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Synchronicity of pyramidal neurones in the neocortex dominates isoflurane-induced burst suppression in mice
Mengyu Yin1, Ransheng Wang1, Zhiwei Cai2
1Department 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.
Background:
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.
Methods:
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.
Results:
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.
Conclusions:
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.
