We tested the hypothesis that populations of ependymal, subependymal and choroid plexus cells proliferate and differentiate after stroke in adult rats. Rats were subjected to 2 h of middle cerebral artery occlusion (n=70) and euthanized at 1, 2, 4, 7, 14, 21 and 28 days (10 per time point). Hematoxylin and eosin staining and immunostaining were performed using antibodies against bromodeoxyuridine, neuronal nuclear antigen and glial fibrillary acidic protein after stroke. In normal nonischemic rats (n=10), single layers of ependymal and choroid plexus cells do not react with bromodeoxyuridine, neuronal nuclear antigen or glial fibrillary acidic protein. Individual subependymal cells express glial fibrillary acidic protein and bromodeoxyuridine, but not neuronal nuclear antigen. After stroke, increased bromodeoxyuridine reactivity was present in multiple layers of ependymal cells and nodules of subependymal cells and in scattered choroid plexus cells from 2 to 28 days and peaked at 7 days. Bromodeoxyuridine immunoreactivity colocalized with neural phenotypes of neuronal nuclear antigen (approximately 0.1-3.5%) and glial fibrillary acidic protein (approximately 8.6%) immunoreactivity in cells in the ventricular zone and the subventricular zone, as well as in the choroid plexus of the ischemia affected hemisphere. Our data suggest that ependymal, subependymal and choroid plexus cells are potential neural precursor cells in the adult mammalian brain.