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去甲纳曲酮可减少剥夺和阿片类药物引起的进食。

Nor-binaltorphimine decreases deprivation and opioid-induced feeding.

作者信息

Levine A S, Grace M, Billington C J, Portoghese P S

机构信息

Neuroendocrine Research Laboratory (151), Veterans Administration Medical Center, Minneapolis, MN 55417.

出版信息

Brain Res. 1990 Nov 26;534(1-2):60-4. doi: 10.1016/0006-8993(90)90112-o.

Abstract

We evaluated the effect of the kappa antagonist, nor-binaltorphimine (nor-BNI) on deprivation and opioid-induced feeding in rats. Intracerebroventricular administration of nor-BNI (100 nmol) decreased deprivation-induced feeding for as long as 24 h, albeit in a fairly weak manner (maximum decrease of approximately 28%). Nor-BNI (1, 10 and 100 nmol) decreased feeding induced by the kappa ligand U-50,488H by as much as 85% during the first hour of the study. This kappa antagonist also decreased feeding induced by the delta agonist DSLET and the mu agonist DAMGO. Based on previous studies indicating that nor-BNI is a selective kappa antagonist, we conclude that not only U-50,488H (kappa), but also DSLET (delta) and DAMGO (mu)-induced feeding are dependent upon an active kappa receptor.

摘要

我们评估了κ阿片受体拮抗剂去甲二氢吗啡酮(nor-BNI)对大鼠禁食及阿片类药物诱导进食的影响。脑室内注射nor-BNI(100 nmol)可使禁食诱导的进食减少长达24小时,尽管作用相当微弱(最大减少约28%)。在研究的第一个小时内,nor-BNI(1、10和100 nmol)可使κ配体U-50,488H诱导的进食减少多达85%。这种κ阿片受体拮抗剂还可减少δ激动剂DSLET和μ激动剂DAMGO诱导的进食。基于先前表明nor-BNI是一种选择性κ阿片受体拮抗剂的研究,我们得出结论,不仅U-50,488H(κ),而且DSLET(δ)和DAMGO(μ)诱导的进食都依赖于活性κ阿片受体。

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