High-frequency gamma connectivity across the cortex is present during consciousness and depressed during unconsciousness. Subanesthetic ketamine (25 mg/kg) administered during isoflurane anesthesia accelerates recovery upon discontinuation of the primary anesthetic and increases gamma power during emergence. In rodents, ketamine reduced emergence time by 44%. During accelerated emergence, frontal-parietal coherence and normalized symbolic transfer entropy in high-frequency gamma bandwidth were increased compared with saline-treated controls. Surrogates of cortical information exchange in high-frequency gamma are increased in association with accelerated recovery from anesthesia, suggesting a functional significance of high-gamma information transfer in consciousness.
The preoptic area of the hypothalamus, long thought to only promote sleep, contains glutamatergic neurons (MLPO_VGLUT2) that actually drive wakefulness and suppress REM sleep. Using fiber photometry in mice, these neurons were highly active during REM sleep, wakefulness, and brief arousals, but minimally active during non-REM sleep. Chemogenetic stimulation of MLPO_VGLUT2 inhibited REM sleep onset, independent of non-REM fragmentation caused by hypothermia, and blocked the REM sleep rebound normally seen after total sleep deprivation. Chemogenetic inhibition increased REM sleep time only during the light phase. Mapping showed these neurons project to brain regions that promote wakefulness and inhibit REM sleep. The authors conclude that MLPO_VGLUT2 powerfully suppress REM sleep, and their overactivation disrupts REM recovery.