CMT神经元burst放电介导皮层gamma爆发波形成在氯胺酮麻醉中的机制

氯胺酮的“分离麻醉”机制是未解之谜。氯胺酮特异性诱发gamma高频振荡，但gamma波与皮层“觉醒”密切相关，无法解释其伴随的意识消失现象。最新研究发现，慢波耦合参与形成的高强度间断性簇状发放的gamma爆发波而非gamma波才是氯胺酮麻醉后意识消失的EEG标志，探明gamma爆发波的慢波起源及耦合机制将为揭示氯胺酮的麻醉机制提供突破口。申请者前期证实丘脑中央正中核（CMT）是不同麻醉药介导皮层低频振荡的“扳机”（J Neurosci）。在CMT注射氯胺酮能够诱发皮层gamma爆发波及镇静状态，促进CMT神经元burst放电，而丘脑神经元burst放电与皮层慢波形成密切相关。因此本课题拟利用光遗传结合OptoTetrode在体电生理等技术，阐明CMT神经元burst放电介导皮层gamma爆发波的形成机制及其在氯胺酮麻醉中的作用，为阐明氯胺酮独特的作用方式提供新的思路和科学依据。

The mechanism of ketamine's "dissociative anesthesia" is a mystery. Ketamine specifically induces gamma high-frequency oscillation, but gamma oscillation is closely related with the cortical "arousal", which can not explain the accompanying phenomenon of unconsciousness. The latest research reported that the high-intensity intermittent gamma burst induced by slow wave coupling, rather than gamma wave itself, was the EEG marker of unconsciousness induced by ketamine anesthesia. Therefore, to find out the origin and coupling mechanism of the slow wave in gamma burst will provide a breakthrough for the study of ketamine anesthesia mechanism. The applicant has previously confirmed that the central medial thalamus (CMT) is the "trigger" for low-frequency oscillation in cortex induced by different anesthetics (J Neurosci). Ketamine injection into CMT induced gamma burst in cortex and the state of sedation, and promoted burst firing of CMT neurons. The burst firing of thalamic neurons is closely related to the formation of cortical slow waves. In this study, by using the optogenetics combined with OptoTetrode in-vivo electrophysiological technology, we are to investigate the mechanism and the role of the cortical gamma burst induced by the burst firing of CMT neurons in the ketamine anesthesia. This study will provide new ideas and scientific basis for understanding the unique mechanism of ketamine anesthesia.