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Chronic early life lead (Pb2+) exposure alters presynaptic vesicle pools in hippocampal synapses

机译:慢性早期生命铅(Pb2 +)暴露会改变海马突触中突触前囊泡池

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摘要

BackgroundLead (Pb2+) exposure has been shown to impair presynaptic neurotransmitter release in both in vivo and in vitro model systems. The mechanism by which Pb2+ impairs neurotransmitter release has not been fully elucidated. In previous work, we have shown that Pb2+ exposure inhibits vesicular release and reduces the number of fast-releasing sites in cultured hippocampal neurons. We have also shown that Pb2+ exposure inhibits vesicular release and alters the distribution of presynaptic vesicles in Shaffer Collateral – CA1 synapses of rodents chronically exposed to Pb2+ during development.
机译:背景铅在体内和体外模型系统中的暴露(Pb 2 + )都会损害突触前神经递质的释放。 Pb 2 + 损害神经递质释放的机制尚未完全阐明。在以前的工作中,我们表明,Pb 2 + 暴露抑制了水泡的释放,并减少了培养的海马神经元中快速释放位点的数量。我们还显示,Pb 2 + 暴露抑制了发育过程中长期暴露于Pb 2 + 的啮齿动物的Shaffer侧支– CA1突触中囊泡的释放并改变了突触前囊泡的分布。

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