Yin Mengyu, Wang Ransheng, Cai Zhiwei, Liang Yi, Mai Fangcai, Wu Kaibin, Kong Deyi, Tang Peiwen, Pan Yidi, Ji Xuying, Li Fengxian, Liang Feixue, Zhang Hong-Fei
Department of Anaesthesiology, Zhujiang Hospital of Southern Medical University, Guangzhou, China; School of Biomedical Engineering, Southern Medical University, Guangzhou, China; Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Southern Medical University, Guangzhou, China; Key Laboratory of Mental Health of the Ministry of Education, Southern Medical University, Guangzhou, China; Guangdong Province Key Laboratory of Psychiatric Disorders, Southern Medical University, Guangzhou, China; Guangdong-Hong Kong Joint Laboratory for Psychiatric Disorders, Southern Medical University, Guangzhou, China; Guangdong Basic Research Center of Excellence for Integrated Traditional and Western Medicine for Qingzhi Diseases, Southern Medical University, Guangzhou, China.
School of Biomedical Engineering, Southern Medical University, Guangzhou, China; Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Southern Medical University, Guangzhou, China; Key Laboratory of Mental Health of the Ministry of Education, Southern Medical University, Guangzhou, China; Guangdong Province Key Laboratory of Psychiatric Disorders, Southern Medical University, Guangzhou, China; Guangdong-Hong Kong Joint Laboratory for Psychiatric Disorders, Southern Medical University, Guangzhou, China; Guangdong Basic Research Center of Excellence for Integrated Traditional and Western Medicine for Qingzhi Diseases, Southern Medical University, Guangzhou, China.
Br J Anaesth. 2025 Apr;134(4):1122-1133. doi: 10.1016/j.bja.2024.10.052. Epub 2025 Jan 30.
Anaesthesia-induced burst suppression signifies profound cerebral inactivation. Although considerable efforts have been directed towards elucidating the electroencephalographic manifestation of burst suppression, the neuronal underpinnings that give rise to isoflurane-induced burst suppression are unclear.
Electroencephalography combined with micro-endoscopic calcium imaging was used to investigate the neural mechanisms of isoflurane-induced burst suppression. Synchronous activities of pyramidal neurones in the auditory cortex and medial prefrontal cortex and inhibitory neurones in the auditory cortex (including parvalbumin [PV], somatostatin [SST], and vasoactive intestinal peptide [Vip]) and subcortical regions (including the medial geniculate body, locus coeruleus, and thalamic reticular nucleus) were recorded during isoflurane anaesthesia. In addition, the effects of chemogenetic manipulation inhibitory neurones in the auditory cortex on isoflurane-induced burst suppression were studied.
Isoflurane-induced burst suppression was highly correlated with the synchronous activities of excitatory neurones in the cortex (∼65% positively and ∼20% negatively correlated neurones). Conversely, a minimal or absent correlation was observed with the neuronal synchrony of inhibitory interneurones and with neuronal activities within subcortical areas. Only activation or inhibition of PV neurones, but not SST or Vip neurones, decreased (P<0.0001) or increased (P<0.0001) isoflurane-induced neuronal synchrony.
Isoflurane-induced burst suppression might be primarily driven by the synchronous activities of excitatory pyramidal neurones in the cortex, which could be bidirectionally regulated by manipulating the activity of inhibitory PV interneurones. Our findings provide new insights into the neuronal mechanisms underlying burst suppression.
麻醉诱导的爆发抑制意味着大脑深度失活。尽管人们已经付出了相当大的努力来阐明爆发抑制的脑电图表现，但导致异氟烷诱导的爆发抑制的神经元基础尚不清楚。
采用脑电图结合显微内镜钙成像技术研究异氟烷诱导的爆发抑制的神经机制。在异氟烷麻醉期间，记录听觉皮层和内侧前额叶皮层锥体细胞以及听觉皮层（包括小白蛋白[PV]、生长抑素[SST]和血管活性肠肽[Vip]）和皮层下区域（包括内侧膝状体、蓝斑和丘脑网状核）抑制性神经元的同步活动。此外，还研究了听觉皮层中化学遗传学操纵抑制性神经元对异氟烷诱导的爆发抑制的影响。
异氟烷诱导的爆发抑制与皮层兴奋性神经元的同步活动高度相关（约65%为正相关神经元，约20%为负相关神经元）。相反，与抑制性中间神经元的神经元同步性以及皮层下区域内的神经元活动相关性最小或不存在。仅激活或抑制PV神经元，而不是SST或Vip神经元，会降低（P<0.0001）或增加（P<0.0001）异氟烷诱导的神经元同步性。
异氟烷诱导的爆发抑制可能主要由皮层兴奋性锥体神经元的同步活动驱动，通过操纵抑制性PV中间神经元的活动可以对其进行双向调节。我们的研究结果为爆发抑制的神经元机制提供了新的见解。
