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NMDA Receptor Activation: Two Targets for Two Co-Agonists

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Abstract

Neuronal N-methyl-d-aspartate receptors (NMDARs) play a critical role in synaptic plasticity. Their activation requires not only binding of their ligand glutamate and membrane depolarization but also the presence of a co-agonist, glycine or d-serine. An increasing body of experimental evidence suggests that different populations of NMDARs could be gated by different co-agonists. Here we discuss how the spatial distribution of co-agonist sources and uptake mechanisms, together with diffusional properties of the synaptic environment, could shape NMDAR co-agonist supply and therefore NMDAR-dependent plasticity.

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Acknowledgments

The work was supported by Wellcome Trust and Medical Research Council UK (D.A.R.), the Fondation pour la Recherche Medicale (L.B.), the European Molecular Biology Organization and European Marie Curie Actions (EMBOCOFUND2010, GA-2010-267146; L.B.), UCL Grand Challenge Program (C.K.), UCL Excellence Fellowship (C.K., C.H.), NRW-Rückkehrerprogramm (C.H.) and the Human Frontiers Science Program (C.H.).

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Henneberger, C., Bard, L., King, C. et al. NMDA Receptor Activation: Two Targets for Two Co-Agonists. Neurochem Res 38, 1156–1162 (2013). https://doi.org/10.1007/s11064-013-0987-2

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  • DOI: https://doi.org/10.1007/s11064-013-0987-2

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