Elucidation of amplification mechanisms in nociceptive signals and therapeutic strategy of intractable pain.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26463056
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Tohoku University
• Principal Investigator: Eiji Masaki 東北大学, 歯学研究科, 教授 (40221577)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 術後痛 / BDNF / ドパミン受容体 / 神経障害性疼痛 / 抗酸化 / 末梢神経記録

Outline of Final Research Achievements

We examined the effects of tissue-neural damage with surgical incision on the modification of primary and secondary afferent neurons in the postoperative pain model. The postoperative pain was established by plantar and infra-orbital nerve incision and the withdrawal responses along with sickness behavior were evaluated. Using the rat glabrous in vitro skin-tibial nerve preparation, afferent activities from single mechanosensitive nociceptors were recorded. 1) The microglial activation inhibitor had no effect on dorsal horn BDNF overexpression during the early post-incision period. 2) The impairment and/or modification of D2-like receptors in the spinal cord is not involved in the postoperative decrease in nociceptive threshold. 3) PAR-2-mediated excitation and sensitization of peripheral primary nociceptors was involved in the neuropathic component of postoperative pain. 4) The confidential results of hydrogen water on the postoperative pain status have not been elucidated yet.

Free Research Field

麻酔疼痛管理学