孤啡肽通过从小鼠外周神经末梢释放P物质诱导伤害性反应。
Nociceptin/orphanin FQ-induced nociceptive responses through substance P release from peripheral nerve endings in mice.
作者信息
Inoue M, Kobayashi M, Kozaki S, Zimmer A, Ueda H
机构信息
Department of Molecular Pharmacology and Neuroscience, Nagasaki University School of Pharmaceutical Sciences, Nagasaki 852-8521, Japan.
出版信息
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10949-53. doi: 10.1073/pnas.95.18.10949.
Abstract
We have studied the in vivo signaling mechanisms involved in nociceptin/orphanin FQ (Noci)-induced pain responses by using a flexor-reflex paradigm. Noci was 10,000 times more potent than substance P (SP) in eliciting flexor responses after intraplantar injection into the hind limb of mice, but the action of Noci seems to be mediated by SP. Mice pretreated with an NK1 tachykinin receptor antagonist or capsaicin, or mice with a targeted disruption of the tachykinin 1 gene no longer respond to Noci. The action of Noci appears to be mediated by the Noci receptor, a pertussis toxin-sensitive G protein-coupled receptor that stimulates inositol trisphosphate receptor and Ca2+ influx. These findings suggest that Noci indirectly stimulates nerve endings of nociceptive primary afferent neurons through a local SP release.
摘要
我们通过使用屈肌反射范式研究了参与孤啡肽/痛敏肽（Noci）诱导的疼痛反应的体内信号传导机制。在小鼠后肢足底注射后，Noci引发屈肌反应的效力比P物质（SP）强10000倍，但Noci的作用似乎是由SP介导的。用NK1速激肽受体拮抗剂或辣椒素预处理的小鼠，或速激肽1基因靶向破坏的小鼠对Noci不再有反应。Noci的作用似乎是由Noci受体介导的，Noci受体是一种对百日咳毒素敏感的G蛋白偶联受体，可刺激肌醇三磷酸受体和Ca2+内流。这些发现表明，Noci通过局部释放SP间接刺激伤害性初级传入神经元的神经末梢。
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