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甘丙肽与阿片类物质在大鼠下丘脑弓状核伤害性调制中的相互作用

Interactions of galanin and opioids in nociceptive modulation in the arcuate nucleus of hypothalamus in rats.

作者信息

Sun Yan-Gang, Yu Long-Chuan

机构信息

Department of Physiology, College of Life Sciences, National Laboratory of Biomembrane and Membrane Biotechnology, Center for Brain and Cognitive Science, Peking University, Beijing 100871, People's Republic of China.

出版信息

Regul Pept. 2005 Jan 15;124(1-3):37-43. doi: 10.1016/j.regpep.2004.06.023.

Abstract

The fact that galanin, beta-endorphin and their receptors are present in the arcuate nucleus of hypothalamus (ARC), coupled with our previous observation that both beta-endorphin and galanin play antinociceptive roles in pain modulation in the ARC, made it of interest to study their interactions. The hindpaw withdrawal latency (HWL) in response to noxious thermal and mechanical stimulation was assessed by the hot-plate test and the Randall Selitto Test. We showed that the antinociceptive effect induced by intra-ARC injection of galanin was dose-dependently attenuated by the following intra-ARC injection of naloxone. Furthermore, intra-ARC administration of the selective mu-opioid receptor antagonist beta-funaltrexamine (beta-FNA) attenuated the increased HWL induced by intra-ARC injection of galanin in a dose-dependent manner, while the delta-opioid receptor antagonist naltrindole or the kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI) did not. Moreover, intra-ARC injection of a galanin receptor antagonist galantide attenuated intraperitoneal morphine-induced increases in HWLs. These results demonstrate that the antinociceptive effect of galanin was related to the opioid system, especially mu-opioid receptor was involved in, and that systemic morphine induced antinociception involves galanin in the ARC.

摘要

甘丙肽、β-内啡肽及其受体存在于下丘脑弓状核(ARC)中,再加上我们之前观察到β-内啡肽和甘丙肽在ARC的疼痛调节中均发挥抗伤害感受作用,这使得研究它们之间的相互作用变得很有意义。通过热板试验和兰德尔·塞利托试验评估对有害热刺激和机械刺激的后爪撤离潜伏期(HWL)。我们发现,ARC内注射甘丙肽所诱导的抗伤害感受作用会被随后ARC内注射纳洛酮以剂量依赖的方式减弱。此外,ARC内给予选择性μ-阿片受体拮抗剂β-芬太尼(β-FNA)会以剂量依赖的方式减弱ARC内注射甘丙肽所诱导的HWL增加,而δ-阿片受体拮抗剂纳曲吲哚或κ-阿片受体拮抗剂诺-宾丙诺啡(nor-BNI)则不会。此外,ARC内注射甘丙肽受体拮抗剂丙谷酰胺会减弱腹腔注射吗啡所诱导的HWL增加。这些结果表明,甘丙肽的抗伤害感受作用与阿片系统有关,尤其是涉及μ-阿片受体,并且全身吗啡诱导的抗伤害感受涉及ARC中的甘丙肽。

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