Literature DB >> 20889142

Sleep deprivation facilitates extinction of implicit fear generalization and physiological response to fear.

Kenichi Kuriyama1, Takahiro Soshi, Yoshiharu Kim.   

Abstract

BACKGROUND: Neuroendocrine hormones, which regulate both homeostasis and stress responses, provide homeostatic recovery and sleep suppression to brains under stress. We examined the effects of total sleep deprivation on subsequent enhancement of aversive event memory, implicit fear recognition, and fear conditioning in healthy humans.
METHODS: Three different recognitions (explicit event, implicit emotion, and physiological response) were assessed in two groups of 14 healthy young volunteers (sleep control and sleep deprived) with aversive (motor vehicle accident films) and nonaversive episodic memory stimuli. Both groups were tested on Day 1 of the experiment and again on Days 3 and 10; the sleep-deprived group was totally deprived of initial nocturnal sleep after the first trial on Day 1.
RESULTS: Event recognition performances were similar in both groups throughout the study. Implicit fear recognition remained high for aversive stimuli, with generalization of implicit fear recognition occurring for nonaversive stimuli on Day 3 in the sleep control group. Physiological fear and generalized fear responses were observed for every episode, and delayed enhancement of physiological response was only observed for misidentified aversive episodes in the sleep control group on Day 3. However, in the sleep-deprived group, generalization of implicit fear recognition for nonaversive stimuli on Day 3 and all physiological and generalized fear responses on Days 3 and 10 were comprehensively extinguished.
CONCLUSIONS: Clinically, trauma-exposed victims often experience acute insomnia, indicating that such insomnia might provide prophylactic benefits in reducing the development of posttraumatic stress disorder via extinction of the fear-magnifying effects of memory.
Copyright © 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

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Year:  2010        PMID: 20889142     DOI: 10.1016/j.biopsych.2010.08.015

Source DB:  PubMed          Journal:  Biol Psychiatry        ISSN: 0006-3223            Impact factor:   13.382


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