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The N-methyl-D-aspartate (NMDA) receptor contributes to synaptic plasticity in the central nervous system and is both serine-threonine and tyrosine phosphorylated. In CA1 pyramidal neurons of the hippocampus, activators of protein kinase C (PKC) as well as the G-protein-coupled receptor ligands muscarine and lysophosphatidic acid enhanced NMDA-evoked currents. Unexpectedly, this effect was blocked by inhibitors of tyrosine kinases, including a Src required sequence and an antibody selective for Src itself. In neurons from mice lacking c-Src, PKC-dependent upregulation was absent. Thus, G-protein-coupled receptors can regulate NMDA receptor function indirectly through a PKC-dependent activation of the non-receptor tyrosine kinase (Src) signaling cascade.

Original publication




Journal article


Nat Neurosci

Publication Date





331 - 338


Alkaloids, Amino Acid Sequence, Animals, Benzophenanthridines, Cells, Cultured, Enzyme Activation, Enzyme Inhibitors, GTP-Binding Proteins, Genistein, Isoflavones, Lysophospholipids, Mice, Mice, Knockout, Microinjections, Molecular Sequence Data, Muscarine, Nerve Tissue Proteins, Neuronal Plasticity, Oocytes, Patch-Clamp Techniques, Phenanthridines, Phenols, Phosphorylation, Protein Kinase C, Protein Processing, Post-Translational, Proto-Oncogene Proteins pp60(c-src), Pyramidal Cells, Rats, Rats, Wistar, Receptors, Cell Surface, Receptors, G-Protein-Coupled, Receptors, Lysophosphatidic Acid, Receptors, Muscarinic, Receptors, N-Methyl-D-Aspartate, Salicylates, Signal Transduction, Tetradecanoylphorbol Acetate, Xenopus laevis, meta-Aminobenzoates