Memory reconsolidation and its maintenance depend on L-voltage-dependent calcium channels and CaMKII functions regulating protein turnover in the hippocampus
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Immediate postretrieval bilateral blockade of long-acting voltage-dependent calcium channels (L-VDCCs), but not of glutamatergic NMDA receptors, in the dorsal CA1 region of the hippocampus hinders retention of long-term spatial memory in the Morris water maze. Immediate postretrieval bilateral inhibition of calcium/calmodulin-dependent protein kinase (CaMK) II in dorsal CA1 does not affect retention of this task 24 h later but does hinder it 5 d later. These two distinct amnesic effects are abolished if protein degradation by proteasomes is inhibited concomitantly. These results indicate that spatial memory reconsolidation depends on the functionality of L-VDCC in dorsal CA1, that maintenance of subsequent reconsolidated memory trace depends on CaMKII, and these results also suggest that the role played by both L-VDCC and CaMKII is to promote the retrieval-dependent, synaptically localized enhancement of protein synthesis necessary to counteract a retrieval-dependent, synaptic-localized enhancement of protein degradation, which has been described as underlying the characteristic labilization of the memory trace triggered by retrieval. Thus, conceivably, L-VDCC and CaMKII would enhance activity-dependent localized protein renewal, which may account for the improvement of the long-term efficiency of the synapses responsible for the maintenance of reactivated long-term spatial memory.
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The regulation of this system has been linked to intracellular calcium signalling and NMDAR activation.
“The regulation of this system has been linked to intracellular calcium signalling (Da Silva et al., 2013; Jarome et al., 2016) and NMDAR activation (Rosenberg et al., 2016).”
From Retrieval-Dependent Mechanisms Affecting Emotional Memory Persistence: Reconsolidation, Extinction, and the Space in Between (2020) · cites this paper as Da Silva et al., 2013
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Amorim, F. E., Chapot, R. L., Moulin, T. C., Lee, J. L. C., & Amaral, O. B. (2021) · Learning & Memory · doi:10.1101/lm.053418.121 · Cited by 2 · see citing works
Fiebrantz, A. K. B., Leite, L. F., Schwab, E. D. P., Bonini, J. S., & da Silva, W. C. (2023) · Learning & memory (Cold Spring Harbor, N.Y.) · doi:10.1101/lm.053785.123 · Cited by 2 · see citing works
Self-citationPrescient Synapses: Gating Future Neuronal Consciousness Through Synaptic Tagging and Metaplasticity
Connor, S. A., & Nguyen, P. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1761-7_11 · Cited by 1 · see citing works
Ubiquitin-dependent protein degradation is necessary for long-term plasticity and memory
Bal, N. V., & Balaban, P. M. (2015) · Neurochemical Journal · doi:10.1134/s1819712415040042 · Cited by 1 · see citing works
Behaviorally Induced Synaptic Tagging
Myskiw, J. D. C., Furini, C. R. G., & Izquierdo, I. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-809324-5.21122-x · Cited by 1 · see citing works
Self-citationDevelopment and Validation of an Epistemological Profile Questionnaire in a Museum Environment
Rosalino, I., & Kasseboehmer, A. C. (2022) · Science & Education · doi:10.1007/s11191-022-00405-4 · Cited by 1 · see citing works
Endocannabinoid Function in Hippocampal Synaptic Plasticity and Spatial Working Memory
Blaskovits, F. (2013) · uO Research (University of Ottawa) · doi:10.20381/ruor-3206
Wells, A. M. (2019) · Carolina Digital Repository (University of North Carolina at Chapel Hill) · doi:10.17615/d55d-4x10
Prelimbic proBDNF facilitates memory destabilization by regulation of neuronal function in juvenilesPreprint
Sun, W., Chen, X., Mei, Y., Yang, Y., Li, X., & An, L. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.12.30.474526
Brownstone, R. M. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.736824839.793567372
Queiroz, R., Marchiori, C., Rosas, H. K., Medeiros, I. S. S., Ferreira, H. Q., Bonini, J. S., & da Silva, W. C. (2026) · Psychopharmacology · doi:10.1007/s00213-026-07161-1
Self-citation
- Authors
- Da Silva, W. C., Cardoso, G., Bonini, J. S., Benetti, F., & Izquierdo, I.
- Affiliations
- Centro de Memória, Instituto do Cérebro, Pontifícia Universidade Católica do Rio Grande do Sul, RS90610-000, Porto Alegre, Brazil;
- Instituto do Cérebro (BR)
- Conselho Nacional de Desenvolvimento Científico e Tecnológico (BR)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2013-04
- Volume
- 110
- Issue
- 16
- Pages
- 6566-6570
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3631664
- OpenAlex
- W2054146070
- Cited by
- 52
- References
- 61
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 5 · 2018: 3 · 2017: 4 · 2016: 7 · 2015: 9 · 2014: 7 · 2013: 2
- FWCI
- 4.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
- Keywords
- memory reconsolidation, CaMKII, hippocampal CA1, spatial memory, proteasome inhibition, protein degradation, protein synthesis, NMDA receptor
- MeSH terms
- Analysis of Variance, Animals, Hippocampus, Male, Nerve Tissue Proteins, Time Factors, Calcium Channels, Rats, Wistar, Long-Term Potentiation, Maze Learning, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Memory, Long-Term
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