Selective protection of benzomorphan binding sites against inactivation by N-ethylmaleimide. Evidence for kappa-opioid receptors in frog brain.
Selective binding of [3H]bremazocine and [3H]-ethylketocyclazocine to kappa-opioid receptor sites in frog (Rana esculenta) brain membranes is irreversibly inactivated by the sulfhydryl group alkylating agent N-ethylmaleimide (NEM). Pretreatment of the membranes with kappa-selective compounds [ethylketocyclazocine (EKC), dynorphin (1-13), or U-50,488H] but not with [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAGO; mu specific ligand) or [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DADLE; delta specific ligand) strongly protects the binding of the radioligands against NEM inactivation. These results provide more evidence for the existence of kappa-opioid receptors in frog brain. The relatively high concentrations of NEM that are needed to decrease the specific binding of [3H]bremazocine together with the observation of an almost complete protection of its binding sites by NaCl suggest that bremazocine may act as an opioid antagonist in frog brain.
D000818:Animals; D001575:Benzomorphans / Q000378:metabolism*; D001665:Binding Sites; D001921:Brain / Q000378:metabolism*; D003496:Cyclazocine / Q000031:analogs & derivatives / Q000378:metabolism; D004399:Dynorphins / Q000494:pharmacology; D016314:Ethylketocyclazocine; D005033:Ethylmaleimide / Q000494:pharmacology*; D009019:Morphinans / Q000378:metabolism*; D010446:Peptide Fragments / Q000494:pharmacology; D011893:Rana esculenta; D011957:Receptors, Opioid / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology
D001575:Benzomorphans; D009019:Morphinans; D010446:Peptide Fragments; D011957:Receptors, Opioid; D012965:Sodium Chloride; D016314:Ethylketocyclazocine; C026843:dynorphin (1-13); D004399:Dynorphins; D003496:Cyclazocine; D005033:Ethylmaleimide