CaMKII binding to GluN2B is critical during memory consolidation
Open accessAbstract
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.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Binding of CaMKII to GluN2B is critical for the synaptic enhancement caused by CaMKII.
“This binding of CaMKII to GluN2B is critical for the synaptic enhancement caused by CaMKII (see sect. 6) (119–122).”
From Synaptic memory and CaMKII (2023) · cites this paper as [120]
Mutations in the GluN2B CTD that cannot bind CaMKII, or competing constructs, produce highly variable effects on LTP, ranging from complete block to no block.
“The second approach utilizes mutations in the CTD of GluN2B that cannot bind CaMKII as replacement for the wt (CaMKII L1298A/R1300Q) (120, 121, 230) or either competing with overexpressed full-length constructs (GluN2B R1300S/Q1303D) (231) or competing by expressing just the wt GluN2B CTD (839–1482) (232). The results are highly variable as reviewed in Ref. 233, ranging from complete block of LTP”
From Synaptic memory and CaMKII (2023) · cites this paper as [120]
Replacement of wild-type GluN2B with GluN2B(L1298A-R1300Q) has no effect on NMDAR synaptic currents, indicating that the mutant is functional.
“Replacement with the mutant GluN2B had no effect on NMDAR synaptic currents, indicating that it is functional.”
From Synaptic memory and CaMKII (2023) · cites this paper as [120]
Ca2+/CaM peeling away the autoinhibitory segment results in the phosphorylation of T286 and also the binding of CaMKII to GluN2B even without prior autophosphorylation, both of which maintain CaMKII in an active state.
“The first step involves Ca2+/CaM peeling away the autoinhibitory segment from the kinase domain. This results in the phosphorylation of T286 and also the binding of CaMKII to GluN2B even without prior autophosphorylation, both of which maintain CaMKII in an active state (64, 78, 119–121, 221).”
From Synaptic memory and CaMKII (2023) · cites this paper as [120]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 94 · Cited by 243
- Authors
- Halt, A. R., Dallapiazza, R. F., Zhou, Y., Stein, I. S., Qian, H., Juntti, S., Wojcik, S., Brose, N., Silva, A. J., & Hell, J. W.
- Affiliations
- University of Iowa (US)
- University of California, Los Angeles (US)
- Max Planck Institute of Experimental Medicine (DE)
- Corresponding author
- Hell, Johannes W
- Venue
- The EMBO Journal
- Published
- 2012-01-10
- Volume
- 31
- Issue
- 5
- Pages
- 1203-1216
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC3297991
- OpenAlex
- W1796178200
- Cited by
- 243
- References
- 94
- Citations by year
- 2026: 9 · 2025: 12 · 2024: 18 · 2023: 16 · 2022: 17 · 2021: 22 · 2020: 20 · 2019: 13 · 2018: 12 · 2017: 18 · 2016: 10 · 2015: 13 · 2014: 28 · 2013: 23 · 2012: 12
- FWCI
- 10.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- GRO (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R56AG017502, R01AG017502, AG017502, R01AG013622)
- National Institute of Mental Health (F31MH079671, P50MH077972)
- National Institute of General Medical Sciences (TG32 GM067795, T32GM067795, T32GM007337)
- National Institute of Neurological Disorders and Stroke (F30NS054423, R01NS035563, R01NS046450, NS-035563)
- National Center for Research Resources (UL1RR024979)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- CaMKII, GluN2B, NMDA receptor, memory consolidation, long-term potentiation, AMPA receptors, GluA1 phosphorylation, TARP, calcium influx, synaptic plasticity, spatial learning, Morris water maze, memory retrieval
- MeSH terms
- Animals, Memory, Protein Binding, Receptors, N-Methyl-D-Aspartate, Point Mutation, Mutation, Missense, Mutant Proteins, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
