Learning deficits induced by sleep deprivation and recovery are not associated with altered [H-3]muscimol and [H-3]flunitrazepam binding

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dc.contributor.authorDubiela, Francisco Paulino [UNIFESP]
dc.contributor.authorOliveira, MGM
dc.contributor.authorMoreira, K. M.
dc.contributor.authorNobrega, J. N.
dc.contributor.authorTufik, S.
dc.contributor.authorHipólide, Débora Cristina [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionCtr Addict & Mental Hlth
dc.date.accessioned2016-01-24T12:37:43Z
dc.date.available2016-01-24T12:37:43Z
dc.date.issued2005-03-10
dc.description.abstractSeveral studies have shown that sleep deprivation produces deficits in learning tasks, but mechanisms underlying these effects remain unclear. Other lines of evidence indicate an involvement of brain GABA systems in cognitive processes. Here, we investigated the possibility that alterations in GABA(A) or benzodiazepine (BDZ) receptor binding might underlie avoidance deficits induced by sleep deprivation. Rats were deprived of sleep for 96 h using the platform method and then trained in a step-through inhibitory avoidance task, or allowed to recover sleep for 24 h before training (sleep rebound group). Thirty minutes after training, animals were given a retention test. Both sleep-deprived and sleep-recovered animals showed a significant impairment in avoidance responding compared to cage controls, and the sleep-deprived group performed significant worse than the sleep-recovered group. A separate group of animals was sacrificed either immediately after 96 h of sleep deprivation or after 96 h of sleep deprivation followed by 24 h of sleep recovery. [H-3]muscimol and [H-3]flunitrazepam binding were examined by quantitative autoradiography in 42 brain regions, including areas involved in cognitive processes. No significant differences among groups were found in any brain region, except for a reduction in [H-3]flunitrazepam binding in the frontal cortex of sleep-recovered animals. These results confirm the deleterious effects of sleep loss on inhibitory avoidance learning, but suggest that such deficits cannot be attributed to altered GABA(A) or BDZ binding in brain. (c) 2005 Elsevier B.V. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, Brazil
dc.description.affiliationCtr Addict & Mental Hlth, Neuroimaging Sect, Toronto, ON, Canada
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent157-163
dc.identifierhttp://dx.doi.org/10.1016/j.brainres.2005.01.005
dc.identifier.citationBrain Research. Amsterdam: Elsevier B.V., v. 1037, n. 1-2, p. 157-163, 2005.
dc.identifier.doi10.1016/j.brainres.2005.01.005
dc.identifier.issn0006-8993
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/28194
dc.identifier.wosWOS:000228251400019
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofBrain Research
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectsleep deprivationen
dc.subjectGABAen
dc.subjectreceptor autoradiographyen
dc.subjectinhibitory avoidance learningen
dc.titleLearning deficits induced by sleep deprivation and recovery are not associated with altered [H-3]muscimol and [H-3]flunitrazepam bindingen
dc.typeinfo:eu-repo/semantics/article
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