Microglia, which are pathological effectors and amplifiers in the central nervous system, undergo various forms of activation. Activation of spinal microglial following peripheral nerve injury (PNI), is a key event for the development of neuropathic pain but the transcription factors contributing to microglial activation are less understood.
Here, we demonstrate that MafB, a dominant transcriptional regulator of mature microglia, is involved in the pathology of neuropathic pain. PNI caused an increase of MafB expression selectively in spinal microglia. We measured expression of mir-152, a microRNA targeting MafB, and found a transient decrease in  its expression in the spinal cord after PNI. Moreover, intrathecal administration of mir-152 mimic suppressed the development of neuropathic pain. Reduced MafB expression using heterozygous Mafb-deficient mice alleviated mechanical hypersensitivity. Furthermore, we found that intrathecal transfer of Mafb-deficient microglia did not induce mechanical hypersensitivity and that conditional Mafb-knockout mice did not develop neuropathic pain. We propose that MafB is a key mediator of the PNI-induced phenotypic alteration of spinal microglia and neuropathic pain development.