백서 대뇌피질에서 (3H) Norepinephrine 유리에 대한 Mu-Opioid 수용체의 역할

• 영문명: Regulation of (3H ) Norepinephrine Release by Mu-Opioid Receptors in Rat Cortical Slices
• 발행기관: 대한신경정신의학회
• 저자명: 이강영 정영철 김기원
• 간행물 정보: 『신경정신의학』제33권 제5호, 1183~1190쪽, 전체 8쪽
• 주제분류: 의약학 > 정신과학
• 파일형태: PDF
• 발행일자: 1994.09.30

영문 초록

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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키워드

Release of (3H)NE u-opioid receptor u 1-,u 2-receptors b-FNA Naloxonazine