Reactive gliosis is a response of astrocytes to a variety of insults that is characterized by hypertrophy of the cell bodies and processes and an increase in the expression of glial fibrillary acidic protein (GFAP). The signal that regulates the transition to the reactive state and the role of vimentin in reactive gliosis are unknown. The experiments here used a model of repeated seizures in the hippocampal-parahippocampal circuits to determine the extent and time course of reactive gliosis, including the appearance of vimentin, in response to seizures. Reactive gliosis, detected by immunohistochemistry for the presence of GFAP and vimentin, was present 2-7 days after the repeated seizures. At least 9 seizures, or at least 250 s of seizure discharge, were needed to induce reactive gliosis. After seizures, cells staining for vimentin were found in the dentate gyrus molecular layer and hilar region, as well as in the molecular layer of CA1. Fewer cells were stained in the CA3 region. These experiments demonstrate that repeated discrete seizures of the hippocampal-parahippocampal circuits can cause reactive gliosis and localized induction of a glial protein (vimentin) that is not normally expressed in the adult brain.