Role of peripheral and central opioid activity in analgesia induced by restraint stress.
Rats subjected to prolonged restraint showed an increase in tail flick latency which outlasted the period of restraint by 15 min. This restraint could be blocked but not reversed by 1 mg/kg of naltrexone hydrochloride given subcutaneously. Naltrexone methobromide, administered subcutaneously in doses of 10 or 25 mg/kg, did not block the analgesia indicating that peripheral opioid receptors were probably not involved. Naltrexone hydrochloride was shown to have no effect on brain tryptophan uptake in restrained rats, a neurochemical event which had previously been shown to be critical to restraint-induced analgesia.
D000698:Analgesia; D000818:Animals; D001933:Brain Stem / Q000378:metabolism; D004723:Endorphins / Q000502:physiology*; D008297:Male; D009271:Naltrexone / Q000031:analogs & derivatives / Q000494:pharmacology; D000644:Quaternary Ammonium Compounds; D051381:Rats; D011957:Receptors, Opioid / Q000502:physiology; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000209:etiology / Q000503:physiopathology*; D014364:Tryptophan / Q000378:metabolism
D004723:Endorphins; D000644:Quaternary Ammonium Compounds; D011957:Receptors, Opioid; C032257:methylnaltrexone; D009271:Naltrexone; D014364:Tryptophan