This study employed Western blotting and qualitative immunohistochemistry to analyze the effects of cortical impact traumatic brain injury (TBI) on acute changes in MAP2 immunoreactivity in the rat cortex. We employed a lateral cortical impact injury device to induce severe TBI, which is associated with focal cortical contusion and neuronal death at the impact site. Three hours following TBI, Western blotting detected substantial MAP2 loss only in the cortex ipsilateral to the site of injury. Light microscopic studies of MAP2 revealed a prominent loss of MAP2 immunofluorescence in apical dendrites of pyramidal neurons within layers 3 and 5, as well as a loss of fine dendritic arborization within layer 1. These changes in MAP2 immunolabeling were associated with, but not exclusively restricted to, the presence of dark shrunken neurons labeled by hematoxylin and eosin staining, suggesting impending cell death. Alterations in MAP2 immunofluorescence were found both within and beyond areas of focal contusion and necrosis in the ipsilateral cortex. Thus, traumatic brain injury in rats can produce rapid and significant dendritic pathology within sites of contusion. However, immunohistochemical changes in MAP2 labeling outside of contused regions suggests that TBI-induced dendritic damage may not be exclusively associated with acute cell death.