Analysis of pain disease model-associated mitochondrial abnormalities in primary sensory neurons

2017 Fiscal Year Final Research Report

• Project/Area Number: 26460706
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pain science
• Research Institution: Keio University
• Principal Investigator: Shibata Mamoru 慶應義塾大学, 医学部(信濃町), 講師 (60286466)
• Co-Investigator(Kenkyū-buntansha): 清水 利彦 慶應義塾大学, 医学部(信濃町), 講師 (40265799)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: ミトコンドリア / 三叉神経節ニューロン / 片頭痛 / オートファジー / ミトファジー / 皮質拡延性抑制

Outline of Final Research Achievements

TRPV1 is activated by capsaicin. We applied 10 mM capsaicin-immersed cotton to the whisker pad for up to 6 days. Electron microscopic analysis revealed that there was extensive destruction of mitochondrial internal structure in small-sized trigeminal ganglion (TG) neurons at Day 4. Nevertheless, no discernible structural alterations were not observed in the small-sized TG neurons at Day 6, implying that there was a restorative process that normalized mitochondrial status in TG neurons exposed to repetitive TRPV1 stimulation. We established a PC12 clone stably expressing TRPV1. When exposed to capsaicin, these cells exhibited mitochondrial structural derangements in a dose-dependent manner. There were significantly increased mitophagy-affected mitochondria in capsaicin-treated cells. Our-cell-based assays imply that mitophagy plays an important role in the reparative process of mitochondrial health in capsaicin-treated cells.

Free Research Field

神経内科