Propofol is an intravenous anesthetic that can active γ-aminobutyric acid A (GABAA) receptors and generate sedative-hypnotic effects. Propofol has been widely applied clinically to achieve sedation comparable to sleep in humans. The basal forebrain (BF) is a brain region that plays an important role in sleep-wake regulation. Previous studies suggest that propofol affects the sleep-wake circuit via the BF; however, the mechanism remains elusive. In the current study we investigated the effects of propofol on the inherent properties of cholinergic neurons and their ability to convert excitatory inputs into spikes in mouse BF slices using whole-cell patch clamp recordings. Bath application of propofol (10 μM) significantly elevated the threshold potentials (Vts), decreased the number of spikes in response to a depolarizing current injection, and augmented the inter-spike intervals (ISIs), energy barrier (Vts-Vrs), and absolute refractory periods (ARPs). These effects were eliminated by co-application of a GABAA receptor antagonist picrotoxin (50 μM). Altogether, our results reveal that propofol decreases the excitability of cholinergic neurons in mouse BF via GABAA receptors.

中文翻译：

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丙泊酚通过GABAA受体降低小鼠基底前脑中胆碱能神经元的兴奋性。

异丙酚是一种静脉麻醉药，可以激活γ-氨基丁酸A（GABAA）受体并产生镇静催眠作用。丙泊酚已在临床上得到广泛应用，以达到与人的睡眠相当的镇静作用。基底前脑（BF）是大脑区域，在睡眠觉醒调节中起重要作用。先前的研究表明，异丙酚会通过BF影响睡眠-觉醒回路。但是，该机制仍然难以捉摸。在当前的研究中，我们研究了异丙酚对胆碱能神经元固有特性的影响，以及它们利用全细胞膜片钳记录将兴奋性输入转化为小鼠BF切片中的尖峰的能力。浴液中异丙酚（10μM）的施加可显着提高阈值电势（Vts），并响应于去极化电流注入而减少了尖峰数，并增加了尖峰间隔（ISI），能垒（Vts-Vrs）和绝对不应期（ARPs）。通过共同应用GABAA受体拮抗剂微毒素（50μM）消除了这些影响。总之，我们的结果表明，丙泊酚通过GABAA受体降低了小鼠BF中胆碱能神经元的兴奋性。