The sleep cycle alternates between REM (rapid eye movement) and NREM (non-rapid movement) sleep, which is a highly characteristic feature of sleep. However, the mechanisms by which this cycle is generated are totally unknown. We found that a periodic transient increase of dopamine (DA) level in the basolateral amygdala (BLA) during non-rapid eye movement (NREM) sleep terminates NREM sleep and initiates REM sleep. DA acts on dopamine receptor D2 (Drd2)-expressing neurons in the BLA to induce a transition from NREM to REM sleep. This mechanism also plays a role in cataplectic attack, which is a pathological intrusion of REM sleep into wakefulness in narcoleptics. These results show a critical role of DA signaling in the amygdala in REM sleep regulation and provide a neuronal basis of sleep cycle generation.