Purinergic signaling mediates neuroglial interactions to modulate sighs
Sighs prevent the collapse of alveoli in the lungs, initiate arousal under hypoxic conditions, and are an expression of sadness and relief. Sighs are periodically superimposed on normal breaths, known as eupnea. Implicated in the generation of these rhythmic behaviors is the preBötzinger complex (pr...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10471608/ https://www.ncbi.nlm.nih.gov/pubmed/37652903 http://dx.doi.org/10.1038/s41467-023-40812-x |
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author | Severs, Liza J. Bush, Nicholas E. Quina, Lely A. Hidalgo-Andrade, Skyler Burgraff, Nicholas J. Dashevskiy, Tatiana Shih, Andy Y. Baertsch, Nathan A. Ramirez, Jan-Marino |
author_facet | Severs, Liza J. Bush, Nicholas E. Quina, Lely A. Hidalgo-Andrade, Skyler Burgraff, Nicholas J. Dashevskiy, Tatiana Shih, Andy Y. Baertsch, Nathan A. Ramirez, Jan-Marino |
author_sort | Severs, Liza J. |
collection | PubMed |
description | Sighs prevent the collapse of alveoli in the lungs, initiate arousal under hypoxic conditions, and are an expression of sadness and relief. Sighs are periodically superimposed on normal breaths, known as eupnea. Implicated in the generation of these rhythmic behaviors is the preBötzinger complex (preBötC). Our experimental evidence suggests that purinergic signaling is necessary to generate spontaneous and hypoxia-induced sighs in a mouse model. Our results demonstrate that driving calcium increases in astrocytes through pharmacological methods robustly increases sigh, but not eupnea, frequency. Calcium imaging of preBötC slices corroborates this finding with an increase in astrocytic calcium upon application of sigh modulators, increasing intracellular calcium through g-protein signaling. Moreover, photo-activation of preBötC astrocytes is sufficient to elicit sigh activity, and this response is blocked with purinergic antagonists. We conclude that sighs are modulated through neuron-glia coupling in the preBötC network, where the distinct modulatory responses of neurons and glia allow for both rhythms to be independently regulated. |
format | Online Article Text |
id | pubmed-10471608 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-104716082023-09-02 Purinergic signaling mediates neuroglial interactions to modulate sighs Severs, Liza J. Bush, Nicholas E. Quina, Lely A. Hidalgo-Andrade, Skyler Burgraff, Nicholas J. Dashevskiy, Tatiana Shih, Andy Y. Baertsch, Nathan A. Ramirez, Jan-Marino Nat Commun Article Sighs prevent the collapse of alveoli in the lungs, initiate arousal under hypoxic conditions, and are an expression of sadness and relief. Sighs are periodically superimposed on normal breaths, known as eupnea. Implicated in the generation of these rhythmic behaviors is the preBötzinger complex (preBötC). Our experimental evidence suggests that purinergic signaling is necessary to generate spontaneous and hypoxia-induced sighs in a mouse model. Our results demonstrate that driving calcium increases in astrocytes through pharmacological methods robustly increases sigh, but not eupnea, frequency. Calcium imaging of preBötC slices corroborates this finding with an increase in astrocytic calcium upon application of sigh modulators, increasing intracellular calcium through g-protein signaling. Moreover, photo-activation of preBötC astrocytes is sufficient to elicit sigh activity, and this response is blocked with purinergic antagonists. We conclude that sighs are modulated through neuron-glia coupling in the preBötC network, where the distinct modulatory responses of neurons and glia allow for both rhythms to be independently regulated. Nature Publishing Group UK 2023-08-31 /pmc/articles/PMC10471608/ /pubmed/37652903 http://dx.doi.org/10.1038/s41467-023-40812-x 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 Severs, Liza J. Bush, Nicholas E. Quina, Lely A. Hidalgo-Andrade, Skyler Burgraff, Nicholas J. Dashevskiy, Tatiana Shih, Andy Y. Baertsch, Nathan A. Ramirez, Jan-Marino Purinergic signaling mediates neuroglial interactions to modulate sighs |
title | Purinergic signaling mediates neuroglial interactions to modulate sighs |
title_full | Purinergic signaling mediates neuroglial interactions to modulate sighs |
title_fullStr | Purinergic signaling mediates neuroglial interactions to modulate sighs |
title_full_unstemmed | Purinergic signaling mediates neuroglial interactions to modulate sighs |
title_short | Purinergic signaling mediates neuroglial interactions to modulate sighs |
title_sort | purinergic signaling mediates neuroglial interactions to modulate sighs |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10471608/ https://www.ncbi.nlm.nih.gov/pubmed/37652903 http://dx.doi.org/10.1038/s41467-023-40812-x |
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