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Previous Article | Next Article
Volume 17, Number 12, Issue of June 15, 1997 pp. 4580-4590
Copyright ©1997 Society for NeuroscienceControl of NMDA Receptor Activation by a Glycine Transporter Co-Expressed in Xenopus Oocytes
Received Jan. 17, 1997; revised March 27, 1997; accepted March 31, 1997.
Stéphane Supplisson and Claude Bergman Laboratoire de Neurobiologie, Centre National de la Recherche Scientifique, Unité de Recherche Associée 1857, Ecole Normale Supérieure, 75005 Paris, France
We present evidence that membrane transporters can control the membrane receptor's agonist concentration in restricted extracellular spaces of a biological model. The model is constructed by co-expressing glycine/Na/Cl cotransporters (GLYT1b) and NMDA receptors (NMDARs) (composed of the subunits NR1 and NR2A or NR2B) in Xenopus oocytes. We use the high-affinity glycine site of the NMDARs as a sensor of the actual juxtamembrane glycine concentration. We show that glycine uptake by GLYT1b dramatically reduces NMDAR currents by reducing the glycine concentration in extracellular spaces in which diffusion is restricted. This effect appears only in oocytes in which GLYT1b and NMDAR are co-expressed. It is Na+- and voltage-dependent, and is abolished when Na+ is replaced by Li+ and when glycine is replaced by D-serine (a coagonist of the NMDAR that is not transported by GLYT1b). These results demonstrate the ability of the GLYT transporter to reduce glycine concentration at the level of NMDARs in restricted diffusion spaces. This observation could account for a prevalent role of membrane transporters in the modulation of synapse transmission in the CNS. From a more general point of view, our results draw attention to possible significant discrepancies between local concentrations at the level of substrate targets in biological membranes and their concentration in the bulk solution when membrane transporters are present.
Key words: glutamate receptor; NMDA; coagonist; D-serine; sarcosine; synaptic cleft
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