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Molecular mechanisms of CaMKII activation in neuronal plasticity
被引:167
作者:

Fink, CC
论文数: 0 引用数: 0
h-index: 0
机构:
Stanford Univ, Dept Mol Pharmacol, Stanford, CA 94305 USA Stanford Univ, Dept Mol Pharmacol, Stanford, CA 94305 USA

Meyer, T
论文数: 0 引用数: 0
h-index: 0
机构:
Stanford Univ, Dept Mol Pharmacol, Stanford, CA 94305 USA Stanford Univ, Dept Mol Pharmacol, Stanford, CA 94305 USA
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.
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页码:293 / 299
页数:7
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