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

页码：3009 / 3013

页数：5

共 18 条

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