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. 2012 May 1;29(7):1469–1482. doi: 10.1089/neu.2011.2161

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Copyright 2012, Mary Ann Liebert, Inc.

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FIG. 6. — (A) High-power views showing β-APP immunoreactivity in different ipsilateral brain regions at 1 day after injury in ACZ-treated animals compared with sham-control and untreated-injured animals. Note that the number of damaged immunoreactive axons (arrows) was significantly reduced in ACZ-treated animals compared with untreated-injured animals (scale bar=20 μm). (B) Bar graph of the mean densities of immunopositive profiles displaying β-APP immunoreactivity in ACZ-treated (solid bars) and untreated-injured rats (open bars) at 3 and 24 h after trauma. There was a significant decrease in the number of β-APP-immunopositive damaged axons in the cingulum, corpus callosum, pericontusion margin, and thalamus in the ACZ group at 24 h. Data are plotted as means±standard error of the mean (Marg, pericontusion margin; Cing, cingulum; Thal, thalamus; CC, corpus callosum; EC, external capsule; IC, internal capsule; ACZ, acetazolamide; β-APP, β-amyloid precursor protein).