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Literature DB >> 17660813

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

Mohammad Reza Hojjati¹, Geeske M van Woerden, William J Tyler, Karl Peter Giese, Alcino J Silva, Lucas Pozzo-Miller, Ype Elgersma.

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.

Entities: Chemical

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Year: 2007 PMID： 17660813 PMCID： PMC2804046 DOI： 10.1038/nn1946

Source DB: PubMed Journal: Nat Neurosci ISSN： 1097-6256 Impact factor: 24.884

15 in total

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Review 6. Short-term synaptic plasticity.

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Authors: W J Tyler; L D Pozzo-Miller
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Review 10. Regulation of synaptic transmission by presynaptic CaMKII and BK channels.

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