This study employed Western blotting and qualitative immunohistochemis
try to analyze the effects of cortical impact traumatic brain injury (
TBI) on acute changes in MAP2 immunoreactivity in the rat cortex, We e
mployed a lateral cortical impact injury device to induce severe TBI,
which is associated with focal cortical contusion and neuronal death a
t the impact site, Three hours following TBI, Western blotting detecte
d 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 with
in layers 3 and 5, as well as a loss of fine dendritic arborization wi
thin layer 1, These changes in MAP2 immunolabeling were associated wit
h, but not exclusively restricted to, the presence of dark shrunken ne
urons labeled by hematoxylin and eosin staining, suggesting impending
cell death, Alterations in MAP2 immunofluorescence were found both wit
hin and beyond areas of focal contusion and necrosis in the ipsilatera
l cortex, Thus, traumatic brain injury in rats can produce rapid and s
ignificant dendritic pathology within sites of contusion, However, imm
unohistochemical changes in MAP2 labeling outside of contused regions
suggests that TBI-induced dendritic damage may not be exclusively asso
ciated with acute cell death.