Elucidation of Sema3A signaling pathway in mechanisms of neuropathic pain

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592352
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: Niigata University
• Principal Investigator: KAMIYA Yoshinori 新潟大学, 医歯学総合病院, 教授 (90381491)
• Co-Investigator(Kenkyū-buntansha): FUNAKOSHI Kengo 横浜市立大学, 医学(系)研究科(研究院), 教授 (60291572) ; YAMASHITA Naoya 横浜市立大学, 医学(系)研究科(研究院), 客員講師 (40508793)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 神経因性疼痛 / 神経ガイダンス因子 / 神経成長因子 / 疼痛メカニズム / シグナルパスウェイ / NMDA受容体

Outline of Final Research Achievements

To clarify the dynamics of Sema3A signaling cascade in peripheral neuropathic pain, we examined Sema3A related proteins CRPM2, CDK5 and NR2B subunit of NMDA receptor in the spinal cord dorsal horn of chronic constriction injury in unilateral sciatic nerve model by Western blotting. Intrathecal intermittent administration of Sema3A induced reduction of pain behavior in pain model rats and increase of CRMP2 and CDK5 expression and decrease of NR2B expression in spinal dorsal horn. On the other hand, in paclitacel-induced pain model rats, NGF and its receptor TrkA is increased in the spinal dorsal horn and dorsal root ganglion. Our findings suggested that the increase of NGF and TrkA might not be neither due to increase of production nor decrease of degradation.

Free Research Field

麻酔科学