Molecular determinants controlling NMDA receptor synaptic incorporation

Synaptic incorporation of NMDA receptors (NMDARs) is regulated by GluN2 subunits with different rules controlling GluN2A- and GluN2B-containing receptors; whereas GluN2B-containing receptors are constitutively incorporated into synapses, GluN2A incorporation is activity-dependent. We expressed elect...

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Bibliographic Details
Published in:The Journal of neuroscience 2011-04, Vol.31 (17), p.6311-6316
Main Authors: Storey, Granville P, Opitz-Araya, Ximena, Barria, Andres
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Biophysics
Brief Communications
Electric Stimulation - methods
Excitatory Amino Acid Antagonists - pharmacology
Excitatory Postsynaptic Potentials - genetics
Excitatory Postsynaptic Potentials - physiology
Green Fluorescent Proteins - genetics
Hippocampus - cytology
Macromolecular Substances - chemistry
Male
Mutation - genetics
Neurons - physiology
Organ Culture Techniques
Patch-Clamp Techniques - methods
Protein Subunits
Rats
Rats, Sprague-Dawley
Receptors, N-Methyl-D-Aspartate - chemistry
Receptors, N-Methyl-D-Aspartate - genetics
Receptors, N-Methyl-D-Aspartate - physiology
Synapses - physiology
Time Factors
Transfection - methods
Valine - analogs & derivatives
Valine - pharmacology
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Summary:Synaptic incorporation of NMDA receptors (NMDARs) is regulated by GluN2 subunits with different rules controlling GluN2A- and GluN2B-containing receptors; whereas GluN2B-containing receptors are constitutively incorporated into synapses, GluN2A incorporation is activity-dependent. We expressed electrophysiologically tagged NMDARs in rat hippocampal slices to identify the molecular determinants controlling the mode of synaptic incorporation of NMDARs. Expressing chimeric GluN2 subunits, we identified a putative N-glycosylation site present in GluN2B, but not in GluN2A, as necessary and sufficient to drive NMDARs into synapses in an activity-independent manner. This suggests a novel mechanism for regulating activity-driven changes and trafficking of NMDARs to the synapse.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.5553-10.2011