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孤啡肽在大鼠杏仁中央核中的抗伤害作用,涉及阿片受体。

Antinociceptive effects of galanin in the central nucleus of amygdala of rats, an involvement of opioid receptors.

机构信息

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

出版信息

Brain Res. 2010 Mar 12;1320:16-21. doi: 10.1016/j.brainres.2009.12.060. Epub 2010 Jan 4.

DOI:10.1016/j.brainres.2009.12.060
PMID:20051236
Abstract

The central nucleus of amygdala (CeA) is a very important brain structure involved in multiple physiological functions, especially in pain modulation. There are high densities of galanin and galanin receptors found in the CeA. The present study was performed to explore the antinociceptive effects of galanin in the CeA of rats, and possible involvements of opioid receptors in the galanin-induced antinociception. Intra-CeA injection of galanin induced dose-dependent increases in hindpaw withdrawal latencies (HWLs) to noxious thermal and mechanical stimulations in rats. Interestingly, the amtinociceptive effect induced by intra-CeA injection of galanin was blocked by intra-CeA injection of naloxone, a common opioid receptor antagonist, indicating an involvement of opioid receptors in the galanin-induced antinociception in the CeA of rats. Moreover, intra-CeA injection of either selective mu-opioid receptor antagonist beta-funaltrexamine (beta-FNA) or delta-opioid receptor antagonist naltrindole, but not kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI), significantly attenuated the galanin-induced increases in HWLs in the CeA of rats. Taken together, the results demonstrate that galanin induces antinociceptive effects in the CeA of rats, and both mu- and delta-opioid receptors are involved in the galanin-induced antinociception.

摘要

杏仁中央核(CeA)是一个非常重要的脑结构,涉及多种生理功能,特别是在疼痛调制中。CeA 中发现有高浓度的甘丙肽和甘丙肽受体。本研究旨在探讨 CeA 中甘丙肽的抗伤害作用,以及甘丙肽诱导的抗伤害作用是否涉及阿片受体。CeA 内注射甘丙肽可剂量依赖性增加大鼠对有害热和机械刺激的后爪退缩潜伏期(HWL)。有趣的是,CeA 内注射纳洛酮,一种常见的阿片受体拮抗剂,可阻断 CeA 内注射甘丙肽引起的抗伤害作用,表明阿片受体参与了 CeA 中甘丙肽诱导的抗伤害作用。此外,CeA 内注射选择性μ-阿片受体拮抗剂β-氟纳曲胺(β-FNA)或 δ-阿片受体拮抗剂纳曲吲哚,而不是 κ-阿片受体拮抗剂 nor-binaltorphimine(nor-BNI),显著减弱了 CeA 中甘丙肽诱导的 HWL 增加。总之,这些结果表明甘丙肽在大鼠 CeA 中诱导抗伤害作用,μ-和 δ-阿片受体都参与了甘丙肽诱导的抗伤害作用。

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