Source:http://linkedlifedata.com/resource/pubmed/id/10719064
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0006104,
umls-concept:C0010124,
umls-concept:C0021753,
umls-concept:C0032005,
umls-concept:C0033684,
umls-concept:C0036667,
umls-concept:C0038435,
umls-concept:C0205178,
umls-concept:C0229671,
umls-concept:C0312418,
umls-concept:C0871261,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
2
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pubmed:dateCreated |
2000-5-9
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pubmed:abstractText |
Activation of peripheral immune cells leads to increases of interleukin-1beta (IL-1beta) mRNA, immunoreactivity, and protein levels in brain and pituitary. Furthermore, IL-1beta in brain plays a role in mediating many of the behavioral, physiological, and endocrine adjustments induced by immune activation. A similarity between the consequences of immune activation and exposure to stressors has often been noted, but the potential relationship between stress and brain IL-1beta has received very little attention. A prior report indicated that exposure to inescapable tailshocks (IS) raised levels of brain IL-1beta protein 2 h after IS, but only in adrenalectomized (and basal corticosterone replaced) subjects. The studies reported here explore this issue in more detail. A more careful examination revealed that IL-1beta protein levels in hypothalamus were elevated by IS in intact subjects, although adrenalectomy, ADX (with basal corticosterone replacement) exaggerated this effect. IL-1beta protein increases were already present immediately after the stress session, both in the hypothalamus and in other brain regions in adrenalectomized subjects, and no longer present 24 h later. Furthermore, IS elevated levels of IL-1beta protein in the pituitary, and did so in both intact and adrenalectomized subjects. IS also produced increased blood levels of IL-1beta, but only in adrenalectomized subjects. Finally, the administration of corticosterone in an amount that led to blood levels in adrenalectomized subjects that match those produced by IS, inhibited the IS-induced rise in IL-1beta in hypothalamus and pituitary, but not in other brain regions or blood.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
24
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pubmed:volume |
859
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
193-201
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10719064-Adrenalectomy,
pubmed-meshheading:10719064-Animals,
pubmed-meshheading:10719064-Brain,
pubmed-meshheading:10719064-Corticosterone,
pubmed-meshheading:10719064-Interleukin-1,
pubmed-meshheading:10719064-Male,
pubmed-meshheading:10719064-Pituitary Gland,
pubmed-meshheading:10719064-Rats,
pubmed-meshheading:10719064-Rats, Sprague-Dawley,
pubmed-meshheading:10719064-Stress, Physiological,
pubmed-meshheading:10719064-Time Factors
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pubmed:year |
2000
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pubmed:articleTitle |
Timecourse and corticosterone sensitivity of the brain, pituitary, and serum interleukin-1beta protein response to acute stress.
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pubmed:affiliation |
Department of Psychology, Campus box 345, University of Colorado, Boulder, CO, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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