Journal
NATURE NEUROSCIENCE
Volume 10, Issue 9, Pages 1125-1127Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn1946
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Funding
- MRC [G0400983] Funding Source: UKRI
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P30HD038985] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P30NS057098, P30NS047466, R01NS040593] Funding Source: NIH RePORTER
- Medical Research Council [G0400983] Funding Source: Medline
- NICHD NIH HHS [P30-HD38985, P30 HD038985] Funding Source: Medline
- NINDS NIH HHS [P30-NS57098, R01 NS040593, P30-NS47466, R01 NS040593-09, P30 NS047466, P30 NS057098] Funding Source: Medline
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Using targeted mouse mutants and pharmacologic inhibition of alpha CaMKII, we demonstrate that the aCaMKII protein, but not its activation, autophosphorylation or its ability to phosphorylate synapsin I, is required for normal short-term presynaptic plasticity. Furthermore, aCaMKII regulates the number of docked vesicles independent of its ability to be activated. These results indicate that aCaMKII has a nonenzymatic role in short-term presynaptic plasticity at hippocampal CA3-CA1 synapses.
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