• A Rodenbeck.
• Institut für Physiologie, Abt. Schlafmedizin, Charité-Universitätsmedizin Berlin, Sankt-Hedwig-Krankenhaus, Große Hamburger Strasse 5-11, Berlin, Germany. arodenb@gwdg.de
• Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2011 Dec 1; 54 (12): 1270-5.

AbstractElectrophysiologically measurable sleep is divided into rapid eye movement (REM) sleep and nonREM sleep--the latter is further structured into several sleep stages, including deep sleep. This internal sleep regulation is explained by the reciprocal interaction model that was validated in 1975. The interdependence of not only the reciprocal discharge of cholinergic REM-on, but also serotonergic and noradrenergic (REM-off) cell populations distributed over the brain stem results in the alternating pattern of nonREM and REM sleep. The timing of sleep onset and waking is described using the two-process model. Thereby, the theoretical sum of all circadian processes (process C) interacts with the homeostatic sleep drive (process S). Because the occurrence of REM sleep also depends on circadian factors, the decrease of deep sleep during the night is accepted as a physiological correlate of process S. Social activity and daylight synchronize the circadian process with the external 24-h day. With the help of the orexin system, the flip-flop model explains why both sleep and wake can be sustained over longer periods. Dependency on age and physiological short and long sleepers are the most prominent variations of normal sleep behavior. Newer therapeutic concepts in sleep medicine have taken into consideration these biological basics, e.g., in the selection of sleep medication and in the development of new sleep-inducing medications.

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