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. 2017 Sep 7;8:473. doi: 10.1038/s41467-017-00618-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Tau^−/− mice are protected from neurological deficits, aberrant hyperexcitation and extensive brain damage after transient MCAO. a Western blotting for murine tau (mTau) in brain extracts from tau^+/+ and tau^−/− mice. GAPDH confirmed equal loading. b Ischemic stroke was induced by middle cerebral artery occlusion (MCAO) for 1.5 h with subsequent reperfusion. Drop in blood flow in the MCA was the same in tau^−/− and tau^+/+ mice during MCAO, as determined by laser Doppler flowmetry (not significant; N = 12; Student’s t-test). Unit, % of baseline flow. c Neurological scoring (with higher numbers indicating more severe impairments) revealed similar deficits directly after MCAO in tau^−/− and tau^+/+ mice. Only tau^+/+ mice showed a worsening of deficits at 24 h (**P < 0.01; N = 12; 2-way ANOVA (Sidak post hoc)). d Representative electroencephalography (EEG) recordings in tau^−/− and tau^+/+ mice at baseline (0 h) and indicated times after transient MCAO. Suppressed EEG signals recovered after 12 h following MCAO in tau^−/− mice, while tau^+/+ mice presented with epileptiform discharges (gray boxed) after 6 h. e Quantification revealed persistently high numbers of epileptiform discharges 6 h after transient MCAO (***p < 0.001 vs. tau^−/− MCAO; N = 5; two-way ANOVA (Bonferroni post hoc)). A small increase in epileptiform spike trains was transient in tau^−/− mice, and reached levels of sham operated tau^−/− and tau^+/+ mice 24 h after transient MCAO. f EEG frequency power spectrum (0–25 Hz) tau^+/+ and tau^−/− mice at baseline (0 h) indicated times following transient MCAO, with recovery only in tau^−/− animals. g Quantification of EEG recordings showed a progressive amplitude decline in tau^+/+ mice that partial recovered tau^−/− animals (*p < 0.05; N = 5; two-way ANOVA (Bonferroni post hoc)). h TTC-stained serial brain sections of tau^+/+ and tau^−/− mice 24 h after MCAO (viable tissue stains red). Note the large infarcted area (white) in tau^+/+, while only minimal brain damage was present in tau^−/− mice (arrow). i Volumetric quantification of infarct and brain volumes in tau^+/+ and tau^−/− mice 24 h after transient MCAO (***p < 0.001; N = 12; Student’s t-test). All error bars are s.e.m