Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl.

Although morphine typically produces analgesia in a variety of species, recent research has identified a biological model in which morphine produces a naloxone-reversible, paradoxical hyperalgesic response to a noxious thermal stimulus in young domestic fowl. The present study examined opioid receptor-mediation of this atypical opiate effect. Patterns of morphine hyperalgesia (1.25 to 5.0 mg/kg IM) were examined on a standard hot-plate test following administration (10 micrograms/5 microliters ICV) of the mu antagonist beta-funaltrexamine, the delta antagonist naltrindole, or the kappa antagonist nor-binaltorphimine in 15-day-old White Leghorn cockerels. Respiration measures were also recorded because they are indicative of opiate effects. Morphine produced a dose-dependent decrease in mean jump latencies (i.e., hyperalgesic effect). Mu receptor antagonism attenuated this morphine-induced hyperalgesic effect. Kappa receptor antagonism attenuated morphine-induced hyperalgesia only at the highest morphine dose (i.e., 5.0 mg/kg) and delta receptor antagonism failed to attenuate morphine-induced hyperalgesia. These results suggest that morphine-induced hyperalgesia, like morphine-induced analgesia, is mediated primarily by mu receptor activation.