Endogenous nociceptin signaling and stress-induced analgesia

被引：35
|
作者：
Rizzi, A
Marzola, G
Bigoni, R
Guerrini, R
Salvadori, S
Mogil, JS
Regoli, D
Calò, G
机构：
[1] Univ Modena, Pharmacol Sect, Dept Expt & Clin Med, I-41100 Modena, Italy
[2] Dept Pharmaceut Sci, I-44100 Ferrara, Italy
[3] Ctr Biotechnol, I-44100 Ferrara, Italy
[4] McGill Univ, Dept Psychol, Montreal, PQ H3A 1B1, Canada
来源：
NEUROREPORT | 2001年 / 12卷 / 14期
关键词：
mouse tail-withdrawal assay (TW); nociceptin/orphanin FQ (NC); Nphe(1)]NC(I-13)NH2; OP4; receptor; swim stress-induced analgesia (SIA);
D O I：
10.1097/00001756-200110080-00006
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Nociceptin/orphanin FQ (NC) and its receptor (OP4) have been implicated in pain transmission. The aim of the present study was to investigate the role of the NC/OP4 system in stress-induced analgesia (SIA). The tail-withdrawal assay was performed in mice stressed by forced swimming in water at 15 degreesC (high severity swims) or 32 degreesC (low severity swims). High severity swims produced a naloxone-insensitive antinociceptive effect which was blocked by supraspinal NC (I nmol). The selective OP4 receptor antagonist, [Nphe(1)]]NC(-13)NH2 (30 nmol), was inactive by itself, but prevented the effect of NC. Low severity swims produced a milder analgesic effect that was partially antagonized by naloxone, completely blocked by NC and potentiated by [Nphe(1)]NC(- 13)NH2. These findings confirm the anti-analgesic role of supraspinal NC and suggest that endogenous NC signaling counteracts the opioid component of SIA. NeuroReport 12:3009-3013 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码：3009 / 3013
页数：5
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