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dc.contributor.author
Beltrán González, Andrea Natalia
dc.contributor.author
Lopez Pazos, Manuel Ignacio
dc.contributor.author
Calvo, Daniel Juan
dc.date.available
2020-12-22T14:26:30Z
dc.date.issued
2020-07
dc.identifier.citation
Beltrán González, Andrea Natalia; Lopez Pazos, Manuel Ignacio; Calvo, Daniel Juan; Reactive Oxygen Species in the Regulation of the GABA Mediated Inhibitory Neurotransmission; Pergamon-Elsevier Science Ltd; Neuroscience; 439; 7-2020; 137-145
dc.identifier.issn
0306-4522
dc.identifier.uri
http://hdl.handle.net/11336/121031
dc.description.abstract
Reactive oxygen species (ROS) are best known for being involved in cellular metabolism and oxidative stress, but also play important roles in cell communication. ROS signaling has become increasingly recognized as a mechanism implicated in the regulation of synaptic neurotransmission, under both physiological and pathological conditions. Hydrogen peroxide (H2O2) and superoxide anion are the main biologically relevant endogenous ROS in the nervous system. They are predominantly produced in the mitochondria of neurons and glial cells and their levels are tightly regulated by the antioxidant cell machinery, which allows for dynamic signaling through these agents. Physicochemical and biological properties of H2O2 enable it to effectively play an important role in signaling. This review brings up some or the most significant evidence supporting ROS as signaling agents in the nervous system and summarizes data showing that ROS modulate γ-aminobutyric acid (GABA)-mediated neurotransmission by pre- and postsynaptic mechanisms. ROS induce changes on both, the activity of phasic and tonic GABAA receptors and GABA release from presynaptic terminals. Based on these facts, ROS signaling is discussed as a possible selective mechanism linking cellular metabolism to inhibitory neurotransmission through the direct or indirect modulation of the GABAA receptor function. This article is part of a Special Issue entitled: Honoring Ricardo Miledi - outstanding neuroscientist of XX-XXI centuries.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Pergamon-Elsevier Science Ltd
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
GABAA RECEPTOR
dc.subject
HYDROGEN PEROXIDE
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INHIBITORY NEUROTRANSMISSION
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REACTIVE OXYGEN SPECIES
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REDOX SIGNALING
dc.subject.classification
Neurociencias
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Reactive Oxygen Species in the Regulation of the GABA Mediated Inhibitory Neurotransmission
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-11-13T20:41:08Z
dc.journal.volume
439
dc.journal.pagination
137-145
dc.journal.pais
Estados Unidos
dc.journal.ciudad
Massachusetts
dc.description.fil
Fil: Beltrán González, Andrea Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
dc.description.fil
Fil: Lopez Pazos, Manuel Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
dc.description.fil
Fil: Calvo, Daniel Juan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
dc.journal.title
Neuroscience
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0306452219303951
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.neuroscience.2019.05.064
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