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Neuron. 2002 Oct 24;36(3):493-505.

Inhibitory autophosphorylation of CaMKII controls PSD association, plasticity, and learning.

Author information

1
Department of Neurobiology, Department of Psychiatry, Department of Psychology, Brain Research Institute, University of California, Los Angeles, CA 90095, USA.

Abstract

To investigate the function of the alpha calcium-calmodulin-dependent kinase II (alphaCaMKII) inhibitory autophosphorylation at threonines 305 and/or 306, we generated knockin mice that express alphaCaMKII that cannot undergo inhibitory phosphorylation. In addition, we generated mice that express the inhibited form of alphaCaMKII, which resembles the persistently phosphorylated kinase at these sites. Our data demonstrate that blocking inhibitory phosphorylation increases CaMKII in the postsynaptic density (PSD), lowers the threshold for hippocampal long-term potentiation (LTP), and results in hippocampal-dependent learning that seems more rigid and less fine-tuned. Mimicking inhibitory phosphorylation dramatically decreased the association of CaMKII with the PSD and blocked both LTP and learning. These data demonstrate that inhibitory phosphorylation has a critical role in plasticity and learning.

PMID:
12408851
DOI:
10.1016/s0896-6273(02)01007-3
[Indexed for MEDLINE]
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