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Zmatrix and gaba11/9/2023 ![]() ![]() Among them, GABAergic signaling has attracted great interest in the last years ( Procacci et al., 2013 Zonouzi et al., 2015 Arellano et al., 2016 Hamilton et al., 2017 Serrano-Regal et al., 2020). Neuronal activity and several signals such as transcriptional and growth factors, axonal ligands, hormones, extracellular matrix components or neurotransmitters regulate OPC/SC precursor differentiation and myelination. In this regard, understanding the mechanisms of action involved in this complex neuron-glia crosstalk will help us in the search for new therapeutic approaches in these pathologies. These immature SCs can generate both myelinating and non-myelinating SCs (or Remak glia) according to PNS requirements, like the presence of specific signals in the microenvironment and the diameter of axons in their vicinity ( Jessen and Mirsky, 2005, 2019 Kidd et al., 2013).ĭifferentiation of OPCs and SC precursors is necessary for remyelination in demyelinating diseases like multiple sclerosis (MS) and myelin formation in dysmyelinating diseases such as leukodystrophies in the CNS or Charcot-Marie Tooth in the PNS. On the other hand, SCs derive from SC precursors, which differentiate into immature SCs. Mature myelinating OLs develop from glial precursors named oligodendrocyte progenitor cells (OPCs), which constitute the main proliferating cell type in the adult CNS ( Dawson et al., 2003). Regarding their specific characteristics, oligodendroglial cells represent a highly diverse and specialized cell population ( Marques et al., 2016). Thus, myelination represents the major function of these cells, although they carry it out with some differences while OLs can myelinate multiple axons simultaneously, each SC wraps one single axon ( Jessen and Mirsky, 2005 Nave and Trapp, 2008). Myelin speeds up nerve impulse propagation and provides metabolic and trophic support to axons ( Nave and Trapp, 2008 Kidd et al., 2013 Philips and Rothstein, 2017). These cells are responsible for myelin building and maintenance, a function highly regulated by neuronal activity ( Gibson et al., 2014 Mitew et al., 2018). In vertebrates, oligodendrocytes (OLs) and Schwann cells (SCs) are the myelin-forming glia of the central nervous system (CNS) and peripheral nervous system (PNS), respectively. Glial cells express a vast repertoire of receptors and transporters for neurotransmitters and neuromodulators and respond to axonal signals, being key and active elements of the nervous system ( Allen and Lyons, 2018). GABAergic signaling in myelinating cells may have potential implications for developing novel reparative therapies in demyelinating diseases. ![]() 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. 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. The composition and function of GABA receptors (GABARs) are well studied in neurons, while their nature and role in glial cells are still incipient. GABA is the main inhibitory neurotransmitter in the central nervous system (CNS) and it is also present in the peripheral nervous system (PNS). 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). Differentiation of oligodendrocyte progenitor cells (OPCs) and Schwann cell (SC) precursors is critical for myelination during development and myelin repair in demyelinating disorders. Myelin facilitates the fast transmission of nerve impulses and provides metabolic support to axons. 5Department of Neurology, Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, United States. ![]()
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