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Role of neurotransmitters, such as PACAP and nociceptin, on the nociceptive transmission in the rat spinal cord.

神经递质（例如 PACAP 和伤害感受肽）对大鼠脊髓伤害感受传递的作用。

基本信息

批准号：
10470314
负责人：
YAMAMOTO Tatsuo
金额：
$ 4.48万
依托单位：
Chiba University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10470314/
关键词：
PAC1 receptor maxadilan Mad.d.4 spinal cord nociceptin ORL1 receptor formalin test neuropathic pain nocistatin 侵害刺激摘出脊髄カプサイシン

项目摘要

Electrophysiological study:I studied the role of spinal PAC1 receptor on the nociceptive information transmission using an isolated neonatal rat spinal cord preparation. Application of maxadilan to the spinal cord, a PAC1 receptor agonist, resulted in a long lasting ventral root depolarizaion in a dose dependent manner. An application of Max.d.4, a PAC1 receptor antagonist, to the spinal cord produced the depressant effect on the dorsal root evoked slow ventral root potential (slow VRP) in a dose dependent manner. These results suggested that PAC1 receptor in the rat neonatal spinal cord plays an important role in the nociceptive information transmission.Behavioral and Immunohistochemical StudyI examined the role of the opioid receptor like 1 (ORL1) receptor on the nociceptive transmission and thfe expression of Fos-like immunoreactivity of the spinal cord. Intrathecal injection of nociceptin, an ORL1 receptor agonist, depressed the agitation behavior induced by paw formalin injection and inhibited the expression of Fos-like immunoreactivity in the laminae I-II of L5 rat spinal cord. In the study of neuropathic pain model, pre-emptively administered nociceptin delayed the development of thermal hyperalgesia induced by the chronic constriction injury of the sciatic nerve, but not by the partial sciatic nerve injury and depressed the expression of Fos-like immunoreactivity induced by the chronic constriction injury of the sciatic nerve, but not by the partial sciatic nerve injury. These data suggested that activation of spinal ORL1 receptor suppressed the nociceptive transmission in the rat spinal cord.

电生理学研究：我使用分离的新生大鼠脊髓制剂研究了脊髓 PAC1 受体在伤害性信息传递中的作用。将 PAC1 受体激动剂 maxadilan 应用于脊髓，以剂量依赖性方式导致持久的腹侧根去极化。将 PAC1 受体拮抗剂 Max.d.4 应用于脊髓，对背根产生抑制作用，以剂量依赖性方式诱发慢腹根电位（慢 VRP）。这些结果表明，新生大鼠脊髓中的PAC1受体在伤害性信息传递中发挥着重要作用。行为和免疫组织化学研究检测了阿片受体样1（ORL1）受体对伤害性传递和脊髓Fos样免疫反应性表达的作用。鞘内注射伤害感受肽（ORL1受体激动剂）可抑制爪福尔马林注射诱导的躁动行为，并抑制L5大鼠脊髓I-II层中Fos样免疫反应性的表达。在神经病理性疼痛模型的研究中，预先给予伤害感受肽可延缓坐骨神经慢性收缩损伤（而非部分坐骨神经损伤）引起的热痛觉过敏的发生，并抑制坐骨神经慢性收缩损伤（而非部分坐骨神经损伤）引起的Fos样免疫反应性的表达。这些数据表明脊髓 ORL1 受体的激活抑制了大鼠脊髓中的伤害性传递。