Brain prolactin is involved in stress-induced REM sleep rebound

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dc.citation.volume89
dc.contributor.authorMachado, Ricardo Borges
dc.contributor.authorRocha, Murilo Ramos [UNIFESP]
dc.contributor.authorSuchecki, Deborah [UNIFESP]
dc.coverageSan Diego
dc.date.accessioned2020-07-17T14:02:46Z
dc.date.available2020-07-17T14:02:46Z
dc.date.issued2017
dc.description.abstractREM sleep rebound is a common behavioural response to some stressors and represents an adaptive coping strategy. Animals submitted to multiple, intermittent, footshock stress (FS) sessions during 96 h of REM sleep deprivation (REMSD) display increased REM sleep rebound (when compared to the only REMSD ones, without FS), which is correlated to high plasma prolactin levels. To investigate whether brain prolactin plays a role in stress-induced REM sleep rebound two experiments were carried out. In experiment 1, rats were either not sleep-deprived (NSD) or submitted to 96 h of REMSD associated or not to FS and brains were evaluated for PRL immunoreactivity (PRL-ir) and determination of PRL concentrations in the lateral hypothalamus and dorsal raphe nucleus. In experiment 2, rats were implanted with cannulas in the dorsal raphe nucleus for prolactin infusion and were sleep-recorded. REMSD associated with FS increased PRL-ir and content in the lateral hypothalamus and all manipulations increased prolactin content in the dorsal raphe nucleus compared to the NSD group. Prolactin infusion in the dorsal raphe nucleus increased the time and length of REM sleep episodes 3 h after the infusion until the end of the light phase of the day cycle. Based on these results we concluded that brain prolactin is a major mediator of stress-induced REMS. The effect of PRL infusion in the dorsal raphe nucleus is discussed in light of the existence of a bidirectional relationship between this hormone and serotonin as regulators of stress induced REM sleep rebound. (C) 2016 Elsevier Inc. All rights reserved.en
dc.description.affiliationUniv Ibirapuera, Psychosomat Res Grp, Dept Psychol, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Ibirapuera, Dept Pharm, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Psychobiol, Escola Paulista Med, Sao Paulo, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Psychobiol, Escola Paulista Med, Sao Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFAPESP
dc.description.sponsorshipCNPq
dc.description.sponsorshipFAPESP
dc.description.sponsorshipCNPq
dc.description.sponsorshipIDFAPESP: 98/14303-3
dc.description.sponsorshipIDCNPq: 486769/2013-5
dc.description.sponsorshipIDFAPESP: 2010/09087-3
dc.description.sponsorshipIDCNPq: 302294/2012-0
dc.format.extent38-47
dc.identifierhttp://dx.doi.org/10.1016/j.yhbeh.2016.12.004
dc.identifier.citationHormones And Behavior. San Diego, v. 89, p. 38-47, 2017.
dc.identifier.doi10.1016/j.yhbeh.2016.12.004
dc.identifier.issn0018-506X
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/55009
dc.identifier.wosWOS:000398007000005
dc.language.isoeng
dc.publisherAcademic Press Inc Elsevier Science
dc.relation.ispartofHormones And Behavior
dc.rightsAcesso restrito
dc.subjectREM sleep deprivationen
dc.subjectStressen
dc.subjectProlactinen
dc.subject5-HTen
dc.subjectHypothalamusen
dc.subjectDorsal raphe nucleusen
dc.titleBrain prolactin is involved in stress-induced REM sleep rebounden
dc.typeArtigo
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