Self D W, Stein L
Department of Pharmacology, College of Medicine, University of California, Irvine 92717.
Pharmacol Toxicol. 1992 Feb;70(2):87-94. doi: 10.1111/j.1600-0773.1992.tb00435.x.
Studies of the behaviourally-reinforcing actions of opioid and stimulant drugs of abuse are reviewed in an attempt to identify their reward-related brain receptors. We focus on data generated by drug self-administration, brain stimulation reinforcement, and conditioned place preference paradigms. A consistent body of evidence supports a role for mu and delta, but not kappa, receptors in opioid reward. Stimulant reward apparently involves both D1 and D2 receptors; the data favour D2 mediation of stimulant drug reinforcement with a permissive or modulatory role for D1 receptors. The reward-relevant opioid and dopamine receptors, as well as the cannabinoid (marijuana) receptor, share the ability to couple Gi proteins that mediate inhibition of adenylate cyclase and stimulation of K+ conductance. These signal transduction mechanisms thus may be generally implicated in the reinforcing properties of diverse drugs of abuse.
本文综述了阿片类药物和精神兴奋剂类滥用药物的行为强化作用的研究,旨在确定与奖励相关的脑内受体。我们重点关注药物自我给药、脑刺激奖赏和条件性位置偏爱范式所产生的数据。大量一致的证据支持μ和δ受体而非κ受体在阿片类奖赏中发挥作用。精神兴奋剂奖赏显然涉及D1和D2受体;数据支持D2介导精神兴奋剂药物强化作用,而D1受体起允许或调节作用。与奖赏相关的阿片类、多巴胺受体以及大麻素(大麻)受体,均具有与Gi蛋白偶联的能力,Gi蛋白介导腺苷酸环化酶的抑制作用及钾离子电导的刺激作用。因此,这些信号转导机制可能普遍与多种滥用药物的强化特性有关。