Heyman J S, Vaught J L, Mosberg H I, Haaseth R C, Porreca F
Department of Pharmacology, University of Arizona Health Sciences Center, Tucson 85724.
Eur J Pharmacol. 1989 Jun 8;165(1):1-10. doi: 10.1016/0014-2999(89)90764-4.
The effect of the delta-selective agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) on the antinociception produced by intracerebroventricular (i.c.v.) administration of the mu agonists morphine, [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAGO), [NMePhe3,D-Pro4]morphiceptin (PLO17), beta-endorphin, phenazocine, etorphine and sufentanil was studied in mice. Only the antinociceptive effects of morphine and normorphine were modulated by i.c.v. coadministration of a dose of DPDPE which did not produce any significant antinociception alone. Both the morphine and normorphine dose-response lines were displaced to the left in the presence of DPDPE. The delta-selective antagonist ICI174,864 (N,N-diallyl-Tyr-Aib-Aib-Phe-Leu-OH) (where Aib is alpha-aminoisobutyric acid) blocked the modulation of morphine antinociception by DPDPE. ICI 174,864 alone failed to produce either a significant increase or decrease of morphine, phenazocine, etorphine or beta-endorphin antinociception. The results of the present study provide support for the hypothesis that the enkephalins may function to modulate antinociception produced at the mu receptor; such modulation may come about via the existence of an opioid mu-delta receptor complex. The mu receptors existing in such a complex may be selectively activated by morphine and normorphine, but not the other mu agonists studied here. Thus, the enkephalins may function both to directly initiate, as well as to modulate, some forms of supraspinal mu receptor-mediated antinociception.
研究了δ-选择性激动剂[D-青霉胺2,D-青霉胺5]脑啡肽(DPDPE)对脑室内(i.c.v.)注射μ激动剂吗啡、[D-丙氨酸2,N-甲基苯丙氨酸4,甘醇5]脑啡肽(DAGO)、[N-甲基苯丙氨酸3,D-脯氨酸4]吗啡肽(PLO17)、β-内啡肽、非那佐辛、依托啡和舒芬太尼所产生的镇痛作用的影响。仅吗啡和去甲吗啡的镇痛作用受到i.c.v.联合给予一定剂量DPDPE的调节,该剂量单独使用时不会产生任何显著的镇痛作用。在存在DPDPE的情况下,吗啡和去甲吗啡的剂量-反应曲线均向左移动。δ-选择性拮抗剂ICI174,864(N,N-二烯丙基-Tyr-Aib-Aib-Phe-Leu-OH)(其中Aib是α-氨基异丁酸)阻断了DPDPE对吗啡镇痛作用的调节。ICI 174,864单独使用时,未能使吗啡、非那佐辛、依托啡或β-内啡肽的镇痛作用显著增加或降低。本研究结果支持以下假说:脑啡肽可能起到调节μ受体产生的镇痛作用;这种调节可能是通过存在阿片μ-δ受体复合物实现的。存在于这种复合物中的μ受体可能被吗啡和去甲吗啡选择性激活,但不是此处研究的其他μ激动剂。因此,脑啡肽可能既直接引发,又调节某些形式的脊髓上μ受体介导的镇痛作用。