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. 2021 Jun 15;11:12613. doi: 10.1038/s41598-021-91998-3

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© The Author(s) 2021

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/.

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Cortical stroke induces delayed microglial activation in the thalamus. Cortical infarction was induced in young C57BL/6 J mice. At 3 days, 1 week and 2 weeks after stroke, brains were isolated and sectioned. Immunostaining with anti-IBA-1 antibody was performed. Brain sections at − 2 mm from bregma were used for the visualization of thalamic microglial activation. (A) Coronal brain section showing activated MG/macrophages (IBA-1) in the posterior region of the primary injury and in the ipsilateral thalamus at PSD 14 (10X obj, stitched image). (B) Enlarged images showing morphology of MG/macrophages in the ipsilateral and contralateral thalamus at PSD 14 (scale bar = 10 µm, 63X obj). (C) The microglial soma size, located in the ipsilateral thalamus, is much bigger than microglia in the contralateral thalamus (# p < 0.05, unpaired t test) (D) Time course of IBA-1 staining showing delayed MG/macrophage activation in the ipsilateral thalamus (scale bar = 20 µm).