SOCS1 regulates neuropathic pain by inhibiting neuronal sensitization and glial activation in mouse spinal cord

Abstract Neuropathic pain is still a basic science and clinical challenge now, the neuronal sensitization and glial activation in the spinal cord (SC) level are more far-reaching for contributing to pain hypersensitivity following chronic constriction injury (CCI). Accumulating evidence indicates that astrocytes and microglia are activated in the spinal cord dorsal horn (SCDH) after CCI. Suppressor of cytokine signaling 1 (SOCS1) plays an important role in regulating of neuronal inflammation. Here, we investigated the role of SOCS1 in SC played in neuropathic pain. We find SOCS1 was persistently downregulated in the spinal neurons after CCI in mice. On the contrary, overexpression of SOCS1 in the SC reversed CCI-induced pain behavioral, activation of neurons, astrocytes, microglia, and the expression of proinflammatory cytokines including tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and IL-6. Over all, these results demonstrate that downregulation of SOCS1 contributed to the development and maintenance of neuropathic pain via activating of neurons, astrocytes, microglia, and proinflammatory cytokines. SOCS1 may be developed into a potential target for treating neuropathic pain.