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Kinase activity is not required for αCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses

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Abstract

Using targeted mouse mutants and pharmacologic inhibition of αCaMKII, we demonstrate that the αCaMKII protein, but not its activation, autophosphorylation or its ability to phosphorylate synapsin I, is required for normal short-term presynaptic plasticity. Furthermore, αCaMKII regulates the number of docked vesicles independent of its ability to be activated. These results indicate that αCaMKII has a nonenzymatic role in short-term presynaptic plasticity at hippocampal CA3-CA1 synapses.

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Figure 1: Phosphorylation of synapsin I and CaMKII-T286/T287 in synaptosomes obtained from αCaMKII mutants.
Figure 2: Presynaptic short-term plasticity requires αCaMKII protein, but not its autophosphorylation, activation or activity.
Figure 3: αCaMKII protein regulates the number of docked vesicles.

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Acknowledgements

We greatly appreciate the help of H. Beck, M. Merkens, R. Anwyl, K. Wang and R. Colbran for their (hands-on) advice on the use of CaMKII inhibitors, and from G. Borst and S. Kushner and members of the Silva and Elgersma lab for stimulating discussions and critically reading the manuscript. We thank M. Elgersma, H. van der Burg and E. Phillips for technical support. This work was supported by grants from NWO-ZonMW (TOP, VIDI) and Neuro-BSIK to Y.E. We also thank the University of Alabama, Birmingham Neuroscience Cores (P30-NS47466, P30-HD38985, P30-NS57098).

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Author notes

  1. William J Tyler

    Present address: Present address: Arizona State University, School of Life Sciences, 1711 South Rural Road, Tempe, Arizona 85287, USA.,

Authors and Affiliations

  1. Department of Neuroscience, Erasmus University Medical Center, Dr. Molewaterplein 50, Rotterdam, 3015 GE, The Netherlands

    Mohammad Reza Hojjati, Geeske M van Woerden & Ype Elgersma

  2. Department of Physiology, Shahrekord University of Medical Sciences, Kashani Blvd, Shahrekord, 88155, Iran

    Mohammad Reza Hojjati

  3. Department of Neurobiology, McKnight Brain Institute, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, 35294-2182, Alabama, USA

    William J Tyler & Lucas Pozzo-Miller

  4. Institute of Psychiatry, King's College London, 125 Coldharbour Lane, London, SE59NU, UK

    Karl Peter Giese

  5. Departments of Neurobiology, Psychiatry and Psychology, Brain Research Institute, 695 Charles Young Drive South, University of California, Los Angeles, 90095-1761, California, USA

    Alcino J Silva & Ype Elgersma

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  1. Mohammad Reza Hojjati
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  2. Geeske M van Woerden
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  3. William J Tyler
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  7. Ype Elgersma
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Correspondence to Ype Elgersma.

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The authors declare no competing financial interests.

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Hojjati, M., van Woerden, G., Tyler, W. et al. Kinase activity is not required for αCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses. Nat Neurosci 10, 1125–1127 (2007). https://doi.org/10.1038/nn1946

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  • DOI: https://doi.org/10.1038/nn1946

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