Role of brain dynorphin in nitrous oxide antinociception in mice
Role of brain dynorphin in nitrous oxide antinociception in mice
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DOI：
10.1016/s0091-3057(99)00202-6
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发表时间：
2000-02-01
影响因子：
3.6
通讯作者：
Quock, RM
中科院分区：
文献类型：
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作者：
Branda, EM;Ramza, JT;Quock, RM
早期的研究表明，一氧化二氮的抗伤害性是由阿片受体介导的，我们假设，一氧化二氮刺激神经元释放的内源性阿片肽（EOP），刺激阿片受体。为了进一步验证这一假设，雄性NIH Swiss小鼠脑室内预处理兔抗血清阿片肽或各种抑制剂的肽酶参与降解的EOPs。小鼠随后暴露于三种不同浓度的一氧化二氮的氧气，并使用乙酸腹部收缩试验测量其抗伤害性反应。一氧化二氮的抗伤害作用显着衰减预处理24小时强啡肽（DYN）的各种片段的抗血清，但不对甲硫氨酸脑啡肽（ME）或β-内啡肽（β-EP）的抗血清。在其他实验中，一氧化二氮的抗伤害作用显着增强30分钟的预处理与phosphoramidon，内肽酶24.11的抑制剂，这是有牵连的DYN降解，但不是bestatin或卡托普利，抑制氨肽酶和血管紧张素转换酶，分别。后一种酶与某些EOP的降解有关，尽管不是DYN。这些发现支持了一氧化二氮在小鼠腹部收缩试验中的抗伤害性感受是由作用于中枢神经系统的内源性DYN介导的假设。(C)2000 Elsevier Science Inc.
Earlier studies indicate that nitrous oxide antinociception is mediated by opioid receptors, and we have hypothesized that nitrous oxide stimulates a neuronal release of an endogenous opioid peptide (EOP) that stimulates opioid receptors. To further test this hypothesis, male NIH Swiss mice were pretreated intracerebroventricularly with rabbit antisera to opioid peptides or with various inhibitors of peptidases involved in the degradation of EOPs. Mice were subsequently exposed to three different concentrations of nitrous oxide in oxygen, and their antinociceptive responsiveness was measured using the acetic acid abdominal constriction test. Nitrous oxide antinociception was significantly attenuated by 24-h pretreatment with antisera to various fragments of dynorphin (DYN) but not by antisera against methionine-enkephalin (ME) or beta-endorphin (beta-EP). In other experiments, nitrous oxide antinociception was significantly enhanced by 30-min pretreatment with phosphoramidon, an inhibitor of endopeptidase 24.11, which has been implicated in DYN degradation, but not bestatin or captopril, which inhibit aminopeptidase and angiotensin-converting enzyme, respectively. The latter enzymes have been implicated in degradation of certain EOPs albeit not DYN. These findings support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test is mediated by endogenous DYN acting in the central nervous system. (C) 2000 Elsevier Science Inc.