Degree Type

Dissertation

Date of Award

1990

Degree Name

Doctor of Philosophy

Department

Psychology

First Advisor

Richard A. Hughes

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.

DOI

https://doi.org/10.31274/rtd-180813-10295

Publisher

Digital Repository @ Iowa State University, http://lib.dr.iastate.edu/

Copyright Owner

Kenneth Joseph Sufka

Language

en

Proquest ID

AAI9035118

File Format

application/pdf

File Size

67 pages

Share

COinS