ArticleProceedings of the National Academy of Sciences of the United States of America2013
Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
171 citing papers in PubMed, 286 citations in OpenAlex.
- AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction.Acta neuropathologica · 2026Article
- Circadian Changes in CA1 LTP Are Driven by Shifts in Excitation-Inhibition Balance and Reverse Direction after Puberty in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Dysfunctional synaptic competition at dendritic spines in Fragile X syndrome.bioRxiv : the preprint server for biology · 2026Article
- Nonionic signaling rapidly remodels postsynaptic DLG to induce retrograde homeostatic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Behavioral Timescale Synaptic Plasticity: A Burst in the Field of Learning and Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Non-ionotropic NMDAR signalling activates Panx1 to induce P2X4R-dependent long-term depression in the hippocampus.The Journal of physiology · 2025Article
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- Prospects and challenges in NMDAR signaling in spinal cord injury recovery and neural circuit remodeling.Regenerative therapy · 2025Review
- Non-ionotropic signaling through the NMDA receptor GluN2B carboxy-terminal domain drives dendritic spine plasticity and reverses fragile X phenotypes.Cell reports · 2025Article
- Structure-Activity Relationship of NMDA Receptor Ligands and Their Activities on the ERK Activation through Metabotropic Signaling Pathway.Biomolecules & therapeutics · 2025Article
- Contrasting patterns of extrasynaptic NMDAR-GluN2B expression in macaque subgenual cingulate and dorsolateral prefrontal cortices.Frontiers in neuroanatomy · 2025Article
- Emergent functions of noise-driven spontaneous activity: homeostatic maintenance of criticality and memory consolidation.Frontiers in neural circuits · 2025Article
- Metabotropic NMDAR Signaling Contributes to Sex Differences in Synaptic Plasticity and Episodic Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Research Progress on NMDA Receptor Enhancement Drugs for the Treatment of Depressive Disorder.CNS drugs · 2024Review
- Non-ionotropic voltage-gated calcium channel signaling.Channels (Austin, Tex.) · 2024Review
- Developmental Spike Timing-Dependent Long-Term Depression Requires Astrocyte d-Serine at L2/3-L2/3 Synapses of the Mouse Somatosensory Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Astrocytes mediate two forms of spike timing-dependent depression at entorhinal cortex-hippocampal synapses.eLife · 2024Article
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111 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
NMDA receptor (NMDAR) activation controls long-term potentiation (LTP) as well as long-term depression (LTD) of synaptic transmission, cellular models of learning and memory. A long-standing view proposes that a high level of Ca(2+) entry through NMDARs triggers LTP; lower Ca(2+) entry triggers LTD. Here we show that ligand binding to NMDARs is sufficient to induce LTD; neither ion flow through NMDARs nor Ca(2+) rise is required. However, basal levels of Ca(2+) are permissively required. Lowering, but not maintaining, basal Ca(2+) levels with Ca(2+) chelators blocks LTD and drives strong synaptic potentiation, indicating that basal Ca(2+) levels control NMDAR-dependent LTD and basal synaptic transmission. Our findings indicate that metabotropic actions of NMDARs can weaken active synapses without raising postsynaptic calcium, thereby revising and expanding the mechanisms controlling synaptic plasticity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.