Since the discovery of rapid eye movement (REM) sleep (also known as paradoxical sleep; PS), it is accepted that sleep is an active process. PS is characterized by EEG rhythmic activity resembling that of waking with a disappearance of muscle tone and the occurrence of REMs, in contrast to slow-wave sleep (SWS, also known as non-REM sleep) identified by the presence of delta waves. I will describe an updated integrated model of the mechanisms responsible for the onset and maintenance of PS. This model introduces the notion that the entrance and exit of PS are induced by different mechanisms. I will hypothesize that the entrance from SWS to PS is due to the intrinsic activation of PS-on GABAergic neurons localized in the lateral hypothalamus, the ventrolateral periaqueductal gray and the dorsal paragigantocellular reticular nucleus. These populations of neurons would inhibit during PS all waking systems and a population of PS-off GABAergic neurons localized at the border between the ventrolateral periaqueductal gray and the mesencephalic reticular formation. This population of PS-off GABAergic neurons tonically inhibits during waking and SWS the glutamatergic neurons triggering the state of PS localized in the pontine sublaterodorsal tegmental nucleus (SLD). The exit from PS would be induced by the inhibition of the PS-on GABAergic neurons by waking systems such as the pontine and medullary noradrenergic neurons and the hypothalamic hypocretin neurons.