Barrett R W, Vaught J L
Eur J Pharmacol. 1982 Jun 4;80(4):427-30. doi: 10.1016/0014-2999(82)90090-5.
Utilizing the mouse tail-flick assay, four opioid peptides, which have been reported to be selective for either mu- or delta-opioid receptors, were examined for their analgesic potency and for their ability to modify morphine-induced analgesia. [D-Ala2,D-Leu5]enkephalin and [D-Ser2,Thr6]leucine-enkephalin, putative delta-receptor selective peptides, produced a potent analgesic response and at subanalgesic doses potentiated morphine-induced analgesia. Morphiceptin and [D-Ala2,Pro5]enkephalinamide, putative mu-receptor selective peptides, were similarly found to produce analgesia. However, in contrast to the delta-receptor selective peptides, three mu-receptor selective peptides were unable to alter the potency of morphine. Thus, it would appear that the potentiation of morphine analgesia is a unique property of delta-receptor selective peptides.
利用小鼠甩尾试验,对四种据报道对μ或δ阿片受体具有选择性的阿片肽进行了镇痛效力以及改变吗啡诱导镇痛作用能力的检测。[D-丙氨酸2,D-亮氨酸5]脑啡肽和[D-丝氨酸2,苏氨酸6]亮氨酸脑啡肽,被认为是δ受体选择性肽,产生了强效镇痛反应,并且在亚镇痛剂量下增强了吗啡诱导的镇痛作用。吗啡肽和[D-丙氨酸2,脯氨酸5]脑啡肽酰胺,被认为是μ受体选择性肽,同样被发现可产生镇痛作用。然而,与δ受体选择性肽不同的是,三种μ受体选择性肽无法改变吗啡的效力。因此,似乎增强吗啡镇痛作用是δ受体选择性肽的独特特性。