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First published online May 24, 2005
Journal of Experimental Biology 208, 2063-2070 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01595

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Glutamate transporter type 3 attenuates the activation of N-methy-D-aspartate receptors co-expressed in Xenopus oocytes

Zhiyi Zuo^* and Hongyu Fang

Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia 22908-0710, USA

^* Author for correspondence (e-mail: zz3c{at}virginia.edu)

Accepted 14 March 2005

We studied the regulation of N-methy-D-aspartate receptor (NMDAR) current/activation by glutamate transporter type 3 (EAAT3), a neuronal EAAT in vivo, in the restricted extracellular space of a biological model. This model involved co-expressing EAAT3 and NMDAR (composed of NMDAR1-1a and NMDAR2A) in Xenopus oocytes. The NMDAR current was reduced in the co-expression oocytes but not in oocytes expressing NMDAR only when the flow of glutamate-containing superfusate was stopped. The degree of this current reduction was glutamate concentration-dependent. No reduction of NMDAR current was observed in Na⁺-free solution or when NMDA, a non-substrate for EAATs, was used as the agonist for NMDAR. In the continuous flow experiments, the dose-response curve of glutamate-induced current was shifted to the right-hand side in co-expression oocytes compared with oocytes expressing NMDAR alone. The degree of this shift depended on the abundance of EAAT3 in the co-expression oocytes. Thus, the glutamate concentrations sensed by NMDAR locally were lower than those in the superfusates. These results suggest that EAAT3 regulates the amplitude of NMDAR currents at pre-saturated concentrations of glutamate to EAAT3. Thus, EAATs, by rapidly regulating glutamate concentrations near NMDAR, modulate NMDAR current/activation.

Key words: glutamate receptor, glutamate transporter, neurotransmission, oocytes

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