About: Pharmacology of Glutamate Transport in the CNS: Substrates and Inhibitors of Excitatory Amino Acid Transporters (EAATs) and the Glutamate/Cystine Exchanger System x(c)(−)

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About: Pharmacology of Glutamate Transport in the CNS: Substrates and Inhibitors of Excitatory Amino Acid Transporters (EAATs) and the Glutamate/Cystine Exchanger System x(c)(−) Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Pharmacology of Glutamate Transport in the CNS: Substrates and Inhibitors of Excitatory Amino Acid Transporters (EAATs) and the Glutamate/Cystine Exchanger System x(c)(−)
Creator	Bridges, Richard Patel, Sarjubhai
Source	PMC
abstract	As the primary excitatory neurotransmitter in the mammalian CNS, l-glutamateparticipates not only in standard fast synaptic communication, but also contributes to higher order signalprocessing, as well as neuropathology. Given this variety of functional roles, interest has been growingas to how the extracellular concentrations of l-glutamate surroundingneurons are regulated by cellular transporter proteins. This review focuses on two prominent systems, eachof which appears capable of influencing both the signaling and pathological actions of l-glutamatewithin the CNS: the sodium-dependent excitatory amino acid transporters (EAATs) and the glutamate/cystineexchanger, system x (c) (−)(Sx (c) (−)). Whilethe family of EAAT subtypes limit access to glutamate receptors by rapidly and efficiently sequesteringl-glutamate in neurons and glia, Sx(c) (−)provides a route for the export of glutamate from cells into the extracellular environment. The primaryintent of this work is to provide an overview of the inhibitors and substrates that have been developedto delineate the pharmacological specificity of these transport systems, as well as be exploited as probeswith which to selectively investigate function. Particular attention is paid to the development of smallmolecule templates that mimic the structural properties of the endogenous substrates, l-glutamate,l-aspartate and l-cystine andhow strategic control of functional group position and/or the introduction of lipophilic R-groups can impactmultiple aspects of the transport process, including: subtype selectivity, inhibitory potency, and substrateactivity.
has issue date	2008-10-16(xsd:dateTime)
bibo:doi	10.1007/7355_2008_026
has license	no-cc
sha1sum (hex)	c4be5ce968a28d7fd0f1ae78c4875f0d780d004a
schema:url	https://doi.org/10.1007/7355_2008_026
resource representing a document's title	Pharmacology of Glutamate Transport in the CNS: Substrates and Inhibitors of Excitatory Amino Acid Transporters (EAATs) and the Glutamate/Cystine Exchanger System x(c)(−)
has PubMed Central identifier	PMC7123079
schema:publication	Transporters as Targets for Drugs
resource representing a document's body	covid:c4be5ce968a28d7fd0f1ae78c4875f0d780d004a#body_text
is schema:about of	named entity 'CNS' named entity 'Glutamate' named entity 'Cystine' named entity 'CNS' named entity 'Pharmacology' named entity 'Substrates' named entity 'Glutamate' named entity 'EAATs' named entity 'Excitatory Amino Acid' named entity 'Glutamate' named entity 'Exchanger' named entity 'Inhibitors' named entity 'Pharmacology' named entity 'Substrates' named entity 'Amino Acid' named entity 'Cystine' named entity 'Glutamate' named entity 'System' named entity 'Transporters' named entity 'EXCITATORY AMINO ACID TRANSPORTERS' named entity 'GLUTAMATE TRANSPORT' named entity 'CNS' named entity 'EXCHANGER' named entity 'PHARMACOLOGY' named entity 'GLUTAMATE' named entity 'SYSTEM' named entity 'INHIBITORS'
is part of of	Pharmacology of Glutamate Transport in the CNS: Substrates and Inhibitors of Excitatory Amino Acid Transporters (EAATs) and the Glutamate/Cystine Exchanger System x(c)(−) As the primary excitatory neurotransmitter in the mammalian CNS, l-glutamateparticipates not only in standard fast synaptic communication, but also contributes to higher order signalprocessing, as well as neuropathology. Given this variety of functional roles, interest has been growingas to how the extracellular concentrations of l-glutamate surroundingneurons are regulated by cellular transporter proteins. This review focuses on two prominent systems, eachof which appears capable of influencing both the signaling and pathological actions of l-glutamatewithin the CNS: the sodium-dependent excitatory amino acid transporters (EAATs) and the glutamate/cystineexchanger, system x (c) (−)(Sx (c) (−)). Whilethe family of EAAT subtypes limit access to glutamate receptors by rapidly and efficiently sequesteringl-glutamate in neurons and glia, Sx(c) (−)provides a route for the export of glutamate from cells into the extracellular environment. The primaryintent of this work is to provide an overview of the inhibitors and substrates that have been developedto delineate the pharmacological specificity of these transport systems, as well as be exploited as probeswith which to selectively investigate function. Particular attention is paid to the development of smallmolecule templates that mimic the structural properties of the endogenous substrates, l-glutamate,l-aspartate and l-cystine andhow strategic control of functional group position and/or the introduction of lipophilic R-groups can impactmultiple aspects of the transport process, including: subtype selectivity, inhibitory potency, and substrateactivity. covid:c4be5ce968a28d7fd0f1ae78c4875f0d780d004a#body_text

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