QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, January 3, 2007, 27(1):111-123; doi:10.1523/JNEUROSCI.4770-06.2007

This Article Full Text Full Text (PDF) Supplemental Data Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map 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 Augustin, H. Articles by Featherstone, D. E. Search for Related Content PubMed PubMed Citation Articles by Augustin, H. Articles by Featherstone, D. E.

 Previous Article  |  Next Article 

Cellular/Molecular
Nonvesicular Release of Glutamate by Glial xCT Transporters Suppresses Glutamate Receptor Clustering In Vivo

Hrvoje Augustin, ^* Yael Grosjean, ^* Kaiyun Chen, Qi Sheng, and David E. Featherstone

Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607

Correspondence should be addressed to David Featherstone, Department of Biological Sciences, University of Illinois at Chicago, 840 West Taylor Street (M/C 067), Chicago, IL 60607. Email: def{at}uic.edu

We hypothesized that cystine/glutamate transporters (xCTs) might be critical regulators of ambient extracellular glutamate levels in the nervous system and that misregulation of this glutamate pool might have important neurophysiological and/or behavioral consequences. To test this idea, we identified and functionally characterized a novel Drosophila xCT gene, which we subsequently named "genderblind" (gb). Genderblind is expressed in a previously overlooked subset of peripheral and central glia. Genetic elimination of gb causes a 50% reduction in extracellular glutamate concentration, demonstrating that xCT transporters are important regulators of extracellular glutamate. Consistent with previous studies showing that extracellular glutamate regulates postsynaptic glutamate receptor clustering, gb mutants show a large (200–300%) increase in the number of postsynaptic glutamate receptors. This increase in postsynaptic receptor abundance is not accompanied by other obvious synaptic changes and is completely rescued when synapses are cultured in wild-type levels of glutamate. Additional in situ pharmacology suggests that glutamate-mediated suppression of glutamate receptor clustering depends on receptor desensitization. Together, our results suggest that (1) xCT transporters are critical for regulation of ambient extracellular glutamate in vivo; (2) ambient extracellular glutamate maintains some receptors constitutively desensitized in vivo; and (3) constitutive desensitization of ionotropic glutamate receptors suppresses their ability to cluster at synapses.

Key words: glia; glutamate; glutamate receptor; neurotransmission; synapse; synaptic plasticity

---

Received Aug. 23, 2006; revised Nov. 26, 2006; accepted Nov. 26, 2006.

Correspondence should be addressed to David Featherstone, Department of Biological Sciences, University of Illinois at Chicago, 840 West Taylor Street (M/C 067), Chicago, IL 60607. Email: def{at}uic.edu

This article has been cited by other articles:

				D. E. Featherstone and S. A. Shippy Regulation of Synaptic Transmission by Ambient Extracellular Glutamate Neuroscientist, April 1, 2008; 14(2): 171 - 181. [Abstract] [PDF]

				K. K. Murai and D. J. Van Meyel Neuron Glial Communication at Synapses: Insights From Vertebrates and Invertebrates Neuroscientist, December 1, 2007; 13(6): 657 - 666. [Abstract] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help