Cited by 328Neuroscience and Neuropharmacology ResearchProtein Kinase Regulation and GTPase SignalingNeurogenesis and neuroplasticity mechanisms

Selective Regulation of Neurite Extension and Synapse Formation by the β but not the α Isoform of CaMKII

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Fink, Charles C, Bayer, Karl-Ulrich, Myers, Jason W, Ferrell, James E, Schulman, Howard, Meyer, Tobias·2003·Neuron

Abstract

Neurite extension and branching are important neuronal plasticity mechanisms that can lead to the addition of synaptic contacts in developing neurons and changes in the number of synapses in mature neurons. Here we show that Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates movement, extension, and branching of filopodia and fine dendrites as well as the number of synapses in hippocampal neurons. Only CaMKIIbeta, which peaks in expression early in development, but not CaMKIIalpha, has this morphogenic activity. A small insert in CaMKIIbeta, which is absent in CaMKIIalpha, confers regulated F-actin localization to the enzyme and enables selective upregulation of dendritic motility. These results show that the two main neuronal CaMKII isoforms have markedly different roles in neuronal plasticity, with CaMKIIalpha regulating synaptic strength and CaMKIIbeta controlling the dendritic morphology and number of synapses.

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Crossref · 10.1016/s0896-6273(03)00428-8

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  • Upon activation CaMKIIβ dissociates from F-actin because of competition with Ca2+/CaM for the F-actin binding region, and dissociation is made more persistent by specific autophosphorylation of CaMKIIβ in the F-actin binding region.

    “Upon activation CaMKIIβ dissociates from F-actin because of competition with Ca2+/CaM for the F-actin binding region, and dissociation is made more persistent by specific autophosphorylation of CaMKIIβ in the F-actin binding region (171–174).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [171]

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References 62 · Cited by 328

Authors
Fink, C. C., Bayer, K.-U., Myers, J. W., Ferrell, J. E., Schulman, H., & Meyer, T.
Affiliations
Stanford Medicine (US)
Corresponding author
Meyer, Tobias
Venue
Neuron
Publisher
Elsevier BV
Published
2003-07
Volume
39
Issue
2
Pages
283-297
ISSN
0896-6273 (ISSN-L)
OpenAlex
W2014549178
Cited by
328
References
62
Citations by year
2026: 5 · 2025: 8 · 2024: 6 · 2023: 8 · 2022: 6 · 2021: 12 · 2020: 7 · 2019: 11 · 2018: 13 · 2017: 12 · 2016: 7 · 2015: 14 · 2014: 14 · 2013: 17 · 2012: 15
FWCI
8.08
Type
journal article
Language
en
Open access
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
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 › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
CaMKII, neurite outgrowth, dendritic branching, filopodia, synaptogenesis, hippocampal neurons, neuroplasticity, dendritic morphology
MeSH terms
Actins, Animals, Animals, Newborn, Bacterial Proteins, Benzylamines, Binding Sites, Cell Fractionation, Cell Movement, Cells, Cultured, Dose-Response Relationship, Drug, Enzyme Inhibitors, Immunohistochemistry, Isoquinolines, Luminescent Proteins, Mutation, Nerve Tissue Proteins, Sulfonamides, Synapses, Time Factors, Transfection, Immunoblotting, Gene Expression Regulation, Enzymologic, Neurites, Calcium-Calmodulin-Dependent Protein Kinases, Microscopy, Confocal, Protein Isoforms, RNA Interference, Green Fluorescent Proteins, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2

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