Hypoxia induces BrdU incorporation into uninjured cells that coexpress markers of proliferating cells and of immature, but not mature, neurons. Cerebral cortical cultures were treated with BrdU, exposed to hypoxia for 8 hours, and labeled with an Ab against BrdU and another marker, and nuclei were counterstained with DAPI. Most cells incorporating BrdU showed no evidence of DNA damage as assayed by PANT labeling (a), Klenow labeling (b), or TUNEL (c), or of caspase activation measured with an Ab against the 17- to 20-kDa caspase-3 cleavage product (d). BrdU incorporation colocalized with the cell proliferation markers PCNA (e) and phospho-histone-H3 (f), with retroviral infectivity reported by a GFP-expressing vector (g), and with the “replication-licensing” protein CDC47 (h). As shown in g, not all pFB-hrGFP–infected cells incorporated BrdU, which may be related to differences in labeling efficiency between the two markers. BrdU incorporation also colocalized with nestin (i) and to a large extent with E-NCAM (j), but not with the mature neuronal markers NeuN (k) and MAP-2 (l). Data are representative fields from at least three experiments per row.