Astrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurologic disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)-positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under basal conditions. Using a chemoconvulsive status epilepticus (SE) model of temporal lobe epilepsy, we show by immunohistochemistry and colocalization analysis that reactive hippocampal astrocytes express kainate receptor (KAR) subunits after SE. In the CA1 region, GluK1, GluK2/3, GluK4, and GluK5 subunit expression was observed in GFAP-positive astrocytes during the seizure-free or "latent" period 1 week after SE. At 8 weeks after SE, a time after SE when spontaneous behavioral seizures occur, the GluK1 and GluK5 subunits remained expressed at significant levels. Kainate receptor subunit expression was found in astrocytes in the hippocampus and surrounding cortex but not in GFAP-positive astrocytes of striatum, olfactory bulb, or brainstem. To examine hippocampal KAR expression more broadly, astroglial-enriched tissue fractions were prepared from dissected hippocampi and were found to have greater GluK4 expression after SE than controls. These results demonstrate that astrocytes begin to express KARs after seizure activity and suggest that their expression may contribute to the pathophysiology of epilepsy.