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GABA inhibitory network: A requirement of maintenance of consciousness

机译：GABA抑制网络：维持意识的要求

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In this EBioMedicine manuscript [1], Dr. Guo and colleagues report that the isoflurane-induced loss of consciousness was associated with numerous interesting phenomena, including general decay of GABA input onto each cortical neuron subtype, and diverse glutamate transient in both excitatory and inhibitory interneurons. By using in vivo two-photon imaging with high spatiotemporal resolution and recently developed genetically-encoded neurotransmitter indicators [2], the authors systematically investigate the dynamics of cortical neurotransmitters in a cell type-specific manner during anesthetic-induced unconsciousness which occurred transitorily within tens of seconds. They found a general decreased GABA transmission among pyramidal neurons as well as Parvalbumin (PV), somatostatin-expressing (SOM) and Vasoactive Intestinal Polypeptide (VIP) interneurons. In contrast, glutamate transmission was almost preserved on pyramidal neurons but reduced on PV, SOM, and VIP interneurons. Furthermore, VIP neuronal activity was delayed, and PV neuronal activity was strongly inhibited and highly synchronized. The authors conclude that anesthetic-induced unconsciousness is a state with a disrupted excitatory-inhibitory network, and that the functional inhibitory network is required in the maintenance of consciousness.
机译：在这个eBiomedicine稿件[1]中，郭和同事博士报告称异氟烷诱导的意识丧失与许多有趣的现象有关，包括GABA投入的一般衰减，并在每种皮质神经元亚型上输入，以及兴奋性和抑制的各种谷氨酸瞬间中间核心。通过使用具有高时空分辨率的Vivo双光子成像，最近开发了遗传编码的神经递质指标[2]，该作者系统地在麻醉诱导的无意识期间以细胞类型特异性方式系统地研究皮质神经递质的动态。几秒钟。他们发现金字塔神经元以及帕瓦尔白蛋白（PV），表达生长抑素（SOM）和血管活性肠多肽（VIP）中间核的一般GABA传播。相比之下，谷氨酸盐传递几乎保存在金字塔神经元上，但在PV，SOM和VIP Interneurons上减少。此外，延迟VIP神经元活性，强烈抑制和高度同步的PV神经元活性。作者得出结论，麻醉引起的无意识是具有破坏兴奋性抑制网络的状态，并且在维持意识中需要功能抑制网络。

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