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

Academic Article


  • 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. © 2007 Nature Publishing Group.
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    Digital Object Identifier (doi)

    Author List

  • Hojjati MR; Van Woerden GM; Tyler WJ; Giese KP; Silva AJ; Pozzo-Miller L; Elgersma Y
  • Start Page

  • 1125
  • End Page

  • 1127
  • Volume

  • 10
  • Issue

  • 9