Molecular mechanisms of CaMKII activation in neuronal plasticity

被引:167
作者
Fink, CC [1 ]
Meyer, T [1 ]
机构
[1] Stanford Univ, Dept Mol Pharmacol, Stanford, CA 94305 USA
关键词
D O I
10.1016/S0959-4388(02)00327-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Calcium/calmodulin-dependent protein kinase 11 (CaMKII) is thought to be a critical mediator of neuronal plasticity that links transiently triggered Ca2+ 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.
引用
收藏
页码:293 / 299
页数:7
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