This study examined the neuropathological changes in different areas of the brain of fetal and postnatal rats after transient maternal hypoxia. At different time intervals following hypoxia, reactive microglia as determined immunohistochemically with the antibody OX-42 that recognizes complement type three (CR3) receptors, responded vigorously to the hypoxic stress. Microglial activation was particularly evident in the cingulate cortex and the corpus callosum between 3 h and 14 days after hypoxia. Massive cell degeneration as determined ultrastructurally and significant neuronal loss as evaluated by cell counts were observed in the cingulate cortex at 1 and 3 days after hypoxic insults; thereafter, however, the neuronal density was restored to normal levels. Present results suggest that the cingulate cortex is most vulnerable to the hypoxic injury probably due to a redistribution of cerebral blood flow and/or metabolic changes. Besides being involved in the phagocytosis of cellular debris, it is suggested that the reactive microglial cells may have both neurotoxic and neurotrophic functions.