Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Jul 26;24(1):96. doi: 10.1186/s10194-023-01628-8

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 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.

PMC Copyright notice

Fig. 5 — Optogenetic CSDs trigger a prolonged neuroinflammatory response in the cortex of FHM1 mutant compared to WT mice. A Representative photomicrographs of HMGB1 immunolabeling of the primary somatosensory cortex (ipsilateral to the side of optogenetic CSD induction) of a WT and a FHM1 mutant mouse. HMGB1 immunolabeling is shown as red fluorescence signal. In naïve (untreated) mice, HMGB1 is located in cell nuclei as indicated with co-labeling with Hoechst-33258 (blue). CSD triggers massive release of HMGB1 from neuronal nuclei to the extracellular space 30 min after three optogenetically-induced CSDs (‘3x CSD’) in both WT and FHM1 mutant mice. At 24 h, in the ipsilateral cortex, release was still pronounced in both WT and mutant mice and less so at 48 h in both groups. B Quantification of the % of cells displaying nuclear HMGB1 release showed that release was higher in naïve (untreated) FHM1 mutant compared to WT mice. At 30 min, both ipsi- and contralateral release were increased in both FHM1 mutant and WT mice, with ipsilateral release being higher than contralateral release in WT mice, whereas in FHM1 mutant mice release was equally high in both hemispheres. Of note, contralateral release was higher in FHM1 mutant mice than WT mice at this time point. At 24 h after CSD, HMGB1 release remained elevated compared to baseline in the ipsilateral and contralateral cortex for both WT and FHM1 mutant mice. Compared to WT mice, at 24 h, FHM1 mutant mice showed a more pronounced HMGB1 release in the contralateral cortex. At 48 h following CSD, cortical HMGB1 release in WT mice remained increased compared to baseline levels whereas release had normalized in both hemispheres for FHM1 mutant mice, but note that baseline levels in FHM1 mutant mice are elevated compared to WT. C Representative photomicrographs of HMGB1 immunolabeling of the primary somatosensory cortex (ipsilateral to the side of sham stimulation) of a WT and a FHM1 mutant mouse. D HMGB1 release in the ipsi- and contralateral cortex is not affected by sham stimulation in either genotype. * p < 0.05, ** p < 0.01. Black asterisks and brackets: uncorrected p-values. Grey symbols: corrected p-values (after Kruskall-Wallis; see Results text for number and nature of corrections). Scale bar: 250 μm (applicable to all photomicrographs)