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. 2012 Jan 20;29(2):218–234. doi: 10.1089/neu.2011.1762

FIG. 8.

FIG. 8.

Lateral traumatic brain injury (TBI) caused a loss of PSD-95 immunoreactivity in forebrain. The ipsilateral and contralateral hemispheres of the hippocampus and neocortex were dissected from adult rats at 18 h, 24 h, and 48 h after lateral fluid percussion TBI, separately homogenized, and subjected to immunoblotting with antibody recognizing the post-synaptic protein PSD-95. Lateral TBI caused a significant loss of PSD-95 immunoreactivity at 18 h, 24 h, and 48 h post-TBI in the ipsilateral hippocampus (A), and at 18 h and 24 h post-TBI in the contralateral hippocampus (B), relative to controls. In the ipsilateral neocortex, PSD-95 immunoreactivity also decreased significantly below control levels at 18 h and 24 h post-TBI (C). In the contralateral neocortex, however, PSD-95 immunoreactivity did not differ significantly from controls at any time point tested (D). All comparisons were made by one-way analysis of variance with Dunnett's post-hoc test (*p<0.05; **p<0.01; n.s., no significant differences).