Glutamate forward and reverse transport: From molecular mechanism to transporter-mediated release after ischemia

DC ElementWertSprache
dc.contributor.authorGrewer, Christof
dc.contributor.authorGameiro, Armanda
dc.contributor.authorZhang, Zhou
dc.contributor.authorTao, Zhen
dc.contributor.authorBraams, Simona
dc.contributor.authorRauen, Thomas
dc.date.accessioned2021-12-23T16:20:58Z-
dc.date.available2021-12-23T16:20:58Z-
dc.date.issued2008
dc.identifier.issn15216543
dc.identifier.urihttps://osnascholar.ub.uni-osnabrueck.de/handle/unios/13672-
dc.description.abstractGlutamate transporters remove the excitatory neurotransmitter glutamate from the extracellular space after neurotransmission is complete, by taking glutamate up into neurons and glia cells. As thermodynamic machines, these transporters can also run in reverse, releasing glutamate into the extracellular space. Because glutamate is excitotoxic, this transporter-mediated release is detrimental to the health of neurons and axons, and it, thus, contributes to the brain damage that typically follows a stroke. This review highlights current ideas about the molecular mechanisms underlying glutamate uptake and glutamate reverse transport. It also discusses the implications of transporter-mediated glutamate release for cellular function under physiological and patho-physiological conditions. (C) 2008 IUBMB.
dc.description.sponsorshipNational Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [R01-NS0493]; Deutsche ForschungsgeineinschaftGerman Research Foundation (DFG) [1393/2-2,3, 753/1-1,2]; NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Neurological Disorders & Stroke (NINDS) [R56NS049335] Funding Source: NIH RePORTER; This work was supported by the National Institutes of Health Grant R01-NS0493 to CG and by the Deutsche Forschungsgeineinschaft Grants GR 1393/2-2,3 to CG and RA 753/1-1,2 to TR.
dc.language.isoen
dc.publisherWILEY
dc.relation.ispartofIUBMB LIFE
dc.subjectAMINO-ACID TRANSPORTER
dc.subjectANION CONDUCTANCE
dc.subjectASPARTATE
dc.subjectBiochemistry & Molecular Biology
dc.subjectCell Biology
dc.subjectCL-COTRANSPORT FUNCTION
dc.subjectelectrophysiology
dc.subjectGLT-1
dc.subjectglutamate release
dc.subjectglutamate transporter
dc.subjectION-BINDING
dc.subjectKINETICS
dc.subjectNA+
dc.subjectreverse transports
dc.subjectSUBSTRATE INTERACTIONS
dc.subjectTRANSLOCATION
dc.subjecttransport mechanism
dc.titleGlutamate forward and reverse transport: From molecular mechanism to transporter-mediated release after ischemia
dc.typereview
dc.identifier.doi10.1002/iub.98
dc.identifier.isiISI:000258893900007
dc.description.volume60
dc.description.issue9
dc.description.startpage609
dc.description.endpage619
dc.contributor.orcid0000-0001-9699-182X
dc.contributor.researcheridA-9082-2012
dc.identifier.eissn15216551
dc.publisher.place111 RIVER ST, HOBOKEN 07030-5774, NJ USA
dcterms.isPartOf.abbreviationIUBMB Life
dcterms.oaStatusGreen Accepted
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