Previous studies suggested that the inhibition of high K+ -or electrically stimulated release of (3H )NE is mediated mainly by ji-opioid receptor. We tested naloxonazine, a selective ji 1-receptor irreversible antagonist, and P — funaltrexamine (p-FNA), a nonselective |i-receptor irrevesiblc antagonist, to detemine whether the agonistic effect was mediated by \x 1-or ji 2- receptors. b-FNA pretreatment produced comparable shifts in the concentration-response curves of each agonist, mostly 2 fold increase of IC 50，except Tyr-D-Arg-Phe-Sar(TAPS)(3.8 fold), and slightly reduced(6〜 17%) the maximum inhibitory effects of each agonist But, the agonists were not discriminated by b-FNA. Naloxonazine pretreatment produces shifts in the concentration-response curves for each agonists. And the maximum inhibitory effects of each agonist were inhibited. It did not antagonize the inhibitory actions of p-endorphin(b-END) (l-3l). This data suggest that subtypes of ji-opioid receptor mediate the inhibition of high K+ -stimulated release of 〔3H〕NE in rat cortex slices. And, the effects of naloxonazine pretreatment support suggestion that (3-END(l-31) acts through receptor differing from those those utilized by DAMGO, TAPS, DESLET and EKC.
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