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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 astrogliosis in the ipsilateral 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-GFAP antibody was performed. Brain sections at − 2 mm from bregma were used for the visualization of thalamic astrocyte activation. (A) Coronal brain section showing activated astrocytes (GFAP) in the posterior region of the primary injury and in the ipsilateral thalamus at PSD 14. A glial scar is evident in the cortical injury, but not within the thalamus (10X obj, stitched image; scale bar = 1 mm). (B) Time course of GFAP staining showing delayed astrocyte activation in the ipsilateral thalamus (20X obj; scale bar = 20 µm).