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dc.creatorĐorđević, Ana D.
dc.creatorAdžić, Miroslav
dc.creatorĐorđević, Jelena D.
dc.creatorRadoičić, Marija B.
dc.date.accessioned2018-03-01T20:58:17Z
dc.date.available2018-03-01T20:58:17Z
dc.date.issued2009
dc.identifier.issn0300-9564 (print)
dc.identifier.issn1435-1463 (electronic)
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/3822
dc.description.abstractSuccessful adaptation to stress involves actions of glucocorticoid receptor (GR), a steroid-dependent transcription factor, abundant in hippocampus. Another transcription factor, nuclear factor kappa B (NF kappa B) is considered as an important stress sensor implicated in adaptive synaptic plasticity. Numerous stress-related genes are regulated by both hippocampal GR and NF kappa B, including neural cell adhesion molecules (NCAM and L1), involved in plasticity, and genes that encode apoptotic proteins (bax and bcl-2). We presumed that the ratio of nuclear NF kappa B to nuclear GR may determine the degree of proplastic or proapoptotic signaling under stress. To test this presumption we have investigated effects of acute, chronic and combined stress on compartmental levels and ratios of NF kappa B and GR proteins, and in parallel, changes in their mRNA expression. In addition, the expression of plasticity (NCAM, L1) and apoptotic (bax, bcl-2) genes, as well as, Bax and Bcl-2 proteins redistribution between mitochondrial and cytoplasmic compartments, were followed. When glucocorticoid levels were low, as found in chronic stress, GR was not efficiently translocated to the nucleus. This resulted in its lower nuclear level relative to the nuclear NF kappa B. Such conditions did not affect proplastic induction of NCAM mRNA, but were related to the onset of proapoptotic signaling illustrated by relocation of mitochondrial Bcl-2 protein to its soluble cytoplasmic form. Because these Bcl-2 rearrangements were not reversed by subsequent acute stress, representing more stable alterations, it is concluded that chronic social isolation of Wistar rats led to the initiation of proapoptotic signaling that may be etiologically related to compromised adaptive response of central nervous system.en
dc.rightsrestrictedAccessen
dc.sourceJournal of Neural Transmissionen
dc.subjectStressen
dc.subjectHippocampusen
dc.subjectGlucocorticoid receptoren
dc.subjectNuclear factor kappa Ben
dc.subjectPlasticityen
dc.subjectApoptosisen
dc.titleChronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampusen
dc.typearticleen
dcterms.abstractЂорђевић Aна Д; Aджић Мирослав; Ђорђевић Јелена Д.; Радоичић Марија;
dc.citation.volume116
dc.citation.issue12
dc.citation.spage1579
dc.citation.epage1589
dc.identifier.wos000271750300004
dc.identifier.doi10.1007/s00702-009-0286-x
dc.citation.rankM22
dc.identifier.pmid19669692
dc.identifier.scopus2-s2.0-70949092301


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