Elucidation of the mechanism of pain using a new pain model.

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08451
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General anatomy (including histology/embryology)
• Research Institution: Kanazawa University
• Principal Investigator: Okuda Hiroaki 金沢大学, 医学系, 准教授 (40453162)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 疼痛 / 神経化学

Outline of Final Research Achievements

In this study, we aimed to elucidate the mechanism of pain through the analysis of Mlc1-tTA mice that has insertion of the transgene into the chromosome and may be caused aberrant expression of the endogenous gene in this region. In Mlc1-tTA mice, the region of chromosome 8qB1.1 was deleted and the expression of three genes in this region was defective. Furthermore, aberrant structure of the bone marrow is observed. Then, we examined the function of bone marrow-derived immune cells. Particularly, the phagocytic ability in primary macrophages derived from bone marrow was upregulated as compared with the wild type. These results suggest that functional abnormality of bone marrow-derived immune cells may cause alteration in the pain threshold level of mechanical and various noxious stimuli.

Free Research Field

神経化学

Academic Significance and Societal Importance of the Research Achievements

慢性痛の予防や治療は社会的にも重要であるが、慢性痛の発生要因が多岐にわたり、その機序に関しても不明な点が多いことが、疼痛への適切な対処を困難にしている。本研究成果は、骨髄由来の免疫細胞の異常が、疼痛に対する閾値を変化させることを示唆しており、慢性痛の発症メカニズムの解明に新たな視点を加えたと考える。今後のさらなる解析が、新たな鎮痛薬・治療の探索と共に、疼痛に悩む患者の生活の質の向上の一助になりうると考える。