Izenwasser Sari, Kornetsky Conan
Laboratory of Behavioral Pharmacology, Boston University School of Medicine, Boston, MA 02118 U.S.A.
Pain. 1988 Jun;33(3):363-368. doi: 10.1016/0304-3959(88)90297-7.
Morphine will raise the threshold for escape from aversive electrical stimulation delivered to the mesencephalic reticular formation and this effect is potentiated by D-amphetamine. In order to study the roles which dopamine and norepinephrine play in modulating opiate analgesia, the effects of amfonelic acid, an indirect dopamine agonist, and nisoxetine, a selective norepinephrine reuptake blocker, were determined alone and in combination with morphine using this supraspinal model of analgesia. Amfonelic acid alone produced hyperalgesia and completely antagonized the analgesic effect of morphine. Nisoxetine had no effect by itself, however, it potentiated the analgesic effect of morphine when the two drugs were administered concomitantly. These findings suggest that norepinephrine and not dopamine plays a predominant role in the potentiation of opiate analgesia by D-amphetamine.
吗啡会提高从中脑网状结构传递的厌恶性电刺激中逃脱的阈值，并且这种效应会被右旋苯丙胺增强。为了研究多巴胺和去甲肾上腺素在调节阿片类镇痛中所起的作用，使用这种脊髓上镇痛模型，单独以及与吗啡联合测定了间接多巴胺激动剂安非尼酸和选择性去甲肾上腺素再摄取阻滞剂尼索西汀的作用。单独使用安非尼酸会产生痛觉过敏，并完全拮抗吗啡的镇痛作用。尼索西汀本身没有作用，然而，当两种药物同时给药时，它会增强吗啡的镇痛作用。这些发现表明，去甲肾上腺素而非多巴胺在右旋苯丙胺增强阿片类镇痛作用中起主要作用。
