Different mechanisms mediate beta-endorphin- and morphine-induced inhibition of the tail-flick response in rats

The studies were done to determine whether inhibition of the tail-flick response induced by beta-endorphin and morphine microinjected into periaqueductal central gray (CG) was mediated by stimulating different types of opioid receptors and by activating different descending pain modulatory systems in rats. beta-Endorphin (0.3-20 micrograms) or morphine (0.3-20 micrograms) microinjected bilaterally into CG produced a dose-dependent inhibition of the tail-flick response. Naloxone (0.3-3 micrograms) injected into CG was more effective in antagonizing inhibition of the tail-flick response induced by CG administered morphine than by beta-endorphin. beta-Endorphin-(1-27) (3 micrograms) injected CG effectively antagonized CG beta-endorphin-induced inhibition of the tail-flick response but slightly potentiated CG morphine-induced inhibition. Intrathecal injection of naloxone (0.3-30 micrograms) dose-dependently reversed inhibition of the tail-flick response induced by beta-endorphin (2 micrograms) but not by morphine (4 micrograms) injected into CG. On the other hand, yohimbine (0.3-30 micrograms) injected intrathecally dose-dependently antagonized inhibition of the tail-flick response induced by morphine (4 micrograms) but not by beta-endorphin (2 micrograms) given into CG. It was concluded that beta-endorphin and morphine produce inhibitions of the tail-flick response by stimulating epsilon and mu opioid receptors, respectively, and the descending pain modulatory system activated by beta-endorphin from CG involves spinal opioid receptors but not alpha-2 adrenoceptors whereas the descending system activated by morphine from CG involves spinal alpha-2 adrenoceptors but not opioid receptors.