GABAA receptors in the basal forebrain mediates emergence from propofol anaesthesia in rats

Purpose The aim of the current study was to explore the role of the basal forebrain (BF) in propofol anaesthesia. Methods In the present study, we observed the neural activities of the BF during propofol anaesthesia using calcium fibre photometry recording. Subsequently, ibotenic acid was injected into the BF to verify the role of the BF in propofol anaesthesia. Finally, to test whether GABA(A) receptors in the BF were involved in modulating propofol anaesthesia, muscimol (GABA(A) receptor agonist) and gabazine (GABA(A) receptor antagonist) were microinjected into the BF. Cortical electroencephalogram (EEG), time to loss of righting reflex (LORR), and recovery of righting reflex (RORR) under propofol anaesthesia were recorded and analysed. Results The activity of BF neurons was inhibited during induction of propofol anaesthesia and activated during emergence from propofol anaesthesia. In addition, non-specifical lesion of BF neurons significantly prolonged the time to RORR and increased delta power in the frontal cortex under propofol anaesthesia. Next, microinjection of muscimol into the BF delayed emergence from propofol anaesthesia, increased delta power of the frontal cortex, and decreased gamma power under propofol anaesthesia. Conversely, infusion of gabazine accelerated emergence times and decreased EEG delta power. Conclusions The basal forebrain is involved in modulating frontal cortex delta activity and emergence from propofol anaesthesia. Additionally, the GABA(A) receptors in the basal forebrain are involved in regulating emergence propofol anaesthesia.

Automated summary

The study aims to explore the role of the basal forebrain in propofol anesthesia. The results show that the activity of basal forebrain neurons is inhibited during propofol induction and activated during emergence. Lesions in the basal forebrain prolong recovery time and increase delta power in the frontal cortex under propofol anesthesia. Muscimol injection delays emergence and increases delta power, while gabazine infusion accelerates recovery time and decreases delta power. The basal forebrain modulates frontal cortex delta activity and emergence from propofol anesthesia, involving GABA(A) receptors.