Methylnalorphinium fails to reverse naloxone-sensitive stress-induced analgesia in mice.
Exposure of mice to cold-restraint stress markedly decreased the number of abdominal constrictions induced by IP acetic acid. Naloxone pretreatment significantly attenuated the antinociceptive effect of cold-restraint stress, suggesting a partial mediation by opioid mechanisms. Pretreatment with the quaternary opioid antagonist methylnalorphinium did not reverse analgesia in stressed mice. Also, nociception in both stressed and non-stressed mice was not modified by pretreatment with the selective alpha 2-adrenoceptor blocker yohimbine. The results suggest that cold-restraint stress promotes analgesia in mice which is mediated in part by opioid but not alpha 2-adrenoceptor mechanisms. Furthermore, the results do not substantiate a peripheral analgesic role for circulating opioids in this model of stress.
D000698:Analgesia; D000818:Animals; D003080:Cold Temperature; D004723:Endorphins / Q000502:physiology*; D008297:Male; D051379:Mice; D009269:Nalorphine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009420:Nervous System / Q000503:physiopathology*; D010146:Pain / Q000503:physiopathology*; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000503:physiopathology*; D009435:Synaptic Transmission; D015016:Yohimbine / Q000494:pharmacology
D004723:Endorphins; D015016:Yohimbine; D009270:Naloxone; C045365:N-methylnalorphine; D009269:Nalorphine