Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl
Date
Authors
Major Professor
Advisor
Committee Member
Journal Title
Journal ISSN
Volume Title
Publisher
Altmetrics
Authors
Research Projects
Organizational Units
Journal Issue
Is Version Of
Versions
Series
Department
Abstract
Morphine typically produces analgesia in a variety of species by acting as an agonist at mu and perhaps delta opioid receptors. Recent research, however, 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 development of opiate receptor antagonists with selective activity at heterogeneous populations of opioid sites may be a useful tool to differentiate the action of an opiate at a particular receptor. In this study, the hyperalgesic actions of morphine (1.25 to 5.0 mg/kg im) on a standard hot-plate test were examined following administration (10 ug/5 ul icv) of the mu antagonist beta-funaltrexamine, the delta antagonist naltrindole, or the kappa antagonist nor-binaltorphamine in 15-day old White Leghorn cockerels. Morphine produced a dose-dependent decrease in mean jump latencies (i.e., hyperalgesia). Mu receptor antagonism attenuated morphine-induced hyperalgesia. 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 support the notion that atypical morphine-induced hyperalgesia, like morphine-induced analgesia, is mediated primarily by mu receptor activation.