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dc.contributor.authorAguilar Calegare, Bruno Frederico [UNIFESP]
dc.contributor.authorFernandes, Leandro [UNIFESP]
dc.contributor.authorTufik, Sergio [UNIFESP]
dc.contributor.authorD'Almeida, Vania [UNIFESP]
dc.date.accessioned2016-01-24T13:59:45Z
dc.date.available2016-01-24T13:59:45Z
dc.date.issued2010-06-01
dc.identifierhttp://dx.doi.org/10.1016/j.psyneuen.2009.11.004
dc.identifier.citationPsychoneuroendocrinology. Oxford: Pergamon-Elsevier B.V., v. 35, n. 5, p. 775-784, 2010.
dc.identifier.issn0306-4530
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/32599
dc.description.abstractEpidemiological and experimental studies suggest a high prevalence of cognitive impairment and social behavior deficits in adolescents and adults that have experienced prenatal exposure to adverse conditions. This study investigated whether sleep deprivation during the preimplantation stage of development alters the physiological, behavioral and oxidative metabolic processes in adult male mouse offspring. One group of dams was continuously sleep-deprived using the platform technique from gestational days 0 to 3 (PSD 72). Three additional groups were sleep-deprived by gentle handling for 6 h on gestational days 1 (GH 1), 2 (GH 2) or 3 (GH 3). After sleep deprivation, homocysteine, cysteine, corticosterone, estrogen and progesterone concentrations were measured from the experimental mothers and time-matched controls. the sizes and weights of the male pups were measured at various stages throughout the experiment. At PND 90, behavioral (Activity Box and Elevated Plus Maze) and biochemical parameters were assessed. the dams' plasma progesterone concentrations decreased in the PSD 72 group, and the levels of plasma estradiol increased in GH 2. Corticosterone levels were found to increase after all sleep-deprivation procedures. Homocysteine concentrations increased in the GH 2 but decreased in the PSD 72 group. the offspring of GH 1 mothers exhibited decreased superoxide dismutase activity. Exposure to sleep deprivation had a long-lasting impact on tissue weight; in particular, there was a decrease in hemilateral epididymal fat weight in mature animals from the PSD 72 group. Although some of the alterations observed in the mothers (elevated estrogen and corticosterone levels and decreased progesterone) might have played a role in the permanent alterations in the adult offspring, they were not the main cause. the homocysteine changes detected in the sleep-deprived dams may contribute to redox changes, controlling gene expression and shaping epigenetic development. (c) 2009 Elsevier B.V. All rights reserved.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipAFIP
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent775-784
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofPsychoneuroendocrinology
dc.rightsAcesso restrito
dc.subjectSleep deprivationen
dc.subjectHomocysteineen
dc.subjectBiometric measurementsen
dc.subjectAntioxidant enzymesen
dc.subjectBehavioren
dc.subjectPregnancyen
dc.subjectMiceen
dc.titleBiochemical, biometrical and behavioral changes in male offspring of sleep-deprived miceen
dc.typeArtigo
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniversidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biosci, BR-04024002 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biosci, BR-04024002 São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: 2007/07624-9
dc.description.sponsorshipIDCNPq: 501248/2005-6
dc.identifier.doi10.1016/j.psyneuen.2009.11.004
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000278431500016


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