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首页> 外文期刊>The European Journal of Neuroscience >Alcohol increases efficacy of immature synapses in a neurosteroid-dependent manner.
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Alcohol increases efficacy of immature synapses in a neurosteroid-dependent manner.

机译：酒精以神经甾体依赖性方式增加未成熟突触的功效。

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摘要

Fetal ethanol exposure persistently affects hippocampal circuits leading to learning and memory disabilities. Although the mechanisms responsible for these effects are not fully understood, several studies implicate neurosteroids as mediators of the actions of ethanol. A neurosteroid that appears to be critical for the fetal actions of ethanol is pregnenolone sulfate (PREGS). We found that chronic prenatal ethanol exposure increases PREGS levels in the fetal brain and that an endogenous PREGS-like neurosteroid strengthens excitatory transmission in the neonatal hippocampus. Therefore, we hypothesized that ethanol could affect synaptic transmission in the developing hippocampus in a PREGS-dependent manner. We used patch-clamp electrophysiological techniques and found that 50 mm ethanol strengthens AMPA receptor-mediated transmission in the CA1 region by reducing the failure rate of low-efficacy synapses. This effect was age-dependent and was occluded by application of exogenous PREGS. An anti-PREGS antibody scavenger and blockade of PREGS synthesis prevented the effect of ethanol. These data indicate that the deleterious effects of ethanol on hippocampal development are mediated in part by alterations in neurosteroid production, which results in premature stabilization of excitatory synapses.
机译：胎儿乙醇暴露持续影响海马回路，导致学习和记忆障碍。尽管引起这些作用的机制尚不完全清楚，但一些研究表明神经甾体是乙醇作用的介质。似乎对乙醇的胎儿行为至关重要的神经甾体是硫酸孕烯醇酮（PREGS）。我们发现，慢性产前乙醇暴露会增加胎儿大脑中的PREGS水平，而内源性PREGS样神经甾体会增强新生儿海马中的兴奋性传递。因此，我们假设乙醇可能以PREGS依赖性方式影响发育中的海马突触传递。我们使用膜片钳电生理技术，发现50 mm乙醇通过降低低效突触的失败率来增强AMPA受体介导的CA1区传递。该效应是年龄依赖性的，并且通过应用外源性PREGS而被遮挡。抗PREGS抗体清除剂和PREGS合成的阻滞阻止了乙醇的作用。这些数据表明乙醇对海马发育的有害作用部分地由神经类固醇产生的变化介导，这导致兴奋性突触的过早稳定。

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