The DOI matches its Crossref record; 51 of the 53 references it cites were found in a registry or an index.
Persistent Accumulation of Calcium/Calmodulin-Dependent Protein Kinase II in Dendritic Spines after Induction of NMDA Receptor-Dependent Chemical Long-Term Potentiation
Open accessAbstract
Calcium/calmodulin-dependent protein kinase II (CaMKII) is a leading candidate for a synaptic memory molecule because it is persistently activated after long-term potentiation (LTP) induction and because mutations that block this persistent activity prevent LTP and learning. Previous work showed that synaptic stimulation causes a rapidly reversible translocation of CaMKII to the synaptic region. We have now measured green fluorescent protein (GFP)-CaMKIIα translocation into synaptic spines during NMDA receptor-dependent chemical LTP (cLTP) and find that under these conditions, translocation is persistent. Using red fluorescent protein as a cell morphology marker, we found that there are two components of the persistent accumulation. cLTP produces a persistent increase in spine volume, and some of the increase in GFP-CaMKIIα is secondary to this volume change. In addition, cLTP results in a dramatic increase in the bound fraction of GFP-CaMKIIα in spines. To further study the bound pool, immunogold electron microscopy was used to measure CaMKIIα in the postsynaptic density (PSD), an important regulator of synaptic function. cLTP produced a persistent increase in the PSD-associated pool of CaMKIIα. These results are consistent with the hypothesis that CaMKIIα accumulation at synapses is a memory trace of past synaptic activity.
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“Calcium ions play a crucial role in initiating downstream signaling during long-term potentiation (LTP) and depression (LTD) and influx of calcium is both necessary and sufficient for structural synaptic plasticity (Pettit et al., 1994; Lledo et al., 1995; Otmakhov et al., 2004).”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Otmakhov et al., 2004
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“A–C: chemical long-term potentiation (chemLTP) induction results in persistent accumulation of CaMKIIα at the PSD.”
From Synaptic memory and CaMKII (2023) · cites this paper as [217]
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“The persistent accumulation of CaMKII at the PSD following an LTP-inducing stimulus is shown in FIGURE 6, A–C (217).”
From Synaptic memory and CaMKII (2023) · cites this paper as [217]
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“In addition, LTP-inducing stimuli result in the persistent accumulation of CaMKII in the PSD (FIGURE 6, A–C) (217).”
From Synaptic memory and CaMKII (2023) · cites this paper as [217]
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Metadata
- Authors
- Otmakhov, N., Tao-Cheng, J.-H., Carpenter, S., Asrican, B., Dosemeci, A., Reese, T. S., & Lisman, J.
- Affiliations
- Brandeis University (US)
- National Institute of Neurological Disorders and Stroke (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-10-20
- Volume
- 24
- Issue
- 42
- Pages
- 9324-9331
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6730088
- OpenAlex
- W2071910925
- Cited by
- 258
- References
- 53
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 2 · 2023: 8 · 2022: 7 · 2021: 8 · 2020: 5 · 2019: 8 · 2018: 17 · 2017: 10 · 2016: 7 · 2015: 13 · 2014: 23 · 2013: 11 · 2012: 18
- FWCI
- 5.05
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Open Access Server of the Woods Hole Scientific Community (Woods Hole Scientific Community) (submittedVersion)
- Funders
- National Institutes of Health (R01 NS)
- National Institute of Neurological Disorders and Stroke (R01NS027337, R01 NS27337)
- 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 › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- CaMKII, calcium/calmodulin-dependent protein kinase II, dendritic spines, NMDA receptor, postsynaptic density, synaptic memory, long-term potentiation, learning
- MeSH terms
- Adenylyl Cyclases, Animals, Colforsin, Phosphodiesterase Inhibitors, Protein Binding, Recombinant Fusion Proteins, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Long-Term Potentiation, Calcium-Calmodulin-Dependent Protein Kinases, Rolipram, Protein Transport, Dendritic Spines, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, In Vitro Techniques
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