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Nat Neurosci. 2007 Sep;10(9):1125-7. Epub 2007 Jul 29.

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

Author information

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

Abstract

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

PMID:
17660813
PMCID:
PMC2804046
DOI:
10.1038/nn1946
[Indexed for MEDLINE]
Free PMC Article

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