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Cited by 166Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsTreatment of Major Depression

The CaMKII/NMDAR complex as a molecular memory

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Sanhueza, Magdalena, Lisman, John·2013·Molecular Brain
DOI 10.1186/1756-6606-6-10PMC PMC3582596
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Abstract

CaMKII is a major synaptic protein that is activated during the induction of long-term potentiation (LTP) by the Ca2+ influx through NMDARs. This activation is required for LTP induction, but the role of the kinase in the maintenance of LTP is less clear. Elucidating the mechanisms of maintenance may provide insights into the molecular processes that underlie the stability of stored memories. In this brief review, we will outline the criteria for evaluating an LTP maintenance mechanism. The specific hypothesis evaluated is that LTP is maintained by the complex of activated CaMKII with the NMDAR. The evidence in support of this hypothesis is substantial, but further experiments are required, notably to determine the time course and persistence of complex after LTP induction. Additional work is also required to elucidate how the CaMKII/NMDAR complex produces the structural growth of the synapse that underlies late LTP. It has been proposed by Frey and Morris that late LTP involves the setting of a molecular tag during LTP induction, which subsequently allows the activated synapse to capture the proteins responsible for late LTP. However, the molecular processes by which this leads to the structural growth that underlies late LTP are completely unclear. Based on known binding reactions, we suggest the first molecularly specific version of tag/capture hypothesis: that the CaMKII/NMDAR complex, once formed, serves as a tag, which then leads to a binding cascade involving densin, delta-catenin, and N-cadherin (some of which are newly synthesized). Delta-catenin binds AMPA-binding protein (ABP), leading to the LTP-induced increase in AMPA channel content. The addition of postsynaptic N-cadherin, and the complementary increase on the presynaptic side, leads to a trans-synaptically coordinated increase in synapse size (and more release sites). It is suggested that synaptic strength is stored stably through the combined actions of the CaMKII/NMDAR complex and N-cadherin dimers. These N-cadherin pairs have redundant storage that could provide informational stability in a manner analogous to the base-pairing in DNA.

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  • NMDAR-dependent LTP has been most tightly associated with intact animal behavioral memory.

    “Additionally, NMDAR-dependent LTP has been most tightly associated with intact animal behavioral memory (19, 43–46).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [44]

    The section on behavioral tests of memory reports that mice with impaired CaMKII/NMDAR complex formation had both reduced LTP and reduced spatial memory, supporting a link in intact animals. The paper does not compare NMDAR-dependent LTP with other forms of plasticity or establish that its association with behavioral memory is the tightest; the Conclusions say further behavioral work is needed. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Upon activation, CaMKII acts as a persistent structural seed or molecular tag that captures proteins, such as densin and delta-catenin, required for spine growth and synaptic stabilization.

    “Upon activation, CaMKII acts as a persistent structural ‘seed’ or molecular tag that captures proteins, such as densin and delta-catenin, required for spine growth and synaptic stabilization.”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [63]

    In the section on trans-synaptic structural growth (Figure 2), the paper proposes that activated CaMKII forms a persistent complex with NMDAR that acts as a tag and structural seed for binding densin and delta-catenin. It presents this as a working hypothesis, not an established action of CaMKII alone. The same section says that whether densin and delta-catenin are required for synapse growth has not been tested. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The CaMKII complex maintains the on-state of synaptic memory through physical interactions within the PSD, effectively functioning as a structural switch that resists protein turnover.

    “This complex maintains the ‘on-state’ of synaptic memory through physical interactions within the PSD, effectively functioning as a structural switch that resists protein turnover [51,52,63,64].”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [63]

    The section on trans-synaptic structural growth (page not provided) proposes that physical interactions can restore the CaMKII/NMDAR complex despite protein turnover. But it calls this mechanism a hypothesis, and the Abstract says further experiments are needed to establish the complex’s persistence. The claim presents the proposed maintenance mechanism as established. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Activity-dependent capture involves a binding cascade of densin, delta-catenin, and N-cadherin, where the CaMKII/NMDAR complex serves as the initial molecular tag that captures these proteins to increase synapse size and stability.

    “This activity-dependent capture involves a binding cascade of densin, delta-catenin, and N-cadherin, where the CaMKII/NMDAR complex serves as the initial molecular tag that captures these proteins to increase synapse size and stability [17,63].”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [63]

    The section on trans-synaptic structural growth describes the CaMKII/NMDAR complex as a tag and structural seed for capturing densin, delta-catenin, and N-cadherin, with proposed effects on synapse size and stability. But it calls this cascade a working hypothesis, whereas the citing sentence presents it as an established mechanism. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • The specificity by which new proteins participate in either LTP or LTD may be determined by specific RNA-binding proteins and an activity-dependent capture mechanism.

    “The specificity by which new proteins participate in either LTP or LTD may be determined by specific RNA-binding proteins and an “activity-dependent capture” mechanism.”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [63]

    The section on structural growth in late LTP (page not provided) describes activity-dependent tagging of a synapse that captures newly synthesized proteins for late LTP. It does not attribute specificity between LTP and LTD to RNA-binding proteins, or discuss that proposed distinction. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

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Authors
Sanhueza, M., & Lisman, J.
Affiliations
  • University of Chile (CL)
  • Brandeis University (US)
Corresponding author
Lisman, John
ORCID
Venue
Molecular Brain
Publisher
Springer Science and Business Media LLC
Published
2013
Volume
6
Issue
1
Pages
10
ISSN
1756-6606 (ISSN-L)
DOI
10.1186/1756-6606-6-10
PMC
PMC3582596
OpenAlex
W2161006430
Cited by
166
References
8
Citations by year
2026: 5 · 2025: 4 · 2024: 12 · 2023: 14 · 2022: 9 · 2021: 17 · 2020: 10 · 2019: 10 · 2018: 19 · 2017: 13 · 2016: 10 · 2015: 14 · 2014: 19 · 2013: 10
FWCI
1.80
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Molecular Brain (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Universidad de Chile (submittedVersion, cc-by-nc-nd)
Funders
  • Universidad de Chile
  • National Institutes of Health
  • National Institute on Drug Abuse (R01DA027807)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords
CaMKII, NMDA receptor, long-term potentiation, LTP maintenance, molecular memory, synaptic plasticity, N-cadherin, δ-catenin, AMPA receptors, memory stability, calcium signaling
MeSH terms
Animals, Humans, Memory, Synaptic Transmission, Protein Kinase C, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Calcium-Calmodulin-Dependent Protein Kinase Type 2

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