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

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 o...

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Detalhes bibliográficos
Main Authors: Hojjati, Mohammad Reza, van Woerden, Geeske M, Tyler, William J, Giese, Karl Peter, Silva, Alcino J, Pozzo-Miller, Lucas, Elgersma, Ype
Formato: Artigo
Idioma:Inglês
Publicado em: 2007
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Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC2804046/
https://ncbi.nlm.nih.gov/pubmed/17660813
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/nn1946
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