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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-157

Jabaudon, D; Scanziani, M; Gähwiler, B H; Gerber, U (2000). Acute decrease in net glutamate uptake during energy deprivation. Proceedings of the National Academy of Sciences of the United States of America (PNAS), 97(10):5610-5615.

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Abstract

The extracellular glutamate concentration ([glu](o)) rises during cerebral ischemia, reaching levels capable of inducing delayed neuronal death. The mechanisms underlying this glutamate accumulation remain controversial. We used N-methyl-D-aspartate receptors on CA3 pyramidal neurons as a real-time, on-site, glutamate sensor to identify the source of glutamate release in an in vitro model of ischemia. Using glutamate and L-trans-pyrrolidine-2,4-dicarboxylic acid (tPDC) as substrates and DL-threo-beta-benzyloxyaspartate (TBOA) as an inhibitor of glutamate transporters, we demonstrate that energy deprivation decreases net glutamate uptake within 2-3 min and later promotes reverse glutamate transport. This process accounts for up to 50% of the glutamate accumulation during energy deprivation. Enhanced action potential-independent vesicular release also contributes to the increase in [glu](o), by approximately 50%, but only once glutamate uptake is inhibited. These results indicate that a significant rise in [glu](o) already occurs during the first minutes of energy deprivation and is the consequence of reduced uptake and increased vesicular and nonvesicular release of glutamate.

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > Brain Research Institute
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2000
Deposited On:11 Feb 2008 13:13
Last Modified:27 Nov 2013 17:35
Publisher:National Academy of Sciences
ISSN:0027-8424
Publisher DOI:10.1073/pnas.97.10.5610
PubMed ID:10805815
Citations:Web of Science®. Times Cited: 141
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