Analysis of the mechanism of neuropathic pain due to lumbar extra-foraminal stenosis

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10419
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Orthopaedic surgery
• Research Institution: Wakayama Medical University
• Principal Investigator: Nishi Hideto 和歌山県立医科大学, 医学部, 博士研究員 (30382344)
• Co-Investigator(Kenkyū-buntansha): 橋爪 洋 和歌山県立医科大学, 医学部, 准教授 (10326382) ; 谷口 亘 和歌山県立医科大学, 医学部, 講師 (20453194)
• Co-Investigator(Renkei-kenkyūsha): Sonekatsu Mayumi 和歌山県立医科大学, 医学部, 学内助教 (40725579) ; Nishio Naoko 和歌山県立医科大学, 医学部, 特別研究員 (40648359)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 腰椎部脊柱外病変 / 神経障害性疼痛 / パッチクランプ法 / 交感神経 / インターフェロンγ / ミクログリア / Interferon-γ / 脊髄後角

Outline of Final Research Achievements

Little is known about the mechanism of neuropathic pain due to lumbar extra-foraminal stenosis. We investigated whether the sympathetic nervous system is involved in this radiculopathy by patch-clamp method. The average frequency of spontaneous excitatory postsynaptic currents (sEPSCs) in spinal nerve ligation (SNL) with resection of sympathetic ganglion model was significantly smaller than that in SNL only model rats. Next, we had investigated the effects of IFNγ on the glutamate-receptor response potentiation recorded from SG neurons of adult rat spinal cord. IFNγ significantly enhanced NMDA-induced inward currents, but not AMPA-induced currents. We found this mechanism was that microglia activated by IFNγ stimulates neuronal CCR2 and increases neuronal NMDA-induced inward currents. These mechanisms are partially a possible explanation for making the persistent neuropathic pain.

Free Research Field

整形外科学