Bals-Kubik R, Shippenberg T S, Herz A
Department of Neuropharmacology, Max Planck Institute for Psychiatry, Planegg-Martinsried, F.R.G.
Eur J Pharmacol. 1990 Jan 3;175(1):63-9. doi: 10.1016/0014-2999(90)90153-w.
An unbiased place preference conditioning procedure was used to identify the central opioid receptor types through which the endogenous opioid peptide, beta-endorphin, acts to exert its reinforcing effects in rats in vivo. The intracerebroventricular administration of beta-endorphin, and selective mu (DAGO) or delta (DPDPE) opioid receptor agonists produced marked preferences for the drug-associated place. Intracerebroventricular pretreatment with the selective mu antagonist, CTOP, eliminated the place preference produced by DAGO but not that produced by DPDPE. Pretreatment with the selective delta antagonist, ICI 174,864, abolished the place preference induced by DPDPE. It did not modify the effect of DAGO. In contrast, pretreatment with either ICI 174,864 or CTOP abolished the effects of beta-endorphin. These data demonstrate that both mu and delta receptors are involved in mediating the reinforcing effect of beta-endorphin and indicate that the activation of both receptor types is required for the expression of the motivational effects of beta-endorphin. Further they suggest that beta-endorphin produces its motivational effects via an interaction with an opioid receptor complex composed of both mu and delta receptors.
采用无偏性位置偏爱条件反射程序，以确定内源性阿片肽β-内啡肽在大鼠体内发挥强化作用所通过的中枢阿片受体类型。脑室内注射β-内啡肽、选择性μ（DAGO）或δ（DPDPE）阿片受体激动剂可使大鼠对与药物相关的位置产生明显偏爱。用选择性μ拮抗剂CTOP进行脑室内预处理，可消除DAGO产生的位置偏爱，但不能消除DPDPE产生的位置偏爱。用选择性δ拮抗剂ICI 174,864预处理，可消除DPDPE诱导的位置偏爱。它不会改变DAGO的作用。相反，用ICI 174,864或CTOP预处理均可消除β-内啡肽的作用。这些数据表明，μ和δ受体均参与介导β-内啡肽的强化作用，并表明两种受体类型的激活都是β-内啡肽动机效应表达所必需的。此外，它们提示β-内啡肽通过与由μ和δ受体组成的阿片受体复合物相互作用产生其动机效应。
