A spinal microglia population involved in remitting and relapsing neuropathic pain

被引：153

作者：

Kohno, Keita ^{[1
,2
]}

Shirasaka, Ryoji ^{[2
]}

Yoshihara, Kohei ^{[2
]}

Mikuriya, Satsuki ^{[1
]}

Tanaka, Kaori ^{[3
]}

Takanami, Keiko ^{[4
,5
]}

Inoue, Kazuhide ^{[6
]}

Sakamoto, Hirotaka ^{[4
]}

Ohkawa, Yasuyuki ^{[3
]}

Masuda, Takahiro ^{[1
,2
]}

Tsuda, Makoto ^{[1
,2
]}

机构：

[1] Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Life Innovat, Fukuoka, Japan

[2] Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Mol & Syst Pharmacol, Fukuoka, Japan

[3] Kyushu Univ, Med Inst Bioregulat, Div Transcript, Fukuoka, Japan

[4] Okayama Univ, Grad Sch Nat Sci & Technol, Ushimado Marine Inst, Setouchi, Japan

[5] Natl Inst Genet, Mouse Genom Resources Lab, Shizuoka, Japan

[6] Kyushu Univ, Inst Adv Study, Fukuoka, Japan

来源：

SCIENCE | 2022年 / 376卷 / 6588期

基金：

日本科学技术振兴机构;

关键词：

GROWTH-FACTOR-I; DENDRITIC CELLS; CHOROID-PLEXUS; BRAIN; MICE; MENINGES; SYSTEM;

D O I：

10.1126/science.abf6805

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

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页码：86 / +

页数：44

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