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.

Understanding the network topology of a cluster of diverse neurons acting in concert requires a detailed expression map of ligand–receptor pairs involved in cell–cell communication. The neuropeptide arginine vasopressin (AVP) and signaling mediated by its cognate receptor V1a have been implicated in dorsal-to-ventral regional communication in the suprachiasmatic nucleus (SCN), a cluster of neurons that acts in concert to generate daily rhythms in behavior and physiology. Here, we show that among vasoactive intestinal peptide (VIP)-ergic neurons in the ventral SCN only a small subpopulation expresses V1a, and we demonstrate the requirement of V1a in these VIP neurons for maintaining the robustness of the circadian clock using a jet-lag paradigm. Notably, we found that V1a expression appears to be minimal in the other major ventral neuronal population expressing gastrin-releasing peptide (GRP). The identified heterogeneity between VIP and GRP neurons, and among VIP neurons, provides a basic map for understanding the cryptic network structure from dorsal AVP neurons to receiver ventral SCN.