Control of stress-induced acth secretion by vasopressin and crh: additional evidence

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dc.contributor.authorRamos, Adriana T. [UNIFESP]
dc.contributor.authorTufik, Sergio [UNIFESP]
dc.contributor.authorTroncone, Lanfranco R. P.
dc.date.accessioned2019-01-21T10:29:56Z
dc.date.available2019-01-21T10:29:56Z
dc.date.issued2016
dc.description.abstractVasopressin and CRH have complementary roles in the secretion of ACTH following different stress modalities. The concomitant use of V-1b and CRF1 receptor antagonists completely inhibits ACTH secretion in response to different stress modalities. The combination of the CRF1 antagonist SSR125543 with the V-1b antagonist SSR149415 effectively suppressed plasma ACTH 1.30 h after injection in rats stressed by ether vapor inhalation for 1 min, restraint stress for 1 h or forced swimming for 5 min. The duration of the effect was also studied. The CRF1 antagonist effectively suppressed ACTH secretion in restraint stress, while the V-1b antagonist was effective against ether inhalation. Both antagonists were necessary to block the forced swimming stress response. SSR125543 induced a prolonged effect and can be used in a model of prolonged HPA axis blockade. (C) 2016 S. Karger AG, Baselen
dc.description.affiliationDepartment of Psychobiology, Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliationLaboratory of Pharmacology, Instituto Butantan
dc.description.affiliationLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil
dc.description.affiliationUnifespDepartment of Psychobiology, Universidade Federal de São Paulo (UNIFESP)
dc.description.sourceWeb of Science
dc.description.sponsorshipAFIP
dc.description.sponsorshipFAPESP [98/14303-3, 04/12871-7, 15/08098-5, 2013/18897-7]
dc.description.sponsorshipCAPES
dc.description.sponsorshipFundacao Butantan
dc.description.sponsorshipIDSanofi-Aventis: SSR125543
dc.description.sponsorshipIDSanofi-Aventis: SSR149415
dc.description.sponsorshipIDFAPESP: 98/14303-3
dc.description.sponsorshipIDFAPESP: 04/12871-7
dc.description.sponsorshipIDFAPESP: 15/08098-5
dc.description.sponsorshipIDFAPESP: 2013/18897-7
dc.format.extent184-190
dc.identifierhttps://doi.org/10.1159/000445480
dc.identifier.citationNeuropsychobiology. Basel, v. 73, n. 3, p. 184-190, 2016.
dc.identifier.doi10.1159/000445480
dc.identifier.issn0302-282X
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/49493
dc.identifier.wosWOS:000377996400007
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofNeuropsychobiology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectActh Secretionen
dc.subjectAnimal Modelsen
dc.subjectAnxietyen
dc.subjectCrf1 Receptoren
dc.subjectDepressionen
dc.subjectEther Inhalationen
dc.subjectForced Swimmingen
dc.subjectRestraint Stressen
dc.subjectVasopressin V-1b ReceptorV-1b Receptor Antagonisten
dc.subjectHydrochloride Ssr125543aen
dc.subjectDisordersen
dc.subjectSsr149415en
dc.subjectAntidepressanten
dc.subjectResponsesen
dc.subjectModelsen
dc.subjectSuppressionen
dc.subjectPotenten
dc.subjectRatsen
dc.titleControl of stress-induced acth secretion by vasopressin and crh: additional evidenceen
dc.typeinfo:eu-repo/semantics/article
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