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. 2015 Oct 20;6:222. doi: 10.3389/fneur.2015.00222

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Copyright © 2015 Turner, Lucke-Wold, Logsdon, Robson, Dashnaw, Huang, Smith, Huber, Rosen and Petraglia.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Blast and closed-head injury models both induced tau hyperphosphorylation. (A) Immunoblots show no significant difference in tau phosphorylation at serine sites 199/202 and threonine site 205 (AT8) at 1 month after single and repeat blast exposures in the ipsilateral rat hippocampus. (B) A significant increase in AT8 expression was measured after single (*p < 0.05 vs. CTRL) and repeat blast exposure (***p < 0.001 vs. CTRL) in the contralateral rat hippocampus. (C) AT8 expression was significantly increased at 1 month after closed-head injury in the ipsilateral mouse hippocampus (*p < 0.05 vs. CTRL). (D) No significant differences were observed in AT8 expression in the contralateral mouse hippocampus. (E) Immunoblots show no significant difference in tau phosphorylation at threonine site 181 (AT270) at 1 month after single and repeat blast exposure in the ipsilateral rat hippocampus. (F) A significant increase in AT270 expression was measured at 1 month after repeat blast exposure (*p < 0.05 vs. CTRL) in the contralateral rat hippocampus. (G) No significant differences were observed in AT270 expression in the ipsilateral mouse hippocampus, (H) or the contralateral mouse hippocampus after closed-head injury. One-way ANOVA Tukey’s post hoc analysis (values represent mean ± SEM; normalized to β-actin) (n = 3–5).