Acute nociceptive pain is a key defense system for detecting danger signals. In contrast, chronic pain (like neuropathic pain occurring after damage of the nervous system) persists for a long period even in the absence of dangerous stimuli or after injuries have healed.  In animal models of neuropathic pain, peripheral nerve injury has been shown to cause a variety of plastic modifications in the somatosensory system at the levels of neuronal synapses, connections, and networks, which leads to the development of neuropathic pain. A number of studies including ours have demonstrated that these pathologically alterations require signals from glial cells, especially microglia (a type of tissue-resident macrophages in the CNS), and have significantly advanced our understanding of the mechanism underlying neuropathic pain development.  On the other hand, the role of microglia after the development remains unknown, but our recent study provide evidence indicating that a subset of microglia contributes to spontaneous recovery from neuropathic pain. These new findings suggest that microglia play a highly dynamic role during the course of neuropathic pain. In my talk, I will show our data including the new role of microglial subset and discuss the new mechanism of neuropathic pain.