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

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

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

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 of docked vesicles independent of its ability to be activated. These results indicate that αCaMKII has a nonenzymatic role in short-term presynaptic plasticity at hippocampal CA3-CA1 synapses.

Original languageEnglish (US)
Pages (from-to)1125-1127
Number of pages3
JournalNature Neuroscience
Volume10
Issue number9
DOIs
StatePublished - Sep 2007

ASJC Scopus subject areas

  • Neuroscience(all)

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    Hojjati, M. R., Van Woerden, G. M., Tyler, W., Giese, K. P., Silva, A. J., Pozzo-Miller, L., & Elgersma, Y. (2007). Kinase activity is not required for αCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses. Nature Neuroscience, 10(9), 1125-1127. https://doi.org/10.1038/nn1946