Abnormalities of REM sleep, i.e. shortening of REM latency, lengthenin
g of the duration of the first REM period and heightening of REM densi
ty, which are frequently observed in patients with a Major Depressive
Disorder (MDD), have attracted considerable interest. Initial hopes th
at these aberrant patterns of sleep constitute specific markers for th
e primary/endogenous subtype of depression have not been fulfilled. Th
e specificity of REM sleep disinhibition for depression in comparison
to other psychopathological groups is also challenged. Demographic var
iables like age and sex exert strong influences on sleep physiology an
d must be controlled when searching for specific markers of depressed
sleep. It is still an open question whether abnormalities of sleep are
statemarkers or trait-markers of depression. Beyond baseline studies,
the cholinergic REM induction test (CRIT) indicated a heightened resp
onsitivity of the REM sleep system to cholinergic challenge in depress
ion compared with healthy controls and other psychopathological groups
, with the exception of schizophrenia. A special role for REM sleep in
depression is supported by the well known REM sleep suppressing effec
t of most antidepressants. The antidepressant effect of selective REM
deprivation by awakenings stresses the importance of mechanisms involv
ed in REM sleep regulation for the understanding of the pathophysiolog
y of depressive disorders. The positive effect of total sleep deprivat
ion on depressive mood which can be reversed by daytime naps, furtherm
ore emphasizes relationships between sleep and depression. Experimenta
l evidence as described above instigated several theories like the REM
deprivation hypothesis, the 2-process model and the reciprocal intera
ction model of nonREM-REM sleep regulation to explain the deviant slee
p pattern of depression. The different models will be discussed with r
eference to empirical data gathered in the field.