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. 2016 Sep 1;4(1):95. doi: 10.1186/s40478-016-0369-5

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — Disruption of oligodendrocyte gap junctions (GJs) in inflamed brainstem. a–f Coronal brainstem sections immunostained for oligodendrocyte marker CC1 (green) and Cx47 (red) with nuclear DAPI staining (blue). In KO T55I tissues all oligodendrocytes transgenically express enhanced green fluorescent protein (EGFP) and were not stained with CC1. There is a reduction of Cx47 formed GJ plaques at oligodendrocyte cell bodies and proximal processes in LPS-injected mouse tissues (b, d, f) compared to saline controls (a, c, e) associated with increased intracellular signal of Cx47 suggesting diffusion (insets in d, f). Scale bars in a–f: 10 μm. Counts of GJ plaques per oligodendrocyte confirm a significant reduction in LPS tissues compared to controls in all genotypes (h, j, l), whereas total oligodendrocyte numbers remain unchanged in LPS compared to control groups (g, i, k) (Student’s t-test, *:p < 0.05, **:p < 0.01, ***:p < 0.001)