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Curr Opin Neurobiol. 2002 Jun;12(3):293-9.

Molecular mechanisms of CaMKII activation in neuronal plasticity.

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Stanford University, Department of Molecular Pharmacology, CCSR Building, Room 3230, 269 Campus Drive, Stanford, California 94305, USA.


Calcium/calmodulin-dependent protein kinase II (CaMKII) is thought to be a critical mediator of neuronal plasticity that links transiently triggered Ca(2+) signals to persistent changes in neuronal physiology. In one of its roles, CaMKII is an essential player in the N-methyl-D-aspartate receptor-mediated increase in conductance at glutamatergic synapses, a process described as long-term potentiation, which serves as a common model for neuronal plasticity and memory. Recent studies have used genetic, biochemical, live cell imaging and mathematical modeling approaches to investigate neuronal CaMKII and have led to a model of the molecular steps of CaMKII translocation and activation that can explain its role in neuronal plasticity.

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