{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T07:03:26Z","timestamp":1792047806418,"version":"4.4.0"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2004,11,10]],"date-time":"2004-11-10T00:00:00Z","timestamp":1100044800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Pineal Research"],"published-print":{"date-parts":[[2005,4]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> In chronically inflamed animals, adrenal hormones exert a positive control on the secretion of melatonin by the pineal gland. In this paper, the mechanism of corticosterone as a modulator of melatonin and <jats:italic>N<\/jats:italic>\u2010acetylserotonin (NAS) was determined. Rat pineal glands in culture, stimulated for 5\u2003hr with noradrenaline (10\u2003n<jats:sc>m<\/jats:sc>), were previously incubated with corticosterone (1.0\u2003n<jats:sc>m<\/jats:sc>\u20131.0\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>m<\/jats:sc>) for 48\u2003hr in the presence or absence of the glucocorticoid receptor (GR) antagonist, mifepristone (1.0\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>m<\/jats:sc>), the proteasome inhibitor, <jats:italic>N<\/jats:italic>\u2010acetyl\u2010leucinyl\u2010leucinyl\u2010norleucinal\u2010H (ALLN, 12.5\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>m<\/jats:sc>) or the antagonist of the nuclear factor kappa B (NF<jats:italic>\u03ba<\/jats:italic>B), pyrrolidinedithiocarbamate (PDTC, 12.5\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>m<\/jats:sc>). Corticosterone potentiated noradrenaline\u2010induced melatonin and NAS production in a bell\u2010shaped manner. The increase in NAS (12.9\u2003\u00b1\u20032.7, n\u2003=\u20036 versus 34.3\u2003\u00b1\u20038.3\u2003ng per pineal) and melatonin (16.3\u2003\u00b1\u20032.0, n\u2003=\u20036 versus 44.3\u2003\u00b1\u200312.9\u2003ng per pineal) content induced by 1\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>m<\/jats:sc> corticosterone was blocked by mifepristone, and mimicked by ALLN and PDTC. The presence of GRs was shown by [<jats:sup>3<\/jats:sup>H]\u2010dexamethasone binding (0.30\u2003\u00b1\u20030.09\u2003pmol\/mg protein) and corticosterone inhibition of NF<jats:italic>\u03ba<\/jats:italic>B nuclear translocation was demonstrated by electromobility shift assay. Therefore, corticosterone potentiates noradrenaline\u2010induced melatonin and NAS production through GR inhibition of NF<jats:italic>\u03ba<\/jats:italic>B nuclear translocation. To the best of our knowledge, this is the first time that this relevant pathway for passive and acquired immune response is shown to modulate melatonin production in pineal gland.<\/jats:p>","DOI":"10.1111\/j.1600-079x.2004.00191.x","type":"journal-article","created":{"date-parts":[[2005,2,22]],"date-time":"2005-02-22T19:40:26Z","timestamp":1109101226000},"page":"182-188","source":"Crossref","is-referenced-by-count":72,"title":["Corticosterone modulates noradrenaline\u2010induced melatonin synthesis through inhibition of nuclear factor kappa B"],"prefix":"10.1111","volume":"38","author":[{"given":"Zulma S.","family":"Ferreira","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pedro A. C. 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