Corticosteroid receptor signalling modes and stress adaptation in the brain
Identifieur interne : 001076 ( Main/Corpus ); précédent : 001075; suivant : 001077Corticosteroid receptor signalling modes and stress adaptation in the brain
Auteurs : Onno C. MeijerSource :
- Hormone Molecular Biology and Clinical Investigation [ 1868-1883 ] ; 2011-02-01.
Abstract
Adrenal glucocorticoid hormones modulate neuronal activity to support an adaptive response to stress. They modulate brain circuitry mediating physiological responses, emotion and cognitive processing. Chronically elevated glucocorticoid exposure is however linked to the development of mental disease. Glucocorticoid effects depend on mineralo- and glucocorticoid receptors, which are powerful transcription factors, but also can act via a diversity of non-genomic mechanisms. Here, I review generic factors that determine neuronal glucocorticoid sensitivity, in relation to brain function. First, pre-receptor mechanisms determine ligand availability. Second, there may be considerable variation in the receptor splice- and translation variants. Third, other transcription factors and many transcriptional coregulators interact with steroid receptors, determining nature and magnitude of steroid responses, in part through epigenetic regulation of DNA accessibility. Which factors underlie adaptive and pathogenic effects of stress hormones is largely unknown. Genome-wide identification of the receptor-DNA interactions in specific behavioural and physiological contexts provides a way of assessing the complete genomic range of glucocorticoid modes of action. Novel ligands that induce selective activation of particular receptor signalling modes will aid our understanding of receptor signalling and may allow selective targeting of glucocorticoid effects in emotional or cognitive domains, in research and, hopefully, in clinical settings.
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DOI: 10.1515/HMBCI.2011.114
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Meijer, Division of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research and Leiden University Medical Center, PO Box 9503, 2300 RA Leiden, The Netherlands Phone: +31 71 5276070, Fax: +31 71 5274715</corresp></author-notes><pub-date pub-type="ppub"><day>01</day><month>02</month><year>2011</year><string-date>October 2011</string-date></pub-date><volume>7</volume><issue>2</issue><issue-title>Issue 2: Special issue Hormones and the Brain - Part A – August</issue-title><fpage>317</fpage><lpage>326</lpage><history><date date-type="received"><day>6</day><month>6</month><year>2011</year></date><date date-type="accepted"><day>11</day><month>7</month><year>2011</year></date></history><permissions><copyright-statement>©2011 by Walter de Gruyter Berlin Boston</copyright-statement><copyright-year>2011</copyright-year></permissions><related-article related-article-type="pdf" xlink:href="hmbci.2011.114.pdf"></related-article><abstract><title>Abstract</title><p>Adrenal glucocorticoid hormones modulate neuronal activity to support an adaptive response to stress. 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Genome-wide identification of the receptor-DNA interactions in specific behavioural and physiological contexts provides a way of assessing the complete genomic range of glucocorticoid modes of action. Novel ligands that induce selective activation of particular receptor signalling modes will aid our understanding of receptor signalling and may allow selective targeting of glucocorticoid effects in emotional or cognitive domains, in research and, hopefully, in clinical settings.</p></abstract><kwd-group><title>Keywords</title><kwd>brain</kwd><x>, </x><kwd>coregulators</kwd><x>, </x><kwd>glucocorticoids</kwd><x>, </x><kwd>selective receptor modulators</kwd><x>, </x><kwd>stress</kwd><x>, </x><kwd>transcription</kwd></kwd-group><counts><fig-count count="1"></fig-count><table-count count="0"></table-count><ref-count count="98"></ref-count></counts></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Corticosteroid receptor signalling modes and stress adaptation in the brain</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Corticosteroid receptor signalling modes and stress adaptation in the brain</title></titleInfo><name type="personal"><namePart type="given">Onno C.</namePart><namePart type="family">Meijer</namePart><affiliation>Division of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research and Leiden University Medical Center, Leiden, The Netherlands</affiliation><affiliation>E-mail: o.meijer@lacdr.leidenuniv.nl</affiliation></name><typeOfResource>text</typeOfResource><genre type="review-article">review-article</genre><subject><genre>heading</genre><topic>Review Articles</topic></subject><originInfo><publisher>Walter de Gruyter</publisher><dateIssued encoding="w3cdtf">2011-02-01</dateIssued><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="references">98</extent></physicalDescription><abstract lang="en">Adrenal glucocorticoid hormones modulate neuronal activity to support an adaptive response to stress. They modulate brain circuitry mediating physiological responses, emotion and cognitive processing. Chronically elevated glucocorticoid exposure is however linked to the development of mental disease. Glucocorticoid effects depend on mineralo- and glucocorticoid receptors, which are powerful transcription factors, but also can act via a diversity of non-genomic mechanisms. Here, I review generic factors that determine neuronal glucocorticoid sensitivity, in relation to brain function. First, pre-receptor mechanisms determine ligand availability. Second, there may be considerable variation in the receptor splice- and translation variants. Third, other transcription factors and many transcriptional coregulators interact with steroid receptors, determining nature and magnitude of steroid responses, in part through epigenetic regulation of DNA accessibility. Which factors underlie adaptive and pathogenic effects of stress hormones is largely unknown. 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