在医学和神经科学的领域中，麻醉机制一直是一个备受关注的研究热点。最近的研究发现，为我们进一步了解麻醉与神经系统之间的关系带来了新的曙光。
研究聚焦于基底前脑（BF）中的GABAergic neurons（γ - 氨基丁酸能神经元），发现它们能够促进皮层激活。在手术中，我们常常使用异氟烷进行麻醉，而麻醉后的恢复过程对于患者来说至关重要。这些位于基底前脑的特殊神经元竟然能够加速从异氟烷麻醉后的行为恢复，这就像是在身体内部有一个天然的“唤醒开关”，帮助我们更快地从麻醉状态中脱离出来。
更令人惊喜的是，研究还发现中央杏仁核（CeA）的GABA能神经元在全身麻醉调节中扮演着重要角色。它们通过GABA能的CeA - BF通路，对异氟烷麻醉后的行为和皮层恢复起到了促进作用。这一发现就像是在一个复杂的神经网络中找到了一条关键的通路，它连接着麻醉状态与清醒状态之间的桥梁。
从临床意义上来看，这一研究成果可能为未来的麻醉实践提供新的思路。例如，是否可以通过靶向调节这些神经元或相关通路，来优化麻醉药物的使用和患者的麻醉后恢复过程？也许在不久的将来，根据患者的个体神经特征，更加精准地控制麻醉剂量和时长，减少麻醉后并发症的发生，让患者在手术后能够小鼠杏仁核中GABA能神经元促进异氟醚麻醉后复苏
摘要译文（供参考）
中央杏仁核中的γ - 氨基丁酸能神经元促进小鼠从异氟烷麻醉中苏醒
背景：近期有证据表明全身麻醉和睡眠 - 觉醒行为存在一些重叠的神经基础。中央杏仁核（CeA）中的γ - 氨基丁酸（GABA）能神经元在清醒状态下具有较高的放电频率，并且在调节与觉醒相关的行为方面起作用。本研究的目的是探究中央杏仁核的GABA能神经元是否参与异氟烷全身麻醉的调节，并揭示潜在的神经回路。
方法：采用光纤光度记录法测定Vgat - Cre小鼠在异氟烷麻醉期间中央杏仁核GABA能神经元钙信号的变化。运用化学遗传学和光遗传学方法操控中央杏仁核GABA能神经元的活性，并通过翻正反射试验测定异氟烷麻醉的诱导和苏醒情况。采用皮层脑电图（EEG）记录分别评估在0.8%和1.4%异氟烷麻醉期间脑电图频谱功率和爆发抑制比的变化。本研究使用了雄性和雌性小鼠。
结果：在异氟烷麻醉诱导过程中，中央杏仁核GABA能神经元的钙信号降低，而在苏醒时恢复。中央杏仁核GABA能神经元的化学遗传学激活延长了异氟烷麻醉的诱导时间（平均值±标准差，赋形剂组对比氯氮平 - N - 氧化物组：58.75±5.42秒对比67.63±5.01秒；n = 8，P = 0.0017）并缩短了苏醒时间（385.50±66.26秒对比214.60±40.21秒；n = 8，P = 0.0017）。中央杏仁核GABA能神经元的光遗传学激活产生了类似的效果。此外，光遗传学激活降低了脑电图的δ波功率（刺激前对比刺激时：46.63%±4.40%对比34.16%±6.47%；n = 8，P = 0.0195）和爆发抑制比（83.39%±5.15%对比52.60%±12.98%；n = 8，P = 0.0002）。而且，对基底前脑（BF）中中央杏仁核GABA能神经元末梢的光遗传学刺激也促进了皮层激活并加速了异氟烷麻醉后的行为恢复。
结论：我们的研究结果表明，中央杏仁核GABA能神经元在全身麻醉调节中起作用，它通过GABA能的中央杏仁核 - 基底前脑通路促进了异氟烷麻醉后行为和皮层的恢复。
原文摘要
GABAergic neurons in the central amygdala promote emergence from isoflurane anesthesia in mice
Background: Recent evidence indicates that general anesthesia and sleep-wake behavior share some overlapping neural substrates. GABAergic neurons in the central amygdala (CeA) have a high firing rate during wakefulness and play a role in regulating arousal-related behaviors. The objective of this study is to investigate whether CeA GABAergic neurons participate in the regulation of isoflurane general anesthesia and uncover the underlying neural circuitry.
Methods: Fiber photometry recording was used to determine the changes in calcium signals of CeA GABAergic neurons during isoflurane anesthesia in Vgat-Cre mice. Chemogenetic and optogenetic approaches were used to manipulate the activity of CeA GABAergic neurons, and a righting reflex test was used to determine the induction and emergence from isoflurane anesthesia. Cortical electroencephalogram (EEG) recording was used to assess the changes in EEG spectral power and burst-suppression ratio during 0.8% and 1.4% isoflurane anesthesia, respectively. Both male and female mice were used in this study.
Results: The calcium signals of CeA GABAergic neurons decreased during the induction of isoflurane anesthesia and was restored during the emergence. Chemogenetic activation of CeA GABAergic neurons delayed induction time (mean ± SD, vehicle vs. clozapine-N-oxide: 58.75±5.42 s vs. 67.63±5.01 s; n=8, P=0.0017) and shortened emergence time (385.50±66.26 s vs. 214.60±40.21 s; n=8, P=0.0017) from isoflurane anesthesia. Optogenetic activation of CeA GABAergic neurons produced a similar effect. Furthermore, optogenetic activation decreased EEG delta power (Pre-stim vs. Stim: 46.63%±4.40% vs. 34.16%±6.47%; n=8, P=0.0195) and burst-suppression ratio (83.39%±5.15% vs. 52.60%±12.98%; n=8, P=0.0002). Moreover, optogenetic stimulation of terminals of CeA GABAergic neurons in the basal forebrain (BF) also promoted cortical activation and accelerated behavioral emergence from isoflurane anesthesia.
Conclusions: Our results suggest that CeA GABAergic neurons play a role in general anesthesia regulation, which facilitates behavioral and cortical emergence from isoflurane anesthesia through the GABAergic CeA-BF pathway.
