Expression and Function of GABA Receptors in Myelinating Cells

Myelin facilitates the fast transmission of nerve impulses and provides metabolic support to axons. Differentiation of oligodendrocyte progenitor cells (OPCs) and Schwann cell (SC) precursors is critical for myelination during development and myelin repair in demyelinating disorders. Myelination is...

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Published inFrontiers in cellular neuroscience Vol. 14; p. 256
Main Authors Serrano-Regal, Mari Paz, Bayón-Cordero, Laura, Ordaz, Rainald Pablo, Garay, Edith, Limon, Agenor, Arellano, Rogelio O, Matute, Carlos, Sánchez-Gómez, María Victoria
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 21.08.2020
Frontiers Media S.A
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Summary:Myelin facilitates the fast transmission of nerve impulses and provides metabolic support to axons. Differentiation of oligodendrocyte progenitor cells (OPCs) and Schwann cell (SC) precursors is critical for myelination during development and myelin repair in demyelinating disorders. Myelination is tightly controlled by neuron-glia communication and requires the participation of a wide repertoire of signals, including neurotransmitters such as glutamate, ATP, adenosine, or γ-aminobutyric acid (GABA). GABA is the main inhibitory neurotransmitter in the central nervous system (CNS) and it is also present in the peripheral nervous system (PNS). The composition and function of GABA receptors (GABARs) are well studied in neurons, while their nature and role in glial cells are still incipient. Recent studies demonstrate that GABA-mediated signaling mechanisms play relevant roles in OPC and SC precursor development and function, and stand out the implication of GABARs in oligodendrocyte (OL) and SC maturation and myelination. In this review, we highlight the evidence supporting the novel role of GABA with an emphasis on the molecular identity of the receptors expressed in these glial cells and the possible signaling pathways involved in their actions. GABAergic signaling in myelinating cells may have potential implications for developing novel reparative therapies in demyelinating diseases.
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Reviewed by: Åsa Fex-Svenningsen, University of Southern Denmark, Denmark; Beatriz Garcia-Diaz, INSERM U1127 Institut du Cerveau et de la Moelle épinière (ICM), France; Maria Cecilia Angulo, Centre National de la Recherche Scientifique (CNRS), France
Edited by: Nicola B. Hamilton-Whitaker, King’s College London, United Kingdom
Specialty section: This article was submitted to Non-Neuronal Cells, a section of the journal Frontiers in Cellular Neuroscience
ORCID: Mari Paz Serrano-Regal orcid.org/0000-0002-1133-7261
ISSN:1662-5102
1662-5102
DOI:10.3389/fncel.2020.00256