Neuropathic pain is a highly debilitating chronic pain condition occurring after insult in the nervous system. Peripheral nerve injury (PNI) is used as a rodent model of neuropathic pain and causes activation of spinal cord microglia, resident immune cells in the central nervous system. Accumulating evidence indicates that microglia activated in the spinal dorsal horn are critical elements for neuropathic pain development. However, the role of microglia in a later phase of neuropathic pain remains unclear. In this study, we found a subpopulation of microglia expressing CD11c (CD11c⁺ microglia) emerged in the late phase. The increase of CD11c⁺ microglia was temporally correlated with recovery of pain hypersensitivity. To explore a role of CD11c⁺ microglia, we depleted these cells specifically using diphtheria toxin. Although control mice showed pain hypersensitivity and subsequent recovery after PNI, the mice in which CD11c⁺ microglia were depleted did not recover from pain hypersensitivity. These findings suggest that spinal microglia during neuropathic pain are heterogeneous and that CD11c⁺ microglia are a subpopulation that has an important role in a recovery of neuropathic pain.