Possible medullary kappa hyperalgesic mechanism. I. A new potential role for endogenous opioid peptides in pain perception.
The kappa-agonist, ethylketazocine, produces hyperalgesia in the acutely decerebrated dog as indicated by a shortening of the skin twitch reflex latency whereas fentanyl is inactive. Naloxone produces analgesia and antagonizes the hyperalgesic effect of ethylketazocine. Spinal cord transection decreases the latency of the skin twitch reflex and allowed the analgesic effect of fentanyl and ethylketazocine on this nociceptive reflex to become manifest. These observations indicate that there is a non-opioid analgesic and kappa hyperalgesic mechanism present in the pontine-medullary region of the dog brainstem. It suggests that the hyperalgesic mechanism is mediated by an endogenous kappa-opioid peptide and that the analgesic effect of naloxone is in part related to antagonism of the activity of this hyperalgesia producing opioid peptide.
D000818:Animals; D003496:Cyclazocine / Q000031:analogs & derivatives / Q000494:pharmacology; D004285:Dogs; D004399:Dynorphins; D004723:Endorphins / Q000494:pharmacology / Q000502:physiology*; D016314:Ethylketocyclazocine; D008526:Medulla Oblongata / Q000502:physiology*; D009270:Naloxone / Q000494:pharmacology; D010146:Pain / Q000503:physiopathology*; D011957:Receptors, Opioid / Q000187:drug effects*; D012018:Reflex / Q000187:drug effects
D004723:Endorphins; D011957:Receptors, Opioid; D009270:Naloxone; D016314:Ethylketocyclazocine; D004399:Dynorphins; D003496:Cyclazocine