A spinal microglia population involved in remitting and relapsing neuropathic pain
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- Keita Kohno
- Department of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
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- Ryoji Shirasaka
- Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
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- Kohei Yoshihara
- Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
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- Satsuki Mikuriya
- Department of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
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- Kaori Tanaka
- Division of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
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- Keiko Takanami
- Ushimado Marine Institute, Graduate School of Natural Science and Technology, Okayama University, Setouchi, Japan.
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- Kazuhide Inoue
- Kyushu University Institute for Advanced Study, Fukuoka, Japan.
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- Hirotaka Sakamoto
- Ushimado Marine Institute, Graduate School of Natural Science and Technology, Okayama University, Setouchi, Japan.
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- Yasuyuki Ohkawa
- Division of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
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- Takahiro Masuda
- Department of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
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- Makoto Tsuda
- Department of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Description
<jats:p> 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 <jats:sup>+</jats:sup> microglial depletion failed to recover spontaneously from this hypersensitivity. CD11c <jats:sup>+</jats:sup> 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 <jats:sup>+</jats:sup> 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. </jats:p>
Journal
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- Science
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Science 376 (6588), 86-90, 2022-04
American Association for the Advancement of Science (AAAS)