Shaik ShavaliBegonia HoPiyarat GovitrapongSaiphon SawlomAmornpan AjjimapornSirirat KlongpanichapakManuchair EbadiUND School of Medicine & Health Sciences - Northeast CampusMahidol University2018-06-212018-06-212005-01-30Brain Research Bulletin. Vol.64, No.6 (2005), 471-479036192302-s2.0-11444268808https://repository.li.mahidol.ac.th/handle/20.500.14594/17149The occurrence of systematic diurnal variations in pain thresholds has been demonstrated in human. Salivary melatonin levels change following acute pain when other factors that could explain the change have been removed or controlled. Melatonin-induced analgesia is blocked by naloxone or pinealectomy. By using selective radioligands [3H]-DAMGO, [3H]-DPDPE, [3-U69593, and 3H]-nociceptin, we have shown that the bovine pinealocytes contain delta and mu, but not kappa or ORL1 opioid receptor subtypes. In the present study, by using melatonin receptor agonists (6-chloromelatonin or 2-iodo-N-butanoyl-5- methoxytryptamine) or melatonin receptor antagonist (2-phenylmelatonin), we have shown that these agents do not compete with opioid receptor subtypes. However, we observed a time-dependent release of β-endorphin an endogenous opioid peptide, by melatonin from mouse pituitary cells in culture. Hence, it is suggested that melatonin exerts its analgesic actions not by binding to opioid receptor subtypes but by binding to its own receptors and increasing the release of β-endorphin. © 2004 Elsevier Inc. All rights reserved.Mahidol UniversityNeuroscienceArticleSCOPUS10.1016/j.brainresbull.2004.09.008