Molecular memory by reversible translocation of calcium/calmodulin-dependent protein kinase II
Abstract
Synaptic plasticity is thought to be a key process for learning, memory and other cognitive functions of the nervous system. The initial events of plasticity require the conversion of brief electrical signals into alterations of the biochemical properties of synapses that last for much longer than the initial stimuli. Here we show that a regulator of synaptic plasticity, calcium/calmodulin-dependent protein kinase IIalpha (CaMKII), sequentially translocates to postsynaptic sites, undergoes autophosphorylation and gets trapped for several minutes until its dissociation is induced by secondary autophosphorylation and phosphatase 1 action. Once dissociated, CaMKII shows facilitated translocation for several minutes. This suggests that trapping of CaMKII by its targets and priming of CaMKII translocation may function as biochemical memory mechanisms that change the signaling capacity of synapses.
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During glutamate-induced translocation of CaMKII in culture, T305A/T306A mutations greatly increase CaMKII resident time at synaptic sites.
“During glutamate-induced translocation of CaMKII in culture, these same mutations greatly increase CaMKII resident time at synaptic sites (88).”
From Synaptic memory and CaMKII (2023) · cites this paper as [88]
Using a T286D mutation alone is problematic because it generates a constitutively active kinase that then results in phosphorylation of T305/T306, which can counteract T286D and alter resident time at the synapse.
“Just using a T286D mutation would be problematic because it generates a constitutively active kinase that then results in the phosphorylation of T305/T306, which can counteract T286D and alter resident time at the synapse (88, 210, 211).”
From Synaptic memory and CaMKII (2023) · cites this paper as [88]
T286 phosphorylation is needed for the persistence of a CaMKII-GluN2B complex.
“This suggests a need for T286 phosphorylation for persistence of a CaMKII-GluN2B complex (88, 169).”
From Synaptic memory and CaMKII (2023) · cites this paper as [88]
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References 31 · Cited by 206
- Authors
- Shen, K., Teruel, M. N., Connor, J. H., Shenolikar, S., & Meyer, T.
- Affiliations
- Duke Medical Center (US)
- Duke University (US)
- Corresponding author
- Meyer, T.
- Venue
- Nature Neuroscience
- Published
- 2000-09
- Volume
- 3
- Issue
- 9
- Pages
- 881-886
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W1585828943
- Cited by
- 206
- References
- 31
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 3 · 2019: 2 · 2018: 5 · 2017: 7 · 2016: 6 · 2015: 3 · 2014: 8 · 2013: 9 · 2012: 11
- FWCI
- 5.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM048113, R01-GM48113)
- 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, calcium/calmodulin-dependent protein kinase II, synaptic plasticity, molecular memory, protein translocation, autophosphorylation, postsynaptic sites, learning and memory
- MeSH terms
- Aniline Compounds, Animals, Animals, Newborn, Cells, Cultured, Electric Stimulation, Fluorescent Dyes, Hippocampus, Indicators and Reagents, Luminescent Proteins, Memory, Neuronal Plasticity, Neurons, Phosphorylation, Synaptic Membranes, Xanthenes, Calcium-Calmodulin-Dependent Protein Kinases, Glutamic Acid, Green Fluorescent Proteins, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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