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. 2023 Nov 6;20:253. doi: 10.1186/s12974-023-02921-8

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 6 — Mertk cKO animals display dysregulated OPC/OL dynamics during cuprizone-mediated demyelination. A Representative immunostaining of the corpus callosum from Mertk WT and cKO animals following 3 and 5 weeks cuprizone-challenge. Hoechst-labelled nuclei in cyan. Scale bar represents 50 µm. Inset scale bar represents 25 µm. B The density of Iba1^+ve microglia was similar between Mertk WT and cKO mice. C The density of PDGFRα^+ve OPCs was altered over the course of cuprizone-induced demyelination, with significantly more OPCs observed following 5 weeks demyelination. D A substantial reduction in CC1^+ve oligodendrocytes was observed in the absence of microglial Mertk, although this did not reach statistical significance. Data obtained from n = 4 mice per group. Data represent means ± SD. Statistical significance was determined using two-way ANOVA with Fisher's LSD