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. 2016 Feb 27;8(1):1759091416630220. doi: 10.1177/1759091416630220

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© The Author(s) 2016

This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — Moderate CCI triggers a significant downregulation of vGlut1-positive glutamatergic innervation of CA1 hippocampal neurons. We have analyzed vGlut1-positive puncta in SR area of the CA1 hippocampus, which immunolabels terminals of CA3 neurons innervating dendrites of CA1 neurons. (a–d) Fluorescent images show a reduced vGlut1-positive puncta in SR at 3 (c) and 7 dpi (d) as compared with control (a), suggesting a reduction in excitatory innervation of CA1 neurons following TBI. (e) Graph shows vGlut1-positive puncta per 100 µm² area (mean ± SEM; n = 3–4 mice, one-way ANOVA followed by Tukey’s post hoc analysis, *p < .05). (f) Graph shows a negative correlation between the mean levels of ephrin-B1 per ephrin-B1-positive astrocyte (x axis, n = 100–300 astrocytes per animal) and the average number of vGlut1-positive puncta per 100 µm² area (y axis, n = 50–100 images per animal) in SR area of CA1 hippocampus of four mice at 3 dpi. SR = stratum radiatum.