LAUSR

The sleep cycle is characterized by alternating non–rapid eye movement (NREM) and rapid eye movement (REM) sleeps. The mechanisms by which this cycle is generated are incompletely understood. We found that a transient increase of dopamine (DA) in the basolateral amygdala (BLA) during NREM sleep terminates NREM sleep and initiates REM sleep. DA acts on dopamine receptor D2 (Drd2)–expressing neurons in the BLA to induce the NREM-to-REM transition. This mechanism also plays a role in cataplectic attacks—a pathological intrusion of REM sleep into wakefulness—in narcoleptics. These results show a critical role of DA signaling in the BLA in initiating REM sleep and provide a neuronal basis for sleep cycle generation. Description Dopamine and the gating of REM sleep Sleep is composed of rapid eye movement (REM) and non-REM sleep, and REM sleep usually appears after periods of non-REM sleep. However, we do not understand the mechanisms by which the brain cycles between those states. Using fiber photometry, Hasegawa et al. found increases in dopamine activation before non-REM to REM transitions but not before non-REM to wake transitions in the basolateral amygdala (see the Perspective by Arrigoni and Fuller). This effect was mediated by dopamine receptor D2-expressing neurons in the amygdala. Artificially activating these neurons induced a transition from non-REM to REM sleep and cataplectic states in awake mice. —PRS Transient dopamine elevation in the amygdala during non-REM sleep plays a role in triggering the non-REM to REM sleep transition.