Abstract
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.
Published Version
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