PubMed · 7774379
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H Spapen, M Diltoer, L Huyghens. 1994. Reduce sympathetic hyperreactivity.. https://doi.org/10.1378/chest.106.2.655
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This work was designed to observe the effects of nociceptin(13-17), one of the main metabolites of nociceptin (also termed orphanin FQ), in pain modulation at supraspinal level in mice. Intracerebroventricular (i.c.v.) administration of nociceptin/orphanin FQ(13-17) (N/OFQ(13-17)) (5, 0.5, 0.05, 0.005 nmol/mouse) dose-dependently induced potent hyperalgesic effects in the 48 degrees C warm-water tail-flick test in mice. I.c.v. pretreatment with N/OFQ(13-17) (5, 0.5, 0.05 nmol/mouse) potentiated the analgesic effects induced by morphine (i.p., 2 mg/kg) and reversed the hyperalgesic effects induced by N/OFQ (i.c.v., 5 nmol/mouse). The hyperalgesic effects induced by N/OFQ(13-17) could not be antagonized by [Nphe((1))]N/OFQ(1-13)NH((2)) or naloxone. These findings suggest that N/OFQ(13-17) may play important roles in pain modulation at supraspinal level in mice and elicits these effects through a novel mechanism independent of the N/OFQ receptor and the mu, delta and kappa opioid receptors.
The Ca(2+) channel blocker, nimodipine, increases the chronic naltrexone-induced supersensitivity to morphine analgesia in mice without affecting the density of up-regulated mu-opioid receptors. In the present study, the change in dihydropyridine-sensitive Ca(2+) channels associated with chronic naloxone-induced supersensitivity to morphine analgesia was studied in rat whole-brain membranes using a radiolabeled Ca(2+) channel blocker, [3H]PN200-110 [isopropyl 4-(2,1,3-benzoxadiazol-4-yl)-1,4-dihydro-2,6-dimethyl-5-methoxycarbonylpyridine-3-carboxylate] (0.02-1.0 nmol/l). Rats were chronically treated with naloxone (1 mg/kg, i.p.), nimodipine (1 mg/kg, i.p.) or their respective vehicles twice daily for 10 days. On the 11th day, 16 h after the last injection of either nimodipine or naloxone, morphine (2 mg/kg, i.p.)-induced tail-flick analgesia was determined or rats were killed for the binding study. Chronic naloxone significantly potentiated (+84%) the morphine-induced analgesia. Chronic nimodipine also potentiated (+76%) morphine analgesia. In rats treated with nimodipine and naloxone, there was an additive increase (206%) in morphine analgesia. In binding studies, chronic naloxone resulted in a significant decrease (-39%) in the density (B(max)) of [3H]PN200-110 binding with no change in K(d) value when compared to the effect of chronic vehicle. Chronic nimodipine resulted in a slight but significant (+14.5%) increase in the B(max) of [3H]PN200-110. However, when nimodipine was co-administered with naloxone, it not only reversed the down-regulation but actually up-regulated (+25%) [3H]PN200-110 binding with no change in K(d) value. Our results show significant down-regulation of [3H]PN200-110 binding in association with naloxone-induced analgesic supersensitivity to morphine. The supersensitivity was also observed following chronic blockade of up-regulated Ca(2+) channels by nimodipine. These results indicate an important role of L-type Ca(2+) channel regulation in naloxone-induced analgesic supersensitivity to morphine.