Evidence for delta-receptor involvement in the post-ictal antinociceptive responses to electroconvulsive shock in rats.
Studies were conducted with the putative delta-opioid receptor antagonist lCl 154,129 (lCl) and the putative mu-receptor antagonist beta-funaltrexamine (beta-FNA) to investigate their ability to block the acute opioid-like effects of a single electroconvulsive shock (ECS). lCl, but not beta-FNA, attenuated the increase in hot-plate escape latencies seen following ECS. From these data, we conclude that ECS activates endogenous opioids which act upon delta rather than mu receptors to result in an increase in hot-plate escape latencies.
D000818:Animals; D004597:Electroshock; D004743:Enkephalin, Leucine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004924:Escape Reaction / Q000187:drug effects; D006358:Hot Temperature; D008297:Male; D009270:Naloxone / Q000031:analogs & derivatives*; D009271:Naltrexone / Q000031:analogs & derivatives* / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology*; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000502:physiology*; D017465:Receptors, Opioid, delta
D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D017465:Receptors, Opioid, delta; D009270:Naloxone; D004743:Enkephalin, Leucine; D009271:Naltrexone; C024524:beta-funaltrexamine; C036405:ICI 154129