Association between mitochondria quality control and chronic pain by NIPSNAP1

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460709
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pain science
• Research Institution: Osaka Institute of Technology
• Principal Investigator: ASHITAKA Emiko 大阪工業大学, 工学部, 教授 (50291802)
• Co-Investigator(Renkei-kenkyūsha): OHMIYA Yoshihiro 産業技術総合研究所, バイオメディカル研究部門, 部門長 (20223951)
• Research Collaborator: OKAMOTO Kazuya 大阪工業大学, 大学院工学研究科, 大学院生 ; OHNO Kana 大阪工業大学, 大学院工学研究科, 大学院生 ; KAWABATA Kenta 大阪工業大学, 大学院工学研究科, 大学院生 ; MATSUOKA Etsuko 大阪工業大学, 大学院工学研究科, 大学院生
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: NIPSNAP1 / ミトコンドリア / マイトファジー / 炎症性疼痛

Outline of Final Research Achievements

4-Nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog (NIPSNAP) 1 is expressed in the synaptic membrane and the mitochondria. Synaptic NIPSNAP1, which interacts with the neuropeptide nocistatin, has been implicated in the inhibition of tactile pain allodynia. Here, we investigated the involvement of NIPSNAP1 in the mitochondrial functions in the dorsal root ganglion neurons prepared from NIPSNAP1-deficient mice. We revealed that NIPSNAP1 is involved in the regulation of reactive oxygen species production and the autophagy of the mitochondria in dorsal root ganglion neurons.

Free Research Field

疼痛学、生化学