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μ-阿片受体和δ-阿片受体参与AMPA受体拮抗剂在大鼠脊髓诱导的抗伤害感受作用。

Involvement of mu- and delta-opioid receptors in the antinociceptive effects induced by AMPA receptor antagonist in the spinal cord of rats.

作者信息

Kong Ling-Ling, Yu Long-Chuan

机构信息

Laboratory of Neurobiology and National Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, PR China.

出版信息

Neurosci Lett. 2006 Jul 10;402(1-2):180-3. doi: 10.1016/j.neulet.2006.03.071. Epub 2006 Apr 27.

DOI:10.1016/j.neulet.2006.03.071
PMID:16644121
Abstract

The present study was performed to explore the involvement of opioid receptors in the antinociception induced by a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor antagonist in rats. The hindpaw withdrawal latency (HWL) to noxious thermal and mechanical stimulation was assessed by hot plate test and the Randall Selitto Test. Intrathecal injection of 20 nmol of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo[f]quinoxaline-7-sulfonamide (NBQX) disodium, a competitive AMPA receptor antagonist, increased significantly the HWLs to both thermal and mechanical stimulation in rats. The increased HWLs induced by NBQX were dose-dependently attenuated by the opioid receptor antagonist naloxone, while naloxone itself had no marked influences on the HWL of rats. Furthermore, the increased HWLs induced by NBQX were inhibited by the mu-opioid antagonist beta-funaltrexamine (beta-FNA) or the delta-opioid antagonist naltrindole, but not by the kappa-opioid antagonist nor-binaltorphimine (nor-BNI). The results suggest that mu- and delta-opioid receptors, not kappa-opioid receptor, are involved in the antinociception induced by AMPA antagonist in the spinal cord of rats.

摘要

本研究旨在探讨阿片受体在α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体拮抗剂诱导的大鼠抗伤害感受中的作用。通过热板试验和Randall Selitto试验评估大鼠对有害热刺激和机械刺激的后爪缩足潜伏期(HWL)。鞘内注射20 nmol的1,2,3,4-四氢-6-硝基-2,3-二氧代[f]喹喔啉-7-磺酰胺(NBQX)二钠,一种竞争性AMPA受体拮抗剂,显著增加了大鼠对热刺激和机械刺激的HWL。阿片受体拮抗剂纳洛酮剂量依赖性地减弱了NBQX诱导的HWL增加,而纳洛酮本身对大鼠的HWL没有明显影响。此外,NBQX诱导的HWL增加被μ-阿片拮抗剂β-芬太尼(β-FNA)或δ-阿片拮抗剂纳曲吲哚抑制,但不被κ-阿片拮抗剂去甲二氢吗啡酮(nor-BNI)抑制。结果表明,μ-和δ-阿片受体而非κ-阿片受体参与了AMPA拮抗剂在大鼠脊髓中诱导的抗伤害感受。

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