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Serotonin and dreaming

Edward F Pace-Schott

Birkhäuser Basel eBooks March 3, 2008 DOI: 10.1007/978-3-7643-8561-3_12 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Dreaming Serotonin
Citations 7
Key findings Reviews evidence that SSRIs can intensify dreaming despite reducing dream recall frequency, with increased dream intensity during steady-state administration and further increases during acute discontinuation, possibly due to REM rebound and brain activation during sleep.

Abstract

Many clinical anecdotes and an experimental study have reported intensification of dreaming by the selective serotonin-reuptake inhibitors (SSRIs). However, no published neurochemical dream model invokes serotonin as a dream-promoting neuromodulator or accounts for serotonergic dream enhancement. An experimental study of normal volunteers showed that, although SSRI treatment decreased dream recall frequency, several subject-rated dream-intensity measures were greater during steady-state drug administration compared with pre-drug baseline and early drug treatment. Additionally, such subject-rated dream intensity as well as dream report length and judge-rated bizarreness were greater during acute discontinuation than during pre-drug baseline and drug administration periods. Nightcap ambulatory monitor data showed increased REM latency during treatment and increased REM density during acute discontinuation, indicative of SSRI-induced REM suppression and REM rebound following drug discontinuation, respectively. The bulk of pharmacological evidence suggests that drugs that enhance serotonergic neurotransmission lighten sleep. Sleep-disruptive effects of SSRIs are accompanied by electroencephalographic and electromyographic signs of brain activation, abnormally prominent eye movements in NREM sleep, and REM rebound following drug discontinuation. Explanations of SSRI-induced dream intensification suggested by these findings include, respectively, generalized brain activation during sleep, enhanced NREM dreaming, and within-night REM rebound. Additional clues as to potential causes of serotonergic dream enhancement are provided by: (i) the cellular pharmacology of hallucinogens that act on 5-HT 2A receptors, (ii) the phenomenological and functional neuroimaging effects of serotonergic hallucinogens, and (iii) putative neurophysiological mechanisms of lesionrelated complex hallucinosis. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.