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

来源：

CURRENT OPINION IN NEUROBIOLOGY | 2002年 / 12卷 / 03期

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

页码：293 / 299

页数：7

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