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.
出处
《四川生理科学杂志》
2022年第2期298-298,共1页
Sichuan Journal of Physiological Sciences
