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Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior
Cortical neural circuits are complex but very precise networks of balanced excitation and inhibition. Yet, the molecular and cellular mechanisms that form the balance are just beginning to emerge. Here, using conditional γ-aminobutyric acid receptor B1- deficient mice we identify a γ-aminobutyric ac...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8927409/ https://www.ncbi.nlm.nih.gov/pubmed/35296664 http://dx.doi.org/10.1038/s41467-022-29020-1 |
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author | Fang, Li-Pao Zhao, Na Caudal, Laura C. Chang, Hsin-Fang Zhao, Renping Lin, Ching-Hsin Hainz, Nadine Meier, Carola Bettler, Bernhard Huang, Wenhui Scheller, Anja Kirchhoff, Frank Bai, Xianshu |
author_facet | Fang, Li-Pao Zhao, Na Caudal, Laura C. Chang, Hsin-Fang Zhao, Renping Lin, Ching-Hsin Hainz, Nadine Meier, Carola Bettler, Bernhard Huang, Wenhui Scheller, Anja Kirchhoff, Frank Bai, Xianshu |
author_sort | Fang, Li-Pao |
collection | PubMed |
description | Cortical neural circuits are complex but very precise networks of balanced excitation and inhibition. Yet, the molecular and cellular mechanisms that form the balance are just beginning to emerge. Here, using conditional γ-aminobutyric acid receptor B1- deficient mice we identify a γ-aminobutyric acid/tumor necrosis factor superfamily member 12-mediated bidirectional communication pathway between parvalbumin-positive fast spiking interneurons and oligodendrocyte precursor cells that determines the density and function of interneurons in the developing medial prefrontal cortex. Interruption of the GABAergic signaling to oligodendrocyte precursor cells results in reduced myelination and hypoactivity of interneurons, strong changes of cortical network activities and impaired social cognitive behavior. In conclusion, glial transmitter receptors are pivotal elements in finetuning distinct brain functions. |
format | Online Article Text |
id | pubmed-8927409 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-89274092022-04-01 Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior Fang, Li-Pao Zhao, Na Caudal, Laura C. Chang, Hsin-Fang Zhao, Renping Lin, Ching-Hsin Hainz, Nadine Meier, Carola Bettler, Bernhard Huang, Wenhui Scheller, Anja Kirchhoff, Frank Bai, Xianshu Nat Commun Article Cortical neural circuits are complex but very precise networks of balanced excitation and inhibition. Yet, the molecular and cellular mechanisms that form the balance are just beginning to emerge. Here, using conditional γ-aminobutyric acid receptor B1- deficient mice we identify a γ-aminobutyric acid/tumor necrosis factor superfamily member 12-mediated bidirectional communication pathway between parvalbumin-positive fast spiking interneurons and oligodendrocyte precursor cells that determines the density and function of interneurons in the developing medial prefrontal cortex. Interruption of the GABAergic signaling to oligodendrocyte precursor cells results in reduced myelination and hypoactivity of interneurons, strong changes of cortical network activities and impaired social cognitive behavior. In conclusion, glial transmitter receptors are pivotal elements in finetuning distinct brain functions. Nature Publishing Group UK 2022-03-16 /pmc/articles/PMC8927409/ /pubmed/35296664 http://dx.doi.org/10.1038/s41467-022-29020-1 Text en © The Author(s) 2022 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 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/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Fang, Li-Pao Zhao, Na Caudal, Laura C. Chang, Hsin-Fang Zhao, Renping Lin, Ching-Hsin Hainz, Nadine Meier, Carola Bettler, Bernhard Huang, Wenhui Scheller, Anja Kirchhoff, Frank Bai, Xianshu Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior |
title | Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior |
title_full | Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior |
title_fullStr | Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior |
title_full_unstemmed | Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior |
title_short | Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior |
title_sort | impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8927409/ https://www.ncbi.nlm.nih.gov/pubmed/35296664 http://dx.doi.org/10.1038/s41467-022-29020-1 |
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