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Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep
Astrocytic Ca(2+) signaling has been intensively studied in health and disease but has not been quantified during natural sleep. Here, we employ an activity-based algorithm to assess astrocytic Ca(2+) signals in the neocortex of awake and naturally sleeping mice while monitoring neuronal Ca(2+) acti...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7338360/ https://www.ncbi.nlm.nih.gov/pubmed/32632168 http://dx.doi.org/10.1038/s41467-020-17062-2 |
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author | Bojarskaite, Laura Bjørnstad, Daniel M. Pettersen, Klas H. Cunen, Céline Hermansen, Gudmund Horn Åbjørsbråten, Knut Sindre Chambers, Anna R. Sprengel, Rolf Vervaeke, Koen Tang, Wannan Enger, Rune Nagelhus, Erlend A. |
author_facet | Bojarskaite, Laura Bjørnstad, Daniel M. Pettersen, Klas H. Cunen, Céline Hermansen, Gudmund Horn Åbjørsbråten, Knut Sindre Chambers, Anna R. Sprengel, Rolf Vervaeke, Koen Tang, Wannan Enger, Rune Nagelhus, Erlend A. |
author_sort | Bojarskaite, Laura |
collection | PubMed |
description | Astrocytic Ca(2+) signaling has been intensively studied in health and disease but has not been quantified during natural sleep. Here, we employ an activity-based algorithm to assess astrocytic Ca(2+) signals in the neocortex of awake and naturally sleeping mice while monitoring neuronal Ca(2+) activity, brain rhythms and behavior. We show that astrocytic Ca(2+) signals exhibit distinct features across the sleep-wake cycle and are reduced during sleep compared to wakefulness. Moreover, an increase in astrocytic Ca(2+) signaling precedes transitions from slow wave sleep to wakefulness, with a peak upon awakening exceeding the levels during whisking and locomotion. Finally, genetic ablation of an important astrocytic Ca(2+) signaling pathway impairs slow wave sleep and results in an increased number of microarousals, abnormal brain rhythms, and an increased frequency of slow wave sleep state transitions and sleep spindles. Our findings demonstrate an essential role for astrocytic Ca(2+) signaling in regulating slow wave sleep. |
format | Online Article Text |
id | pubmed-7338360 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-73383602020-07-09 Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep Bojarskaite, Laura Bjørnstad, Daniel M. Pettersen, Klas H. Cunen, Céline Hermansen, Gudmund Horn Åbjørsbråten, Knut Sindre Chambers, Anna R. Sprengel, Rolf Vervaeke, Koen Tang, Wannan Enger, Rune Nagelhus, Erlend A. Nat Commun Article Astrocytic Ca(2+) signaling has been intensively studied in health and disease but has not been quantified during natural sleep. Here, we employ an activity-based algorithm to assess astrocytic Ca(2+) signals in the neocortex of awake and naturally sleeping mice while monitoring neuronal Ca(2+) activity, brain rhythms and behavior. We show that astrocytic Ca(2+) signals exhibit distinct features across the sleep-wake cycle and are reduced during sleep compared to wakefulness. Moreover, an increase in astrocytic Ca(2+) signaling precedes transitions from slow wave sleep to wakefulness, with a peak upon awakening exceeding the levels during whisking and locomotion. Finally, genetic ablation of an important astrocytic Ca(2+) signaling pathway impairs slow wave sleep and results in an increased number of microarousals, abnormal brain rhythms, and an increased frequency of slow wave sleep state transitions and sleep spindles. Our findings demonstrate an essential role for astrocytic Ca(2+) signaling in regulating slow wave sleep. Nature Publishing Group UK 2020-07-06 /pmc/articles/PMC7338360/ /pubmed/32632168 http://dx.doi.org/10.1038/s41467-020-17062-2 Text en © The Author(s) 2020 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Bojarskaite, Laura Bjørnstad, Daniel M. Pettersen, Klas H. Cunen, Céline Hermansen, Gudmund Horn Åbjørsbråten, Knut Sindre Chambers, Anna R. Sprengel, Rolf Vervaeke, Koen Tang, Wannan Enger, Rune Nagelhus, Erlend A. Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep |
title | Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep |
title_full | Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep |
title_fullStr | Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep |
title_full_unstemmed | Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep |
title_short | Astrocytic Ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep |
title_sort | astrocytic ca(2+) signaling is reduced during sleep and is involved in the regulation of slow wave sleep |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7338360/ https://www.ncbi.nlm.nih.gov/pubmed/32632168 http://dx.doi.org/10.1038/s41467-020-17062-2 |
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