The role of colony-stimulating factors on microglial proliferation and neuropathic pain in rats

Research Project

Project/Area Number	16K19220
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Pain science
Research Institution	Hyogo Medical University
Principal Investigator	Okubo Masamichi 兵庫医科大学, 医学部, 助教 (70581495)
Project Period (FY)	2016-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000) Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000) Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords	神経障害性疼痛 / 末梢神経 / 損傷 / マイクログリア / 増殖 / コロニー刺激因子 / 脊髄 / 後根神経節
Outline of Final Research Achievements	We examined the expression of mRNAs for macrophage-CSF (M-CSF), granulocyte macrophage-CSF (GM-CSF), granulocyte-CSF (G-CSF) and IL-34 in the dorsal root ganglion (DRG) and spinal cord after peripheral nerve injury in rats. RT-PCR and ISHH revealed that M-CSF and IL-34, but not GM- or G-CSF, mRNAs were constitutively expressed in the DRG, and M-CSF robustly increased in injured-DRG neurons. M-CSF receptor mRNA was expressed in naive rats and increased in spinal microglia following peripehral nerve injury. Intrathecal injection of M-CSF receptor inhibitor partially but significantly reversed the proliferation of spinal microglia and mechanical allodynia induced by peripheral nerve injury. Furthermore, intrathecal injection of recombinant M-CSF induced microglial proliferation and mechanical allodynia.