The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
CaMKII Autophosphorylation Is Necessary for Optimal Integration of Ca 2+ Signals during LTP Induction, but Not Maintenance
Open accessAbstract
CaMKII plays a critical role in decoding calcium (Ca 2+) signals to initiate long-lasting synaptic plasticity. However, the properties of CaMKII that mediate Ca 2+ signals in spines remain elusive. Here, we measured CaMKII activity in spines using fast-framing two-photon fluorescence lifetime imaging. Following each pulse during repetitive Ca 2+ elevations, CaMKII activity increased in a stepwise manner. Thr286 phosphorylation slows the decay of CaMKII and thus lowers the frequency required to induce spine plasticity by several fold. In the absence of Thr286 phosphorylation, increasing the stimulation frequency results in high peak mutant CaMKII T286A activity that is sufficient for inducing plasticity. Our findings demonstrate that Thr286 phosphorylation plays an important role in induction of LTP by integrating Ca 2+ signals, and it greatly promotes, but is dispensable for, the activation of CaMKII and LTP.
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“In essence, T286 autophosphorylation and CaM trapping would produce a frequency dependence for CaMKII activation.”
From Synaptic memory and CaMKII (2023) · cites this paper as [94]
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“This representation is strikingly similar to actual CaMKII responses in synaptic spines stimulated by repetitive glutamate uncaging and, as in FIGURE 3, shows little integrated activation with T286A CaMKII, unless substantially higher frequencies are used (94).”
From Synaptic memory and CaMKII (2023) · cites this paper as [94]
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“Despite these findings suggesting a critical role of T286, it should be noted that Chang et al. (94) reported that LTP can be expressed in the absence of T286 phosphorylation.”
From Synaptic memory and CaMKII (2023) · cites this paper as [94]
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Cites
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Structural basis of long-term potentiation in single dendritic spines
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Inhibition of Postsynaptic PKC or CaMKII Blocks Induction But Not Expression of LTP
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Sensitivity of CaM Kinase II to the Frequency of Ca 2+ Oscillations
De Koninck, P., & Schulman, H. (1998) · Science · doi:10.1126/science.279.5348.227 · Cited by 1,269
Mechanisms of CaMKII action in long-term potentiation
Lisman, J., Yasuda, R., & Raghavachari, S. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3192 · Cited by 1,134
Self-citationAutophosphorylation at Thr 286 of the α Calcium-Calmodulin Kinase II in LTP and Learning
Giese, K. P., Fedorov, N. B., Filipkowski, R. K., & Silva, A. J. (1998) · Science · doi:10.1126/science.279.5352.870 · Cited by 1,055
Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation
Barria, A., Muller, D., Derkach, V., Griffith, L. C., & Soderling, T. R. (1997) · Science · doi:10.1126/science.276.5321.2042 · Cited by 1,049
Activation of CaMKII in single dendritic spines during long-term potentiation
Lee, S.-J. R., Escobedo-Lozoya, Y., Szatmari, E. M., & Yasuda, R. (2009) · Nature · doi:10.1038/nature07842 · Cited by 685
Self-citationA critical time window for dopamine actions on the structural plasticity of dendritic spines
Yagishita, S., Hayashi-Takagi, A., Ellis-Davies, G. C. R., Urakubo, H., Ishii, S., & Kasai, H. (2014) · Science · doi:10.1126/science.1255514 · Cited by 614
Local, persistent activation of Rho GTPases during plasticity of single dendritic spines
Murakoshi, H., Wang, H., & Yasuda, R. (2011) · Nature · doi:10.1038/nature09823 · Cited by 564
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CaMKII: a central molecular organizer of synaptic plasticity, learning and memory
Yasuda, R., Hayashi, Y., & Hell, J. W. (2022) · Nature Reviews Neuroscience · doi:10.1038/s41583-022-00624-2 · Cited by 431
Self-citationCaM Kinase: Still Inspiring at 40
Bayer, K. U., & Schulman, H. (2019) · Neuron · doi:10.1016/j.neuron.2019.05.033 · Cited by 314
Plasticity of Spine Structure: Local Signaling, Translation and Cytoskeletal Reorganization
Nakahata, Y., & Yasuda, R. (2018) · Frontiers in Synaptic Neuroscience · doi:10.3389/fnsyn.2018.00029 · Cited by 209
Self-citationCaMKII Isoforms in Learning and Memory: Localization and Function
Zalcman, G., Federman, N., & Romano, A. G. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00445 · Cited by 185
Borovac, J., Bosch, M., & Okamoto, K. (2018) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2018.07.001 · Cited by 193
Metadata
- Authors
- Chang, J.-Y., Parra-Bueno, P., Laviv, T., Szatmari, E. M., Lee, S.-J. R., & Yasuda, R.
- Affiliations
- Duke University (US)
- Max Planck Florida Institute for Neuroscience (US)
- Duke Medical Center (US)
- Corresponding author
- Yasuda, Ryohei
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2017-05
- Volume
- 94
- Issue
- 4
- Pages
- 800-808.e4
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC5573161
- OpenAlex
- W2616355480
- Cited by
- 161
- References
- 44
- Citations by year
- 2026: 3 · 2025: 16 · 2024: 20 · 2023: 22 · 2022: 21 · 2021: 19 · 2020: 24 · 2019: 19 · 2018: 13 · 2017: 3
- FWCI
- 7.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- NIH (R01MH080047, 1DP1NS096787)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- CaMKII, autophosphorylation, long-term potentiation, calcium signaling, synaptic plasticity, dendritic spines, LTP maintenance, stimulation frequency
- MeSH terms
- Animals, Calcium, Hippocampus, Microscopy, Fluorescence, Neuronal Plasticity, Phosphorylation, Long-Term Potentiation, Pyramidal Cells, Patch-Clamp Techniques, Calcium Signaling, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2, CA1 Region, Hippocampal
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