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J. Biol. Chem., Vol. 282, Issue 48, 34719-34726, November 30, 2007

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Neuronal Glutamate Transporters Vary in Substrate Transport Rate but Not in Unitary Anion Channel Conductance^*

Delany Torres-Salazar and Christoph Fahlke¹

From the Institut für Neurophysiologie, Medizinische Hochschule, D-30625 Hannover, Germany and Zentrum für Systemische Neurowissenschaften, D-30625 Hannover, Germany

Excitatory amino acid transporters (EAATs) not only sustain a secondary active glutamate transport but also function as anion-selective ion channels. The relative proportion of currents generated by glutamate transport or by the chloride conductance varies for each cloned EAAT subtype. For EAAT1, EAAT2, and EAAT3, the anion current is only a small component of the total transporter-associated current amplitude, whereas EAAT4 and EAAT5 transporters mediate predominantly anion currents. We here demonstrate that the distinct current proportions are entirely due to differences in glutamate transport rates. EAAT3 and EAAT4 differ in unitary glutamate transport rates as well as in the voltage and substrate dependence of anion channel opening, but ion conduction properties are very similar. Noise analysis revealed identical unitary current amplitudes and similar absolute open probabilities for the two anion channels. The low glutamate transport rate of EAAT4 allows regulation of cellular excitability without interfering with extracellular glutamate homeostasis and makes this EAAT isoform ideally suited to regulate excitability in dendritic spines of Purkinje neurons.

Received for publication, May 18, 2007 , and in revised form, August 20, 2007.

^* This work was supported by Deutsche Forschungsgemeinschaft Grant FOR450 (to Ch. F.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Table S1 and supplemental Fig. S1.

¹ To whom correspondence should be addressed: Institut für Neurophysiologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany. Tel.: 49-511-532-2777; Fax: 49-511-532-2776; E-mail: fahlke.christoph{at}mh-hannover.de.

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