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dc.creatorFilipović, Dragana
dc.creatorGavrilović, Ljubica
dc.creatorDronjak, Slađana
dc.creatorRadojčić, Marija
dc.date.accessioned2018-03-01T19:36:34Z
dc.date.available2018-03-01T19:36:34Z
dc.date.issued2005
dc.identifier.issn0302-282X
dc.identifier.issn1423-0224
dc.identifier.urihttps://vinar.vin.bg.ac.rs/handle/123456789/2871
dc.description.abstractThe pattern and intensity of glucocorticoid receptor (GR) and heat shock 70 protein (Hsp 70) changes in the hippocampus and brain cortex of adult Wistar rat males exposed to acute (immobilization, cold) and chronic (social isolation, crowding, daily swimming) stress or their combinations were followed by Western immunoblotting. Plasma ACTH and CORT were measured by chemiluminescent method and RIA. A significant decrease in cytosol GR and Hsp 70 was observed after acute stress, while chronic stresses led to negligible changes in both these proteins and caused a reduced responsiveness to a novel acute stress. This was valid irrespective of the type of chronic or acute stress combinations for both hippocampal and cortical GR and Hsp 70. The results support the hypothesis that chronic stress-induced deregulation of the LHPA axis may be caused, at least in part, by partial disruption of intracelullar negative feedback control in the higher centers of the brain. Copyright (C) 2005 S. Karger AG, Basel.en
dc.rightsrestrictedAccessen
dc.sourceNeuropsychobiologyen
dc.subjectstressen
dc.subjectglucocorticoid receptoren
dc.subjectheat shock protein 70en
dc.subjecthippocampusen
dc.subjectbrain cortexen
dc.titleBrain glucocorticoid receptor and heat shock protein 70 levels in rats exposed to acute, chronic or combined stressen
dc.typearticleen
dcterms.abstractФилиповић Драгана; Гавриловић Љубица; Дроњак Слађана; Радоичић Марија;
dc.citation.volume51
dc.citation.issue2
dc.citation.spage107
dc.citation.epage114
dc.identifier.wos000227789600008
dc.identifier.doi10.1159/000084168
dc.citation.rankM22
dc.identifier.pmid15741752
dc.type.versionpublishedVersion
dc.identifier.scopus2-s2.0-17144396312


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