[Biological foundations for the use of sleep privation in the treatment of depression (author's transl)].

A cursory review of the literature reveals that the sleep characteristics of normal subjects required to nap in the morning when their central temperature and Cortisol circadian rhythms are on their rising slopes are much similar to those observed in endogenous depressive patients. From this initial observation an overview of our knowledge of the structures and mechanisms responsible for the circadian organization of REM sleep and Slow Wave Sleep (SWS) indicates that whereas the Pineal gland is likely to be involved in the REM sleep circadian organization, the Supra Chiasmatic Nuclei (SCN) as well as the Dorsal Raphe Nucleus (DRN) control both sleep stages, i.e, REM ans SWS, circadian pattern together with that of cortisol through serotoninergic mechanisms. The biochemical effects of sleep deprivation, whether total, partial or limited to REM, possibly impinge upon the three central biogenic amines which are thought to be involved in the phenomenology and/or biochemical etiopathogenesis of depressive disorders: by increasing serotonin turnover, avoiding the blockade of noradrenaline release which occurs during the REM episodes, and modifying dopamine metabolism, since the latter appears to be of importance in some of the aspects of REM sleep. The rapid onset of action of sleep deprivation could be due to a synergistic action upon these three transmitters at a moment when the auto-or postsynaptic receptors could be in a different state of sensitivity.