Investigation of pain regulation mechanism via novel intracellular transport modulation factor.

2015 Fiscal Year Final Research Report

• Project/Area Number: 24592798
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: Mukogawa Women's University (2014-2015); Hiroshima University (2012-2013)
• Principal Investigator: Kitayama Tomoya 武庫川女子大学, 薬学部, 講師 (60363082)
• Co-Investigator(Kenkyū-buntansha): MORITA Katsuya 広島文化学園大学, 看護学部, 教授 (10116684)
• Co-Investigator(Renkei-kenkyūsha): KANEMATSU Takashi 広島大学, 医歯薬保健学研究院, 教授 (10264053)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 神経障害性疼痛 / クロライドイオン / 抑制性シグナル

Outline of Final Research Achievements

To determine the involvement of PRIPs in pain sensation, a hind paw withdrawal test was performed before and after partial sciatic nerve ligation (PSNL) in PRIPs knockout mice (DKO). DKO mice that underwent PSNL surgery showed hard-wired ipsilateral paw withdrawal threshold. To further investigate the inverse phenotype in DKO mice, we produced mice with specific siRNA-mediated knockdown of PRIPs in the spinal cord. Consistent with the phenotypes of KO mice, PRIPs knockdown (DKD) mice with PSNL showed decreased pain-related behavior. This indicates that reduced expression of both PRIPs in the spinal cord induces resistance towards a painful sensation. The expression of KCC2, which controls the balance of neuronal excitation and inhibition, was normal level in DKO mice after PSNL. Suppressed expression of PRIPs induces an elevated expression of KCC2 in the spinal cord, resulting in inhibition of nociception and amelioration of neuropathic pain in DKO mice.

Free Research Field

神経科学