Objective To observe the changes of rat microglial inflammation and migration after exposure to sodium metavanadate(NaVO₃·2H₂O), and to analyze the possible mechanisms of vanadium neurotoxicity. Methods Primary cultured rat microglial cells were incubated with NaVO₃·2H₂O. Morphological changes and the Iba1 expression of microglia were tested by immunofluorescence assay. iNOS, Cox-2, ERK and p-ERK protein expressions were determined by western blotting. The levels of TNF-α and IL-1β in the culture medium were tested by enzyme-linked immunosorbent assay. The migration of microglia was tested by immunofluorescence staining using wound-healing assay. Results Microglia changed from resting state with ramous shape to round shape in activated state after NaVO₃·2H₂O exposure, and the expression of Iba1 increased obviously. The protein expressions of iNOS and COX-2 increased significantly compared with the control. The levels of TNF-α and IL-1β were also increased significantly. NaVO₃·2H₂O promotes the migration of microglia through ERK pathway. Conclusions Exposure to NaVO₃·2H₂O promotes primary cultured rat microglial inflammation and migration. These results suggest that the inflammatory reaction of microglia may be one of the possible mechanisms of neurotoxicity caused by vanadium exposure.