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We have used the brain lesion method and chronically maintained cats to elucidate the contribution of key encephalic structures to the control of REM sleep. The results indicate that the physiological processes that participate in REM sleep generation and maintenance are all located in the pons, with the exception of those involved in REM sleep homeostasis. As we have shown, after a mesencephalic transection, REM sleep-deprived cats show a strong REM sleep pressure, but rebound does not occur. This finding indicates that the pontine mechanisms are modulated by a complex forebrain system, which, as we have shown, originates in the neocortex and has a powerful diencephalic stage. Part of this descending influence is a permissive mechanism for REM sleep rebound, which probably originates in the hypothalamus. Therefore the ultimate control of REM sleep rebound originates in the forebrain. This makes sense because it allows for a needed tight coupling with NREM sleep, which, as is well known, is also controlled by the forebrain. We have demonstrated that the electrocortical desynchronization induced by REM sleep is stronger that the one seen during waking (W), and this allows for REM sleep to accomplish what, we believe, is perhaps an REM sleep main function, i.e., to maintain the continuity of true sleep (S) given the limited duration of NREM sleep periods (by co-opting W at the end of NREM sleep periods).