ArticleThe EMBO journal2012
CaMKII binding to GluN2B is critical during memory consolidation.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.
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Who cites it
162 citing papers in PubMed, 243 citations in OpenAlex.
- CaMKII monomers are sufficient for GluN2B binding, co-condensation, and synaptic potentiation.Molecular cell · 2026Article
- CaMKIIα holoenzymes self-organize into chain-like mesoscale clusters.Science advances · 2026Article
- Dynamic recruitment of CaMKII into SHANK3 phase-separated condensates tunes postsynaptic density remodeling during long-term potentiation.Nature communications · 2026Article
- BDNF Signaling in Glutamatergic Neurons During Long-Term Potentiation (LTP): A Spatio-Temporal Exploration of Events.Molecular neurobiology · 2025Review
- Acute intermittent hypoxia enhances nucleus of the solitary tract neuronal activity and requires NMDARs and CaMKII for phrenic long-term facilitation.Journal of neurophysiology · 2025Article
- Synaptic accumulation of GluN2B-containing NMDA receptors mediates the effects of BDNF-TrkB signalling on synaptic plasticity and in hyperexcitability during status epilepticus.Journal of biomedical science · 2025Article
- Aβ impairs the LTP-related movement of endogenous CaMKII but not of exogenous GFP-CaMKII.Molecular biology of the cell · 2025Article
- The neuroprotective γ-hydroxybutyrate analog 3-hydroxycyclopent-1-enecarboxylic acid does not directly affect CaMKIIα autophosphorylation at T286 or binding to GluN2B.Molecular pharmacology · 2025Article
- Ventral Hippocampal CA1 GADD45B Regulates Susceptibility to Social Stress by Influencing NMDA Receptor-Mediated Synaptic Plasticity.Neuroscience bulletin · 2025Article
- AMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases.Cellular and molecular neurobiology · 2025Review
- Activity-Dependent Internalization of Glun2B-Containing NMDARs Is Required for Synaptic Incorporation of Glun2A and Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- GluN2B influences the progression of status epilepticus by modulating calcium ion homeostasis through its interaction with CaMKIIα.Frontiers in pharmacology · 2025Article
- A revised view of the role of CaMKII in learning and memory.Nature neuroscience · 2025Review
- Data Hazards as An Ethical Toolkit for Neuroscience.Neuroethics · 2025Article
- LTP expression mediated by autonomous activity of GluN2B-bound CaMKII.Cell reports · 2024Article
- Synaptic rearrangement of NMDA receptors controls memory engram formation and malleability in the cortex.Science advances · 2024Article
- Myosin Va-dependent Transport of NMDA Receptors in Hippocampal Neurons.Neuroscience bulletin · 2024Article
- Induction of LTP mechanisms in dually innervated dendritic spines.Scientific reports · 2024Article
- CaMKII autophosphorylation is the only enzymatic event required for synaptic memory.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
102 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Memory is essential for our normal daily lives and our sense of self. Ca(2+) influx through the NMDA-type glutamate receptor (NMDAR) and the ensuing activation of the Ca(2+) and calmodulin-dependent protein kinase (CaMKII) are required for memory formation and its physiological correlate, long-term potentiation (LTP). The Ca(2+) influx induces CaMKII binding to the NMDAR to strategically recruit CaMKII to synapses that are undergoing potentiation. We generated mice with two point mutations that impair CaMKII binding to the NMDAR GluN2B subunit. Ca(2+)-triggered postsynaptic accumulation is largely abrogated for CaMKII and destabilized for TARPs, which anchor AMPA-type glutamate receptors (AMPAR). LTP is reduced by 50% and phosphorylation of the AMPAR GluA1 subunit by CaMKII, which enhances AMPAR conductance, impaired. The mutant mice learn the Morris water maze (MWM) as well as WT but show deficiency in recall during the period of early memory consolidation. Accordingly, the activity-driven interaction of CaMKII with the NMDAR is important for recall of MWM memory as early as 24 h, but not 1-2 h, after training potentially due to impaired consolidation.
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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.