Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal Cord

GABAergic signaling and GABA<sub>B</sub> receptors play crucial roles in regulating the physiology of oligodendrocyte-lineage cells, including their proliferation, differentiation, and myelination. Therefore, they are promising targets for studying how spinal oligodendrocyte precursor ce...

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Main Authors: Davide Gobbo, Phillip Rieder, Li-Pao Fang, Emeline Buttigieg, Moritz Schablowski, Elisa Damo, Nathalie Bosche, Eleonora Dallorto, Pascal May, Xianshu Bai, Frank Kirchhoff, Anja Scheller
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Language:English
Published: MDPI AG 2024-12-01
Series:Cells
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Online Access:https://www.mdpi.com/2073-4409/13/23/2014
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author Davide Gobbo
Phillip Rieder
Li-Pao Fang
Emeline Buttigieg
Moritz Schablowski
Elisa Damo
Nathalie Bosche
Eleonora Dallorto
Pascal May
Xianshu Bai
Frank Kirchhoff
Anja Scheller
author_facet Davide Gobbo
Phillip Rieder
Li-Pao Fang
Emeline Buttigieg
Moritz Schablowski
Elisa Damo
Nathalie Bosche
Eleonora Dallorto
Pascal May
Xianshu Bai
Frank Kirchhoff
Anja Scheller
author_sort Davide Gobbo
collection DOAJ
description GABAergic signaling and GABA<sub>B</sub> receptors play crucial roles in regulating the physiology of oligodendrocyte-lineage cells, including their proliferation, differentiation, and myelination. Therefore, they are promising targets for studying how spinal oligodendrocyte precursor cells (OPCs) respond to injuries and neurodegenerative diseases like multiple sclerosis. Taking advantage of the temporally controlled and cell-specific genetic downregulation of GABA<sub>B</sub> receptors from OPCs, our investigation addresses their specific influence on OPC behavior in the gray and white matter of the mouse spinal cord. Our results show that, while GABA<sub>B</sub> receptors do not significantly alter spinal cord myelination under physiological conditions, they distinctly regulate the OPC differentiation and Ca<sup>2+</sup> signaling. In addition, we investigate the impact of OPC-GABA<sub>B</sub> receptors in two models of toxic demyelination, namely, the cuprizone and the lysolecithin models. The genetic downregulation of OPC-GABA<sub>B</sub> receptors protects against demyelination and oligodendrocyte loss. Additionally, we observe the enhanced resilience to cuprizone-induced pathological alterations in OPC Ca<sup>2+</sup> signaling. Our results provide valuable insights into the potential therapeutic implications of manipulating GABA<sub>B</sub> receptors in spinal cord OPCs and deepen our understanding of the interplay between GABAergic signaling and spinal cord OPCs, providing a basis for future research.
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spelling doaj-art-7d696dd40dfd490c85a08ff72feb59992025-08-20T02:38:46ZengMDPI AGCells2073-44092024-12-011323201410.3390/cells13232014Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal CordDavide Gobbo0Phillip Rieder1Li-Pao Fang2Emeline Buttigieg3Moritz Schablowski4Elisa Damo5Nathalie Bosche6Eleonora Dallorto7Pascal May8Xianshu Bai9Frank Kirchhoff10Anja Scheller11Department of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyDepartment of Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, GermanyGABAergic signaling and GABA<sub>B</sub> receptors play crucial roles in regulating the physiology of oligodendrocyte-lineage cells, including their proliferation, differentiation, and myelination. Therefore, they are promising targets for studying how spinal oligodendrocyte precursor cells (OPCs) respond to injuries and neurodegenerative diseases like multiple sclerosis. Taking advantage of the temporally controlled and cell-specific genetic downregulation of GABA<sub>B</sub> receptors from OPCs, our investigation addresses their specific influence on OPC behavior in the gray and white matter of the mouse spinal cord. Our results show that, while GABA<sub>B</sub> receptors do not significantly alter spinal cord myelination under physiological conditions, they distinctly regulate the OPC differentiation and Ca<sup>2+</sup> signaling. In addition, we investigate the impact of OPC-GABA<sub>B</sub> receptors in two models of toxic demyelination, namely, the cuprizone and the lysolecithin models. The genetic downregulation of OPC-GABA<sub>B</sub> receptors protects against demyelination and oligodendrocyte loss. Additionally, we observe the enhanced resilience to cuprizone-induced pathological alterations in OPC Ca<sup>2+</sup> signaling. Our results provide valuable insights into the potential therapeutic implications of manipulating GABA<sub>B</sub> receptors in spinal cord OPCs and deepen our understanding of the interplay between GABAergic signaling and spinal cord OPCs, providing a basis for future research.https://www.mdpi.com/2073-4409/13/23/2014spinal cordGABA<sub>B</sub> receptorsoligodendrocyte precursor cellsdemyelinationcuprizone
spellingShingle Davide Gobbo
Phillip Rieder
Li-Pao Fang
Emeline Buttigieg
Moritz Schablowski
Elisa Damo
Nathalie Bosche
Eleonora Dallorto
Pascal May
Xianshu Bai
Frank Kirchhoff
Anja Scheller
Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal Cord
Cells
spinal cord
GABA<sub>B</sub> receptors
oligodendrocyte precursor cells
demyelination
cuprizone
title Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal Cord
title_full Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal Cord
title_fullStr Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal Cord
title_full_unstemmed Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal Cord
title_short Genetic Downregulation of GABA<sub>B</sub> Receptors from Oligodendrocyte Precursor Cells Protects Against Demyelination in the Mouse Spinal Cord
title_sort genetic downregulation of gaba sub b sub receptors from oligodendrocyte precursor cells protects against demyelination in the mouse spinal cord
topic spinal cord
GABA<sub>B</sub> receptors
oligodendrocyte precursor cells
demyelination
cuprizone
url https://www.mdpi.com/2073-4409/13/23/2014
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