慢性酗酒者前额叶皮质突触素I升高。

Richard Henriksson, Alexander Kuzmin, Anna Okvist, Clive Harper, Donna Sheedy, Therese Garrick, Tatjana Yakovleva, Georgy Bakalkin
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引用次数: 11

摘要

越来越多的证据表明,慢性乙醇暴露后谷氨酸能突触增强,并表明其突触前效应是对突触强度的调节而不是对谷氨酸释放的执行。为了在人类乙醇依赖的背景下解决这一假设,我们使用半定量免疫印迹法比较了慢性酒精成瘾者和对照者前额叶和运动皮层突触素I、syntaxin 1A、突触体相关蛋白25和囊泡相关膜蛋白的免疫反应性。我们发现嗜酒者前额叶皮层突触体素I的免疫反应性有区域特异性升高,但其他三种蛋白的免疫反应性在两组之间没有显著差异。我们的研究结果与反复乙醇暴露对突触强度调节剂的影响一致,但对谷氨酸释放的执行者没有影响,并表明突触素I在与乙醇依赖相关的前额皮质谷氨酸回路的持久神经可塑性中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Elevated synaptophysin I in the prefrontal cortex of human chronic alcoholics.

Convergent lines of evidence suggest potentiation of glutamatergic synapses after chronic ethanol exposure, and indicate that the presynaptic effect hereof is on modulators of synaptic strength rather than on executors of glutamate release. To address this hypothesis in the context of ethanol dependence in humans, we used semiquantitative immunoblotting to compare the immunoreactivities of synaptophysin I, syntaxin 1A, synaptosome-associated protein 25, and vesicle-associated membrane protein in the prefrontal and motor cortices between chronic alcoholics and control subjects. We found a region-specific elevation in synaptophysin I immunoreactivity in the prefrontal cortex of alcoholics, but detected no significant differences between the groups in the immunoreactivities of the other three proteins. Our findings are consistent with an effect of repeated ethanol exposure on modulators of synaptic strength but not on executors of glutamate release, and suggest a role for synaptophysin I in the enduring neuroplasticity in the prefrontal cortical glutamate circuitry that is associated with ethanol dependence.

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