Cited by 8Sleep and Wakefulness ResearchNeurotransmitter Receptor Influence on BehaviorSleep and related disorders

Serotonin and dreaming

Pace-Schott, Edward F.·2008·Serotonin and Sleep: Molecular, Functional and Clinical Aspects

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.

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Crossref · 10.1007/978-3-7643-8561-3_12

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  • The fear extinction function proposed by the NM-AND model to occur during sleep is similar in some respects to the affective contextualization function proposed for the default mode network, which partially overlaps (vmPFC, ACC) the NM-AND network and which may also be active during dreaming.

    “The fear extinction function proposed by the NM-AND model to occur during sleep is similar in some respects to the affective contextualization function proposed for the default mode network (188), which partially overlaps (vmPFC, ACC) the NM-AND network and which, intriguingly, may also be active during dreaming (189–192).”

    From The Stress Acceleration Hypothesis of Nightmares (2017) · cites this paper as [192]

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Authors
Pace-Schott, E. F.
Affiliations
Beth Israel Deaconess Medical Center (US)
Corresponding author
Pace-Schott, Edward F.
Venue
Serotonin and Sleep: Molecular, Functional and Clinical Aspects
Published
2008-03-03
Pages
307-324
OpenAlex
W1904266856
Cited by
8
References
112
Citations by year
2018: 1 · 2017: 3 · 2016: 1 · 2015: 1 · 2012: 1
FWCI
0.51
Type
book chapter
Language
en
Open access
closed
Locations
Birkhäuser Basel eBooks (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
Keywords
serotonin, dreams, selective serotonin reuptake inhibitors, REM rebound, REM latency, REM density, dream recall, hallucinogens, 5-HT2A receptor, hallucinosis

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