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Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia
Resting state networks (RSN), which show the connectivity in the brain in the absence of any stimuli, are increasingly important to assess brain function. Here, we investigate the changes in RSN as well as the hemodynamic changes during acute, global hypoxia. Mice were imaged at different levels of...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10427674/ https://www.ncbi.nlm.nih.gov/pubmed/37582847 http://dx.doi.org/10.1038/s41598-023-40321-3 |
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author | Bakker, Marleen E. Djerourou, Ismaël Belanger, Samuel Lesage, Frédéric Vanni, Matthieu P. |
author_facet | Bakker, Marleen E. Djerourou, Ismaël Belanger, Samuel Lesage, Frédéric Vanni, Matthieu P. |
author_sort | Bakker, Marleen E. |
collection | PubMed |
description | Resting state networks (RSN), which show the connectivity in the brain in the absence of any stimuli, are increasingly important to assess brain function. Here, we investigate the changes in RSN as well as the hemodynamic changes during acute, global hypoxia. Mice were imaged at different levels of oxygen (21, 12, 10 and 8%) over the course of 10 weeks, with hypoxia and normoxia acquisitions interspersed. Simultaneous GCaMP and intrinsic optical imaging allowed tracking of both neuronal and hemodynamic changes. During hypoxic conditions, we found a global increase of both HbO and HbR in the brain. The saturation levels of blood dropped after the onset of hypoxia, but surprisingly climbed back to levels similar to baseline within the 10-min hypoxia period. Neuronal activity also showed a peak at the onset of hypoxia, but dropped back to baseline as well. Despite regaining baseline sO2 levels, changes in neuronal RSN were observed. In particular, the connectivity as measured with GCaMP between anterior and posterior parts of the brain decreased. In contrast, when looking at these same connections with HbO measurements, an increase in connectivity in anterior–posterior brain areas was observed suggesting a potential neurovascular decoupling. |
format | Online Article Text |
id | pubmed-10427674 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-104276742023-08-17 Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia Bakker, Marleen E. Djerourou, Ismaël Belanger, Samuel Lesage, Frédéric Vanni, Matthieu P. Sci Rep Article Resting state networks (RSN), which show the connectivity in the brain in the absence of any stimuli, are increasingly important to assess brain function. Here, we investigate the changes in RSN as well as the hemodynamic changes during acute, global hypoxia. Mice were imaged at different levels of oxygen (21, 12, 10 and 8%) over the course of 10 weeks, with hypoxia and normoxia acquisitions interspersed. Simultaneous GCaMP and intrinsic optical imaging allowed tracking of both neuronal and hemodynamic changes. During hypoxic conditions, we found a global increase of both HbO and HbR in the brain. The saturation levels of blood dropped after the onset of hypoxia, but surprisingly climbed back to levels similar to baseline within the 10-min hypoxia period. Neuronal activity also showed a peak at the onset of hypoxia, but dropped back to baseline as well. Despite regaining baseline sO2 levels, changes in neuronal RSN were observed. In particular, the connectivity as measured with GCaMP between anterior and posterior parts of the brain decreased. In contrast, when looking at these same connections with HbO measurements, an increase in connectivity in anterior–posterior brain areas was observed suggesting a potential neurovascular decoupling. Nature Publishing Group UK 2023-08-15 /pmc/articles/PMC10427674/ /pubmed/37582847 http://dx.doi.org/10.1038/s41598-023-40321-3 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Bakker, Marleen E. Djerourou, Ismaël Belanger, Samuel Lesage, Frédéric Vanni, Matthieu P. Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia |
title | Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia |
title_full | Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia |
title_fullStr | Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia |
title_full_unstemmed | Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia |
title_short | Alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia |
title_sort | alteration of functional connectivity despite preserved cerebral oxygenation during acute hypoxia |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10427674/ https://www.ncbi.nlm.nih.gov/pubmed/37582847 http://dx.doi.org/10.1038/s41598-023-40321-3 |
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