{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T23:47:23Z","timestamp":1794008843827,"version":"4.8.0"},"reference-count":33,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,8,14]],"date-time":"2006-08-14T00:00:00Z","timestamp":1155513600000},"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":[[2006,11]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> A retino\u2010hypothalamic\u2010sympathetic pathway drives the nocturnal surge of pineal melatonin production that determines the synchronization of pineal function with the environmental light\/dark cycle. In many studies, melatonin has been implicated in the modulation of the inflammatory response. However, scant information on the feedback action of molecules present in the blood on the pineal gland during the time course of an inflammatory response is available. Here we analyzed the effect of tumor necrosis factor\u2010<jats:italic>\u03b1<\/jats:italic> (TNF\u2010<jats:italic>\u03b1<\/jats:italic>) and corticosterone on the transcription of the <jats:italic>Aa\u2010nat<\/jats:italic>, <jats:italic>hiomt<\/jats:italic> and <jats:italic>14\u20103\u20103<\/jats:italic> protein genes in denervated pineal glands of rats stimulated for 5\u2003hr with norepinephrine, using real\u2010time reverse transcription\u2010polymerase chain reaction. The transcription of <jats:italic>Aa\u2010nat<\/jats:italic>, a gene encoding the key enzyme in melatonin biosynthesis, together with the synthesis of the melatonin precursor <jats:italic>N<\/jats:italic>\u2010acetylserotonin, was inhibited by TNF\u2010<jats:italic>\u03b1<\/jats:italic>. This inhibition was transient, and a preincubation of TNF\u2010<jats:italic>\u03b1<\/jats:italic> for more than 24\u2003hr had no detectable effect. In fact, a protein(s) transcribed, later on, as shown by cycloheximide, was responsible for the reversal of the inhibition of <jats:italic>Aa\u2010nat<\/jats:italic> transcription. In addition, corticosterone induced a potentiation of norepinephrine\u2010induced <jats:italic>Aa\u2010nat<\/jats:italic> transcription even after 48\u2003hr of incubation. These data support the hypothesis that the nocturnal surge in melatonin is impaired at the beginning of an inflammatory response and restored either during the shutdown of an acute response or in a chronic inflammatory pathology. Here, we introduce a new molecular pathway involved in the feedback of an inflammatory response on pineal activity, and provide a molecular basis for understanding the expression of circadian timing in injured organisms.<\/jats:p>","DOI":"10.1111\/j.1600-079x.2006.00373.x","type":"journal-article","created":{"date-parts":[[2006,8,14]],"date-time":"2006-08-14T12:50:50Z","timestamp":1155559850000},"page":"344-350","source":"Crossref","is-referenced-by-count":94,"title":["Effect of TNF\u2010<i>\u03b1<\/i> on the melatonin synthetic pathway in the rat pineal gland: basis for a \u2018feedback\u2019 of the immune response on circadian timing"],"prefix":"10.1111","volume":"41","author":[{"given":"Pedro A.C.M.","family":"Fernandes","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erika","family":"Cecon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Regina 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