Does melatonin modulate beta-endorphin, corticosterone, and pain threshold?

Converging lines of evidence suggest that the pineal hormone, melatonin, ma y regulate changes in pain threshold by modulating fluctuations in opioid r eceptor expression and levels of beta-endorphin (beta-END). This study inve stigated whether the circadian oscillation in plasma melatonin is involved in the modulation of plasma beta-END immunoreactivity (beta-END-ir), and wh ether fluctuations in pain threshold measured using the hotplate test are c ontingent upon the fluctuation of these two hormones in Rattus Norvegicus. The role of melatonin was explored using light-induced functional pinealect omy (LFPX) to suppress nocturnal melatonin release. Pinealectomized rats we re found to have significantly elevated levels of beta-END-ir compared to c ontrol animals at both photophase (398 +/- 89 pg/ml versus 180 +/- 23 pg/ml ) and scotophase (373 +/- 45 pg/ml versus 203 +/- 20 pg/ml) test-periods, t hus supporting the putative melatonin-opioid axis. Similarly, latency to pa in threshold of LFPX rats was significantly longer when compared to control animals at photophase (7.3 +/- 1.4 sec versus 4.8 +/- 0.7 sec) and scotoph ase (6.3 +/- 0.7 sec versus 5.1 +/- 0.7 sec). Previous studies have produce d conflicting data regarding the role of the pineal system in modulating le vels of corticosterone (CORT). We observed a moderate, but non-significant, increase in the CORT concentration of LFPX rats during the photophase test period.