ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025
Activity-Dependent Internalization of Glun2B-Containing NMDARs Is Required for Synaptic Incorporation of Glun2A and Synaptic Plasticity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Differential and state-dependent effects of the GluN2A-selective positive allosteric modulator GNE-5729 on executive functions.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Kynurenine pathway dysregulation in attention-deficit hyperactivity disorder: Impact on N-methyl-D-aspartate receptors and phasic dopamine maturation.World journal of clinical pediatrics · 2026Review
- Reduced expression of N-methyl-D-aspartate receptor and calcium signaling genes in gray matter is associated with cancer-related cognitive impairment.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Article
- Anti-P antibodies that impair memory perturb hippocampal glutamatergic receptor trafficking, synapse structure and microglia.Molecular medicine (Cambridge, Mass.) · 2025Article
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3 authors.
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Abstract
NMDA-type glutamate receptors are heterotetrameric complexes composed of two GluN1 and two GluN2 subunits. The precise composition of the GluN2 subunits determines the channel's biophysical properties and influences its interaction with postsynaptic scaffolding proteins and signaling molecules involved in synaptic physiology and plasticity. The precise regulation of NMDAR subunit composition at synapses is crucial for proper synaptogenesis, neuronal circuit development, and synaptic plasticity, a cellular model of memory formation. In the forebrain during early development, NMDARs contain solely the GluN2B subunit, which is necessary for proper synaptogenesis and synaptic plasticity. In rodents, GluN2A subunit expression begins in the second postnatal week, replacing GluN2B-containing NMDARs at synapses in an activity- or sensory experience-dependent process. This switch in NMDAR subunit composition at synapses alters channel properties and reduces synaptic plasticity. The molecular mechanism regulating the switch remains unclear. We have investigated the role of activity-dependent internalization of GluN2B-containing receptors in shaping synaptic NMDAR subunit composition. Using molecular, pharmacological, and electrophysiological approaches in cultured organotypic hippocampal slices from rats of both sexes, we show that the process of incorporating GluN2A-containing NMDAR receptors requires activity-dependent internalization of GluN2B-containing NMDARs. Interestingly, blockade of GluN2A synaptic incorporation was associated with impaired potentiation of AMPA-mediated synaptic transmission, suggesting a potential coupling between the trafficking of AMPARs into synapses and that of GluN2A-containing NMDARs. These insights contribute to our understanding of the molecular mechanisms underlying synaptic trafficking of glutamate receptors and synaptic plasticity. They may also have implications for therapeutic strategies targeting NMDAR function in neurological disorders.
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