Linked Life Data

15390112

Source:http://linkedlifedata.com/resource/pubmed/id/15390112

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-10-27
pubmed:abstractText
Release of glutamine from astrocytes is an essential step of the glutamate-glutamine cycle, and hence for the maintenance of neuronal glutamate and gamma-aminobutyric acid (GABA) pools. The glutamine transporter SNAT3 (SN1) has recently been identified as one of the major mediators of glutamine efflux from astrocytes. We investigated the regulation of SNAT3 mediated glutamine transport in cultured astrocytes. Incubation of primary astrocyte cultures with physiological concentrations of glutamate resulted in a rapid, about twofold, upregulation of SNAT3-mediated transport activity. The effect was not mediated by glutamate receptors but required uptake of glutamate into astrocytes. Both net uptake and net efflux increased after treatment of cells with glutamate, excluding an acceleration of the transport by way of an exchange mechanism. Elevated intracellular glutamate most likely reduces the K(m) of SNAT3 for its substrate glutamine. The results suggest that astrocytes respond actively to the release of glutamate by increasing glutamine release and thereby may modulate glutamatergic neurotransmission.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0894-1491
pubmed:author
pubmed:copyrightInfo
copyright 2004 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
298-310
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Astroglial glutamine transport by system N is upregulated by glutamate.
pubmed:affiliation
School of Biochemistry and Molecular Biology, Australian National University, Canberra, Australia.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't