New data bearing on the neurobiological basis of REM sleep and on mechanisms of EEG synchronization/desynchronization are presented. The revision of the limit cycle reciprocal interaction model (LCRIM) of REM cycle control incorporates new information on monoamine inhibition of mesopontine cholinergic neurons and of cholinergic mechanisms promoting REM sleep. New data also show cortical slow-wave activity is controlled by thalamocortical neurons' membrane potential level, which, in turn, is strongly controlled during sleep by brainstem cholinergic input arising from REM-on neurons. This new knowledge leads to a neurobiologically justified integration of the LCRIM and of the two-process model of sleep control.