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

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.

SUBMITTER: Hojjati MR

PROVIDER: S-EPMC2804046 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature

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

Hojjati Mohammad Reza MR van Woerden Geeske M GM Tyler William J WJ Giese Karl Peter KP Silva Alcino J AJ Pozzo-Miller Lucas L Elgersma Ype Y

Nature neuroscience 20070729 9

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 sy ...[more]

PMID: 17660813

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