Anesthetic propofol normalized the increased release of glutamate and γ-amino butyric acid in hippocampus after paradoxical sleep deprivation in rats

Multiple lines of evidence suggest that general anesthesia helps the recovery from sleep deprivation. However, little is known about the underlying neurochemical mechanisms. In the current study, we investigated the effect of anesthetic propofol on the release of glutamate (Glu) and γ-amino butyric acid (GABA) in the hippocampal CA1 region of rat with 24 h-paradoxical sleep deprivation (PSD).A guide cannula for microdialysis was inserted into the CA1 region of hippocampus in rats. At six days after cannula implantation, rats received 24 h-PSD by using the platform-water tank method. The rats were then subjected to natural sleep or propofol anesthesia (100 mg/kg, i.p.), respectively, after 24-h PSD. Microdialysis samples from hippocampus were collected before and at the end of PSD, and also at 1, 3, 6, and 8 h post-PSD. The concentrations of Glu and GABA in collected samples were determined by using high performance liquid chromatography.The current study showed that 24 h-PSD significantly increased the release of Glu and GABA in the hippocampus in rats. In both natural sleep and propofol anesthesia groups, the upregulated Glu and GABA levels after PSD gradually decreased and returned to the baseline level by 8 h post-PSD.Our data indicate that propofol anesthesia promotes the restoration of disturbed excitatory and inhibitory neurotransmitter release in the hippocampus after PSD, similar to the beneficial effects of natural sleep. This finding suggests that propofol anesthesia may be a viable pharmacotherapeutic strategy for the treatment of certain sleep disorders that share similar mechanisms with PSD.