CB2R activation inhibits pain responses without adverse, most often psychotropic effects that are produced by CB1R agonists. The aim of this study was to examine the dorsal column nuclei for CB2R expression following peripheral nerve injury and to explore a possibility of its contribution to neuropathic pain. Using immunohistochemistry and in situ hybridization in two rat neuropathic pain models, sciatic nerve chronic constriction injury (CCI) and spared nerve injury (SNI), we investigated CB2R synthesis and protein distribution in the dorsal column nuclei.Our results demonstrate that expression of CB2 receptors coincides with hyperactivity of medullary microglia what may contribute to the pathogenesis of neuropathic pain.