Expression and Function of GABA Receptors in Myelinating Cells.
GABA
GABA receptor
Schwann cell
differentiation
myelination
oligodendrocyte
Journal
Frontiers in cellular neuroscience
ISSN: 1662-5102
Titre abrégé: Front Cell Neurosci
Pays: Switzerland
ID NLM: 101477935
Informations de publication
Date de publication:
2020
2020
Historique:
received:
25
05
2020
accepted:
24
07
2020
entrez:
25
9
2020
pubmed:
26
9
2020
medline:
26
9
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 32973453
doi: 10.3389/fncel.2020.00256
pmc: PMC7472887
doi:
Types de publication
Journal Article
Langues
eng
Pagination
256Subventions
Organisme : NIA NIH HHS
ID : R21 AG053740
Pays : United States
Organisme : NIMH NIH HHS
ID : R21 MH113177
Pays : United States
Informations de copyright
Copyright © 2020 Serrano-Regal, Bayón-Cordero, Ordaz, Garay, Limon, Arellano, Matute and Sánchez-Gómez.
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