Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides
Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides
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DOI：
10.1159/000025463
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发表时间：
2000-07-01
影响因子：
11
通讯作者：
Quock, RM
中科院分区：
文献类型：
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作者：
Cahill, FJ;Ellenberger, EA;Quock, RM
以前的研究表明，在小鼠腹部收缩试验中，一氧化二氮的抗伤害作用是由κ-阿片受体介导的，由于一氧化二氮被认为是引起神经元释放内源性阿片肽以刺激阿片受体，因此本研究旨在鉴定所涉及的阿片肽，特别是在脊髓中，通过确定一氧化二氮抗伤害感受是否可以通过鞘内（i.t.）给予针对不同阿片肽的抗血清，将雄性NIH Swiss小鼠i. t.用兔抗阿片肽抗血清，24小时后暴露于三种不同浓度的一氧化二氮中的一种。根据数据建立的剂量-反应曲线表明，一氧化二氮的抗伤害作用可被各种强啡肽（DYN）和甲硫氨酸脑啡肽（ME）抗血清显著拮抗，而不被β-内啡肽（β-EP）抗血清拮抗。DYN和ME的抗血清可显著提高一氧化二氮抗伤害感受的AD（50）值，而β-EP则无此作用。本研究的这些发现支持了一氧化二氮抗伤害感受在小鼠腹部收缩试验中涉及脊髓中DYN和ME的神经元释放的假设，Copyright（C）2000 National Science理事会，ROC和S. Karger AG，巴塞尔。
Previously it was demonstrated that nitrous oxide antinociception in the mouse abdominal constriction test is mediated by kappa-opioid receptors, Since nitrous oxide is thought to cause the neuronal release of endogenous opioid peptide to stimulate opioid receptors, this study was designed to identify the opioid peptides involved, especially in the spinal cord, by determining whether nitrous oxide antinociception can be differentially inhibited by intrathecally (i.t.) administered antisera to different opioid peptides, Male NIH Swiss mice were pretreated i.t. with rabbit antisera to opioid peptides then exposed 24 h later to one of three different concentrations of nitrous oxide in oxygen, Dose-response curves constructed from the data indicated that the antinociceptive effect of nitrous oxide was significantly antagonized by antisera to various dynorphins (DYNs) and methionine-enkephalin (ME), but not by antiserum to P-endorphin (beta-EP). The AD(50) values for nitrous oxide antinociception were significantly elevated by antisera to DYNs a nd ME bur not beta-EP, These findings of th is study support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test involves the neuronal release of DYN and ME in the spinal cord, Copyright (C) 2000 National Science Council, ROC and S. Karger AG, Basel.