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Glutamatergic Transmission: A Matter of Three

Glutamatergic transmission in the vertebrate brain requires the involvement of glia cells, in a continuous molecular dialogue. Glial glutamate receptors and transporters are key molecules that sense synaptic activity and by these means modify their physiology in the short and long term. Posttranslat...

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Detalles Bibliográficos
Autores principales: Martínez-Lozada, Zila, Ortega, Arturo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539489/
https://www.ncbi.nlm.nih.gov/pubmed/26345375
http://dx.doi.org/10.1155/2015/787396
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author Martínez-Lozada, Zila
Ortega, Arturo
author_facet Martínez-Lozada, Zila
Ortega, Arturo
author_sort Martínez-Lozada, Zila
collection PubMed
description Glutamatergic transmission in the vertebrate brain requires the involvement of glia cells, in a continuous molecular dialogue. Glial glutamate receptors and transporters are key molecules that sense synaptic activity and by these means modify their physiology in the short and long term. Posttranslational modifications that regulate protein-protein interactions and modulate transmitter removal are triggered in glial cells by neuronal released glutamate. Moreover, glutamate signaling cascades in these cells are linked to transcriptional and translational control and are critically involved in the control of the so-called glutamate/glutamine shuttle and by these means in glutamatergic neurotransmission. In this contribution, we summarize our current understanding of the biochemical consequences of glutamate synaptic activity in their surrounding partners and dissect the molecular mechanisms that allow neurons to take control of glia physiology to ensure proper glutamate-mediated neuronal communication.
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spelling pubmed-45394892015-09-06 Glutamatergic Transmission: A Matter of Three Martínez-Lozada, Zila Ortega, Arturo Neural Plast Review Article Glutamatergic transmission in the vertebrate brain requires the involvement of glia cells, in a continuous molecular dialogue. Glial glutamate receptors and transporters are key molecules that sense synaptic activity and by these means modify their physiology in the short and long term. Posttranslational modifications that regulate protein-protein interactions and modulate transmitter removal are triggered in glial cells by neuronal released glutamate. Moreover, glutamate signaling cascades in these cells are linked to transcriptional and translational control and are critically involved in the control of the so-called glutamate/glutamine shuttle and by these means in glutamatergic neurotransmission. In this contribution, we summarize our current understanding of the biochemical consequences of glutamate synaptic activity in their surrounding partners and dissect the molecular mechanisms that allow neurons to take control of glia physiology to ensure proper glutamate-mediated neuronal communication. Hindawi Publishing Corporation 2015 2015-08-04 /pmc/articles/PMC4539489/ /pubmed/26345375 http://dx.doi.org/10.1155/2015/787396 Text en Copyright © 2015 Z. Martínez-Lozada and A. Ortega. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Martínez-Lozada, Zila
Ortega, Arturo
Glutamatergic Transmission: A Matter of Three
title Glutamatergic Transmission: A Matter of Three
title_full Glutamatergic Transmission: A Matter of Three
title_fullStr Glutamatergic Transmission: A Matter of Three
title_full_unstemmed Glutamatergic Transmission: A Matter of Three
title_short Glutamatergic Transmission: A Matter of Three
title_sort glutamatergic transmission: a matter of three
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539489/
https://www.ncbi.nlm.nih.gov/pubmed/26345375
http://dx.doi.org/10.1155/2015/787396
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