Cited by 258Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsProtein Kinase Regulation and GTPase Signaling

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Persistent Accumulation of Calcium/Calmodulin-Dependent Protein Kinase II in Dendritic Spines after Induction of NMDA Receptor-Dependent Chemical Long-Term Potentiation

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Otmakhov, Nikolai, Tao-Cheng, Jung-Hwa, Carpenter, Stephen, Asrican, Brent, Dosemeci, Ayse, Reese, Thomas S., Lisman, John·2004·The Journal of Neuroscience

DOI 10.1523/jneurosci.2350-04.2004PMC PMC6730088

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Abstract

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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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)
ORCID: Tao-Cheng, Jung-Hwa
Carpenter, Stephen
Asrican, Brent
Reese, Thomas S.
Lisman, John
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
DOI: 10.1523/jneurosci.2350-04.2004
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: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 182 d)
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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Persistent Accumulation of Calcium/Calmodulin-Dependent Protein Kinase II in Dendritic Spines after Induction of NMDA Receptor-Dependent Chemical Long-Term Potentiation

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