 中国公共卫生, 2013, 29(5): 688-691. DOI: 10.11847/zgggws2013-29-05-21
引用本文: 宋静, 张慧芳, 刘莹, 牛侨. 麦芽酚铝对大鼠在体海马长时程增强影响[J]. 中国公共卫生, 2013, 29(5): 688-691. DOI: 10.11847/zgggws2013-29-05-21
SONG Jing, ZHANG Hui-fang, LIU Ying.et al, . Effect of aluminum-maltolate complex on long-term potentiation in rat hippocampus in vivo[J]. Chinese Journal of Public Health, 2013, 29(5): 688-691. DOI: 10.11847/zgggws2013-29-05-21
Citation: SONG Jing, ZHANG Hui-fang, LIU Ying.et al, . Effect of aluminum-maltolate complex on long-term potentiation in rat hippocampus in vivo[J]. Chinese Journal of Public Health, 2013, 29(5): 688-691. DOI: 10.11847/zgggws2013-29-05-21

麦芽酚铝对大鼠在体海马长时程增强影响

Effect of aluminum-maltolate complex on long-term potentiation in rat hippocampus in vivo

  • 摘要: 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、60.75 μg Al(mal)3,给药容积为5 μL,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。

     

    Abstract: Objective To study the effect of aluminum-maltolate(Almal3) complex on long-term potentiation(LTP) in rat hippocampus in vivo.Methods The rats were exposed to Al(mal)3 by acute intracerebroventricular injection.Field excitatory postsynapic potenial(fEPSP) in CAI region of hippocampus was recorded by field potentiation technique in vivo.Results The basal fEPSP of high dose Al(mal)3(60.75 μg) groups with preinjection and postinjection were 109±4% and 111±7%,respectively,without significant difference(P>0.05).In 60 min-post high frequency stimulation,the fEPSP of 2.43μg,12.15 μg,and 60.75 μg groups were 157±8%,140±13%,and 110±7%,with significant differences compared to that of the control group.But under the same dose of exposure,Al(mal)3 did not affect paired pulse facilitation(PPF)ratio.Conclusion Al(mal)3 obviously suppresses the LTP in rat hippocampal CA1 region in a dose-dependent manner in vivo,probably through postsynaptic mechanism but not presynaptic transmitter release.

     

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