The author summarizes clinical data showing parallels between REM sleep
and depressive phenomena; e.g., patients with endogenous depression show a
first REM period that has a shorter than normal latency and a higher
density of eye movement. The author discusses evidence for his hypothesis
that the following commonalities in neurobiological control systems
generate these parallels: 1) brainstem norepinephrine and serotonin systems
suppress both REM sleep and depressive phenomena, 2) acetylcholine systems
promote both REM and depressive phenomena, and 3) in control of depressive
phenomena, as acetylcholine neuronal systems interact and the balance of
activity between these two systems, rather than absolute activity levels in
either, is the critical factor.Abstract Teaser