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阿片类药物的激励特性:δ受体激活介导强化过程的证据。

Motivational properties of opioids: evidence that an activation of delta-receptors mediates reinforcement processes.

作者信息

Shippenberg T S, Bals-Kubik R, Herz A

机构信息

Department of Neuropharmacology, Max-Planck-Institut für Psychiatrie, Planegg-Martinsried, F.R.G.

出版信息

Brain Res. 1987 Dec 15;436(2):234-9. doi: 10.1016/0006-8993(87)91667-2.

DOI:10.1016/0006-8993(87)91667-2
PMID:2829990
Abstract

The role of central delta-opioid receptors in the mediation of opioid reinforcement and endogenous reward processes was examined using a non-biased place-preference conditioning procedure. Intracerebroventricular (i.c.v.) administration of the selective delta-receptor agonist, [D-Pen2, D-Pen5]-enkephalin (DPDPE, 10.0-25.0 micrograms) produced a significant preference for the drug-associated place and a similar effect was observed following i.c.v. injections of morphine (10.0 micrograms). Administration of the delta-receptor antagonist, ICI 174,864, at doses (1.0-5.0 micrograms, i.c.v.) which had no aversive effects when tested alone, abolished the reinforcing properties of DPDPE. Such treatment did not, however, modify the effect of morphine. These findings demonstrate the involvement delta- as well as mu-receptors in the motivational properties of opioids and suggest that the activation of either receptor type is sufficient for the elicitation of appetitively reinforcing effects.

摘要

使用无偏倚的位置偏好条件反射程序研究了中枢δ-阿片受体在介导阿片类药物强化作用和内源性奖赏过程中的作用。脑室内(i.c.v.)注射选择性δ-受体激动剂[D-青霉胺2,D-青霉胺5]-脑啡肽(DPDPE,10.0 - 25.0微克)产生了对药物相关位置的显著偏好,并且在脑室内注射吗啡(10.0微克)后也观察到了类似的效果。以单独测试时无厌恶作用的剂量(1.0 - 5.0微克,脑室内)给予δ-受体拮抗剂ICI 174,864,消除了DPDPE的强化特性。然而,这种处理并没有改变吗啡的作用。这些发现证明δ-受体以及μ-受体参与了阿片类药物的动机特性,并表明激活任何一种受体类型都足以引发奖赏性强化作用。

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Motivational properties of opioids: evidence that an activation of delta-receptors mediates reinforcement processes.阿片类药物的激励特性:δ受体激活介导强化过程的证据。
Brain Res. 1987 Dec 15;436(2):234-9. doi: 10.1016/0006-8993(87)91667-2.
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Evidence for delta receptor mediation of [D-Pen2,D-Pen5]-enkephalin (DPDPE) analgesia in mice.小鼠中δ受体介导[D-青霉胺2,D-青霉胺5]-脑啡肽(DPDPE)镇痛作用的证据。
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