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.,
Nature Neuroscience
Erasmus MC: University Medical Center Rotterdam

Hojjati, M. R., van Woerden, G., Tyler, W., Giese, K. P., Silva, A., 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. doi:10.1038/nn1946