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Dynamics of Forward and Reverse Transport by the Glial Glycine Transporter, Glyt1b

Karin R. Aubrey ^*, Robert J. Vandenberg ^* and John D. Clements 

^* Department of Pharmacology, Institute for Biomedical Research, University of Sydney, NSW 2006, Australia; and John Curtin School of Medical Research, Australian National University, Canberra, ACT 0200, Australia

Correspondence: Address reprint requests to K. R. Aubrey at her present address, Laboratoire de Neurobiologie Moleculaire et Cellulaire (CNRS UMR 8544), Ecole Normale Superieure, 46 rue d'Ulm, 75230 Paris Cedex 05, France. Tel.: 33-01-44-32-40-90; Fax: 33-0-1-44-32-40-87; Email: aubrey{at}biologie.ens.fr.

Glycine is a coagonist at the N-methyl-D-aspartate receptor. Changes in extracellular glycine concentration may modulate N-methyl-D-aspartate receptor function and excitatory synaptic transmission. The GLYT1 glycine transporter is present in glia surrounding excitatory synapses, and plays a key role in regulating extracellular glycine concentration. We investigated the kinetic and other biophysical properties of GLYT1b, stably expressed in CHO cells, using whole-cell patch-clamp techniques. Application of glycine produced an inward current, which decayed within a few seconds to a steady-state level. When glycine was removed, a transient outward current was observed, consistent with reverse transport of accumulated glycine. The outward current was enhanced by elevating intracellular or lowering extracellular [Na⁺], and was modulated by changes in extracellular [glycine] and time of glycine application. We developed a model of GLYT1b function, which accurately describes the time course of the transporter current under a range of experimental conditions. The model predicts that glial uptake of glycine will decay toward zero during a sustained period of elevated glycine concentration. This property of GLYT1b may permit spillover from glycinergic terminals to nearby excitatory terminals during a prolonged burst of inhibitory activity, and reverse transport may extend the period of elevated glycine concentration beyond the end of the inhibitory burst.

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