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

电生理学研究：利用分离的新生大鼠脊髓标本，研究了脊髓PAC1受体在伤害性信息传递中的作用。脊髓应用PAC1受体激动剂Maxadilan可引起长时间的前根去极化，并呈剂量依赖关系。脊髓应用PAC1受体拮抗剂Max.d.4对背根诱发的慢腹根电位(Slow VRP)有抑制作用，且呈剂量依赖关系。这些结果提示，新生大鼠脊髓中的PAC1受体在伤害性信息传递中起重要作用。行为学和免疫组织化学研究了阿片受体样受体1(ORL1)受体在脊髓伤害性信息传递和Fos样免疫反应表达中的作用。鞘内注射ORL1受体激动剂一氧化氮合酶抑制福尔马林致痛大鼠的兴奋行为，并抑制L5脊髓板层I-II层Fos样免疫反应的表达。在神经病理性疼痛模型的研究中，预先给予伤害素可延缓坐骨神经慢性压迫所致的热痛敏，但不能抑制坐骨神经慢性压迫所致的Fos样免疫反应的表达，但不能抑制部分坐骨神经所致的Fos样免疫反应的表达。这些结果提示，脊髓ORL1受体的激活抑制了大鼠脊髓伤害性信息的传递。

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.