Journal
SCIENCE
Volume 376, Issue 6588, Pages 86-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.abf6805
Keywords
-
Categories
Funding
- Japanese Society for the Promotion of Science (JSPS KAKENHI) [JP19H05658, JP20H05900, JP20K22687, JP21H02752, JP21H00204, JP16H06280]
- Japan Science and Technology Agency [JST Moonshot RD] [JPMJMS2024, JP21gm0910006]
- AMED [JP20gm6310016 AMED-PRIME JP21wm0425001]
- Platform Project for Supporting Drug Discovery and Life Science Research (BINDS AMED) [JP21am0101091]
- Shionogi Co., Ltd.
Ask authors/readers for more resources
This study reveals the role of CD11c-expressing spinal microglia in the remission and recurrence of neuropathic pain. These microglia express IGF1, and interference with IGF1 signaling impairs pain recovery. Depletion of CD11c(+) microglia or interruption of IGF1 signaling leads to relapse in pain hypersensitivity.
Neuropathic pain is often caused by injury and diseases that affect the somatosensory system. Although pain development has been well studied, pain recovery mechanisms remain largely unknown. Here, we found that CD11c-expressing spinal microglia appear after the development of behavioral pain hypersensitivity following nerve injury. Nerve-injured mice with spinal CD11c(+) microglial depletion failed to recover spontaneously from this hypersensitivity. CD11c(+) microglia expressed insulin-like growth factor-1 (IGF1), and interference with IGF1 signaling recapitulated the impairment in pain recovery. In pain-recovered mice, the depletion of CD11c(+) microglia or the interruption of IGF1 signaling resulted in a relapse in pain hypersensitivity. Our findings reveal a mechanism for the remission and recurrence of neuropathic pain, providing potential targets for therapeutic strategies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available