The study investigates the neural mechanisms underlying the homeostatic control of REM sleep. Using fiber photometry, the authors found that POAGAD2→TMN neurons in the preoptic area of the hypothalamus become most active during REM sleep. Optogenetic inhibition of these neurons specifically reduced the amount of REM sleep, without affecting non-REM sleep or wakefulness.
During periods of REM sleep restriction, the POAGAD2→TMN neurons exhibited an increased number and amplitude of calcium transients, reflecting the accumulation of REM sleep pressure. Importantly, inhibiting these neurons during REM sleep restriction prevented the subsequent rebound increase in REM sleep, suggesting that their activity is required for the homeostatic regulation of REM sleep.
The authors propose that the POAGAD2→TMN neurons in the hypothalamus integrate the homeostatic need for REM sleep and facilitate the compensatory increase in REM sleep following its restriction. These findings reveal a hypothalamic circuit that encodes REM sleep pressure and is necessary for the homeostatic regulation of REM sleep.
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by Maur... at www.biorxiv.org 08-23-2023
https://www.biorxiv.org/content/10.1101/2023.08.22.554341v2Deeper Inquiries