Chien C C, Pasternak G W
Department of Neurology and Neuroscience, Cornell II Medical College, New York, NY 10021, USA.
Eur J Pharmacol. 1995 Dec 27;294(1):303-8. doi: 10.1016/0014-2999(95)00552-8.
(-)-Pentazocine is active in the tailflick assay in CD-1 mice, although it shows a biphasic dose-response curve with a peak effect of only 30%. Co-administration of haloperidol shifts the dose-response curve to the left and elevates the maximal response to 70% through a blockade of sigma 1 receptors, but the curve remains biphasic. (+)-Pentazocine is inactive in all antinociceptive assays, either alone or with haloperidol. The analgesic actions of (-)-pentazocine are readily reversed by nor-binaltorphimine, but not by the mu-selective opioid receptor antagonist beta-funaltrexamine, implying a kappa 1-opioid receptor mechanism of action. This conclusion is supported by the ability of antisense oligodeoxynucleotides directed against the KOR-1 clone, which encodes the kappa 1-opioid receptor, to block (-)-pentazocine analgesia.
（-）-喷他佐辛在CD-1小鼠的甩尾试验中具有活性，尽管它呈现双相剂量反应曲线，最大效应仅为30%。氟哌啶醇的共同给药使剂量反应曲线向左移动，并通过阻断σ1受体将最大反应提高到70%，但曲线仍为双相。（+）-喷他佐辛在所有抗伤害感受试验中均无活性，无论是单独使用还是与氟哌啶醇联合使用。（-）-喷他佐辛的镇痛作用很容易被去甲二氢吗啡酮逆转，但不能被μ选择性阿片受体拮抗剂β-芬太尼胺逆转，这意味着其作用机制为κ1阿片受体机制。针对编码κ1阿片受体的KOR-1克隆的反义寡脱氧核苷酸能够阻断（-）-喷他佐辛的镇痛作用，这一结论得到了该结果的支持。
