No evidence for a protracted change in endogenous opioid activity following chronic opiate treatment in mice: parallel recovery of cross tolerance to stress and morphine antinociception.
The involvement of central endogenous opioids in swim-induced antinociception in mice is well documented. The response is attenuated by central or systemic naloxone, displays two-way cross tolerance with morphine and is correlated with apparent occupation of central opiate receptors by endogenous ligands. Swim-induced antinociception was utilised as an in vivo model of endogenous opioid function to investigate a possible protracted functional change in endogenous opioid release or inactivation following chronic opiate treatment. Antinociceptive responses (tail-flick latency) to morphine (4.4 mg/kg, SC) and swimming were determined at various times following chronic methadone (24 days treatment, 102 mg/kg day in drinking water for the last 20 days) and chronic morphine (1 g/kg sustained release) treatment. In both experiments, parallel recovery from cross tolerance was observed for morphine-and swim-induced antinociception. These results were consistent with the view that no protracted functional change in the release or inactivation of endogenous opioids had occurred following chronic opiate treatment.
D000818:Animals; D004361:Drug Tolerance; D004723:Endorphins / Q000378:metabolism*; D005260:Female; D006801:Humans; D008691:Methadone / Q000494:pharmacology; D051379:Mice; D009020:Morphine / Q000494:pharmacology*; D009619:Nociceptors / Q000187:drug effects*; D011930:Reaction Time / Q000187:drug effects; D013315:Stress, Psychological / Q000503:physiopathology*
D004723:Endorphins; D009020:Morphine; D008691:Methadone