中文摘要：

瞄准：乙醇，大多数之一经常在我们的社会使用了并且滥用物质，穿上深刻影响镇静。然而，位于它的镇静的效果下面的 neuronal 机制仍然保持不清楚。在这研究，我们在 tuberomammillary 原子核(TMN ) 在 histaminergic 神经原上调查了乙醇的效果，为 wakefulness.Methods 批评的一个大脑区域想法：花冠大脑片(250 μ； m 厚) 包含 TMN 从 GAD67-GFP 敲门在里面老鼠被准备。GAD67-GFP 被用来在 TMN 识别 histaminergic 神经原。到这些神经原上的自发的开火和 histaminergic 神经原，和 GABAergic 传播的膜潜力用整个房间的补丁夹钳记录被记录。药通过 superfusion.Results 被使用：在 GAD67-GFP 老鼠的 TMN 的 Histaminergic 和表示 GAD67 神经原是高度 co 局部性的。没有开火冲破， TMN GFP 积极的神经原以 2-4 Hz 的率展出了常规自发的分泌物。乙醇(64， 190，和 560 mmol/L ) 的简短 superfusion dose-dependently 并且 reversibly 压制了在 TMN 的神经原的自发的开火；当 synaptic 传播被 tetrodotoxin 堵住时(1 μ； mol/L ) ，乙醇引起了膜潜力的 hyperpolarization。而且，乙醇的 superfusion 显著地增加了自发、缩小的禁止的 postsynaptic 水流(sIPSCs 和 mIPSCs ) 的频率和振幅，它面对 GABA 受体对手 bicuculline (20 μ； mol/L ) 。最后，当片是有 GABA _B 收缩筋 baclofen (30 μ； mol/L ).Conclusion：乙醇在老鼠 TMN 片禁止 histaminergic 神经原的易兴奋性，可能经由加强 GABAergic 传播到在 pre- 和 postsynaptic 地点的神经原上。

英文摘要：

Aim： Ethanol, one of the most frequently used and abused substances in our society, has a profound impact on sedation. However, the neuronal mechanisms underlying its sedative effect remain unclear. In this study, we investigated the effects of ethanol on histaminergic neurons in the tuberomammillary nucleus （TMN）, a brain region thought to be critical for wakefulness. Methods： Coronal brain slices （250 pm thick） containing the TMN were prepared from GAD67-GFP knock-in mice. GAD67-GFP was used to identify histaminergic neurons in the TMN. The spontaneous firing and membrane potential of histaminergic neurons, and GABAergic transmission onto these neurons were recorded using whole-cell patch-clamp recordings. Drugs were applied through superfusion. Results： Histaminergic and GAD67-expressing neurons in the TMN of GAD67-GFP mice were highly co-localized. TMN GFP-positive neurons exhibited a regular spontaneous discharge at a rate of 2-4 Hz without burst firing. Brief superfusion of ethanol （64, 190, and 560 mmol/L） dose-dependently and reversibly suppressed the spontaneous firing of the neurons in the TMN; when synaptic transmission was blocked by tetrodotoxin （1 μmol/L）, ethanol caused hyperpolarization of the membrane potential. Furthermore, superfusion of ethanol markedly increased the frequency and amplitude of spontaneous and miniature inhibitory postsynaptic currents （slPSCs and mlPSCs）, which were abolished in the presence of the GABAA receptor antagonist bicuculline （20 μmol/L）. Finally, ethanolmediated enhancement of slPSCs and mlPSCs was significantly attenuated when the slices were pretreated with the GABAB agonist baclofen （30 μmoVL）. Conclusion： Ethanol inhibits the excitability of histaminergic neurons in mouse TMN slices, possibly via potentiating GABAergic transmission onto the neurons at both pre- and postsynaptic sites.