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This Article Full Text Full Text (PDF) All Versions of this Article: 577/2/591    most recent jphysiol.2006.116830v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Owe, S. G. Articles by Attwell, D. Search for Related Content PubMed PubMed Citation Articles by Owe, S. G. Articles by Attwell, D. Related Collections Neuroscience

¹ Department of Physiology, University College London, London, WC1E 6BT, UK

Maintaining a low extracellular glutamate concentration in the central nervous system is important for terminating synaptic transmission and preventing excitotoxic cell death. The stoichiometry of the most abundant glutamate transporter, GLT-1, predicts that a very low glutamate concentration, 2 nM, should be reached in the absence of glutamate release, yet microdialysis measurements give a value of 1 µM. If other glutamate transporters had a different stoichiometry, the predicted minimum glutamate concentration could be higher, for example if those transporters were driven by the cotransport of 2 Na⁺ (rather than of 3 Na⁺ as for GLT-1). Here we investigated the ionic stoichiometry of the glutamate transporter GLAST, which is the major glutamate transporter expressed in the retina and cerebellum, is expressed in other adult brain areas at a lower level than GLT-1, and is present throughout the brain early in development when expression of GLT-1 is low. Glutamate transport by GLAST was found to be driven, as for GLT-1, by the cotransport of 3 Na⁺ and 1 H⁺ and the counter-transport of 1 K⁺, suggesting that the minimum extracellular glutamate concentration should be similar during development and in the adult brain. A less powerful accumulation of glutamate by GLAST than by GLT-1 cannot be used to explain the high glutamate concentration measured by microdialysis.

(Received 10 July 2006; accepted after revision 25 September 2006; first published online 28 September 2006)
Corresponding author D. Attwell: Department of Physiology, University College London, London, WC1E 6BT, UK.  Email: D.Attwell{at}ucl.ac.uk

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