Brief Communication abstract
Nature Neuroscience 10, 1125 - 1127 (2007)
Published online: 29 July 2007 | doi:10.1038/nn1946
Kinase activity is not required for 
CaMKII-dependent presynaptic plasticity at CA3-CA1 synapses
Mohammad Reza Hojjati1,2, Geeske M van Woerden1, William J Tyler3,6, Karl Peter Giese4, Alcino J Silva5, Lucas Pozzo-Miller3 & Ype Elgersma1,5
Using targeted mouse mutants and pharmacologic inhibition of 
CaMKII, we demonstrate that the CaMKII protein, but not its activation, autophosphorylation or its ability to phosphorylate synapsin I, is required for normal short-term presynaptic plasticity. Furthermore, CaMKII regulates the number of docked vesicles independent of its ability to be activated. These results indicate that CaMKII has a nonenzymatic role in short-term presynaptic plasticity at hippocampal CA3-CA1 synapses.
- Department of Neuroscience, Erasmus University Medical Center, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands.
- Department of Physiology, Shahrekord University of Medical Sciences, Kashani Blvd, Shahrekord 88155, Iran.
- Department of Neurobiology, McKnight Brain Institute, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, Alabama 35294-2182, USA.
- Institute of Psychiatry, King's College London, 125 Coldharbour Lane, London SE59NU, UK.
- Departments of Neurobiology, Psychiatry and Psychology, Brain Research Institute, 695 Charles Young Drive South, University of California, Los Angeles, California 90095-1761, USA.
- Present address: Arizona State University, School of Life Sciences, 1711 South Rural Road, Tempe, Arizona 85287, USA.
Correspondence to: Ype Elgersma1,5 e-mail: y.elgersma@erasmusmc.nl
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