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首页> 外文期刊>The European Journal of Neuroscience >Very low concentrations of ethanol suppress excitatory synaptic transmission in rat visual cortex
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Very low concentrations of ethanol suppress excitatory synaptic transmission in rat visual cortex

机译：非常低浓度的乙醇抑制大鼠视觉皮层中的兴奋性突触传递

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Abstract Ethanol is one of the most commonly used substances in the world. Behavioral effects of alcohol are well described, however, cellular mechanisms of its action are poorly understood. There is an apparent contradiction between measurable behavioral changes produced by low concentrations of ethanol, and lack of evidence of synaptic changes at these concentrations. Furthermore, effects of ethanol on synaptic transmission in the neocortex are poorly understood. Here, we set to determine effects of ethanol on excitatory synaptic transmission in the neocortex. We show that 150爉m ethanol suppresses excitatory synaptic transmission to layer 2/3 pyramidal neurons in rat visual cortex in a concentrationdependent manner. To the best of our knowledge, this is the first demonstration of the effects of very low concentrations of ethanol (from 1爉m ) on synaptic transmission in the neocortex. We further show that a selective antagonist of A1 adenosine receptors, 8cyclopentyl1,3dipropylxanthine (DPCPX ), blocks effects of 110爉m ethanol on synaptic transmission. However, the reduction in excitatory postsynaptic potential amplitude by 50爉m ethanol was not affected byDPCPX . We propose that ethanol depresses excitatory synaptic transmission in the neocortex by at least two mechanisms, engaged at different concentrations: low concentrations of ethanol reduce synaptic transmission via A1 Rdependent mechanism and involve presynaptic changes, while higher concentrations activate additional, adenosineindependent mechanisms with predominantly postsynaptic action. Involvement of adenosine signaling in mediating effects of low concentrations of ethanol may have important implications for understanding alcohol's effects on brain function, and provide a mechanistic explanation to the interaction between alcohol and caffeine.
机译：摘要乙醇是世界上最常用的物质之一。醇的行为效应很好地描述，然而，其作用的细胞机制尚不清楚。通过低浓度的乙醇产生的可测量行为变化之间存在明显矛盾，并且缺乏这些浓度的突触变化的证据。此外，乙醇对Neocortex中突触传递的影响很差。在这里，我们设定了乙醇对新生兴奋性突触传递的影响。我们表明，150毫升乙醇以浓度依赖的方式抑制大鼠视觉皮层的兴奋性突触传递到大鼠的2/3金字塔神经元。据我们所知，这是第一次证明非常低浓度乙醇（从1‰M）对Neocortex中突触传递的影响。我们进一步表明，A1腺苷受体的选择性拮抗剂，8cyclopetyl1,3-二丙基吡啶（DPCPX），嵌段110℃乙醇对突触传递的影响。然而，减少兴奋性突触潜力幅度50℃乙醇的影响不受DPCPX的影响。我们提出乙醇在Neocortex中抑制了至少两种机制，从事不同浓度的机制下降：低浓度的乙醇通过A1 R依赖性机制降低突触传播，涉及突触型变化，而较高浓度的腺嘌呤依赖性机制具有主要的突触后作用。腺苷信号传导在低浓度乙醇中的介导效果中可能具有重要意义，可以对理解酒精对脑功能的影响，并为酒精和咖啡因之间的相互作用提供机械解释。

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