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Curr Biol. 2011 Dec 6;21(23):2029-32. doi: 10.1016/j.cub.2011.10.052. Epub 2011 Nov 23.

REM sleep depotentiates amygdala activity to previous emotional experiences.

Author information

1
Sleep and Neuroimaging Laboratory, Department of Psychology, University of California, Berkeley, Berkeley, CA 94720-1650, USA.

Abstract

Clinical evidence suggests a potentially causal interaction between sleep and affective brain function; nearly all mood disorders display co-occurring sleep abnormalities, commonly involving rapid-eye movement (REM) sleep. Building on this clinical evidence, recent neurobiological frameworks have hypothesized a benefit of REM sleep in palliatively decreasing next-day brain reactivity to recent waking emotional experiences. Specifically, the marked suppression of central adrenergic neurotransmitters during REM (commonly implicated in arousal and stress), coupled with activation in amygdala-hippocampal networks that encode salient events, is proposed to (re)process and depotentiate previous affective experiences, decreasing their emotional intensity. In contrast, the failure of such adrenergic reduction during REM sleep has been described in anxiety disorders, indexed by persistent high-frequency electroencephalographic (EEG) activity (>30 Hz); a candidate factor contributing to hyperarousal and exaggerated amygdala reactivity. Despite these neurobiological frameworks, and their predictions, the proposed benefit of REM sleep physiology in depotentiating neural and behavioral responsivity to prior emotional events remains unknown. Here, we demonstrate that REM sleep physiology is associated with an overnight dissipation of amygdala activity in response to previous emotional experiences, altering functional connectivity and reducing next-day subjective emotionality.

PMID:
22119526
PMCID:
PMC3237718
DOI:
10.1016/j.cub.2011.10.052
[Indexed for MEDLINE]
Free PMC Article
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