CaMKII regulation in information processing and storage

被引：270
作者：
Coultrap, Steven J. [1 ]
Bayer, K. Ulrich [1 ]
机构：
[1] Univ Colorado, Denver Sch Med, Dept Pharmacol, Aurora, CO 80045 USA
来源：
TRENDS IN NEUROSCIENCES | 2012年 / 35卷 / 10期
基金：
美国国家卫生研究院;
关键词：
CaMKII; NMDA receptor; autonomy; long-term potentiation; long-term depression.learning and memory; PROTEIN-KINASE-II; LONG-TERM POTENTIATION; HIPPOCAMPAL SYNAPTIC PLASTICITY; CALCIUM-INDEPENDENT ACTIVATION; POSTSYNAPTIC DENSITY; ALPHA-CAMKII; SUBUNIT COMPOSITION; DENDRITIC SPINES; AMPA RECEPTORS; F-ACTIN;
D O I：
10.1016/j.tins.2012.05.003
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The Ca2+/Calmodulin(CaM)-dependent protein kinase II (CaMKII) is activated by Ca2+/CaM, but becomes partially autonomous (Ca2+-independent) upon autophosphorylation at T286. This hallmark feature of CaMKII regulation provides a form of molecular memory and is indeed important in long-term potentiation (LTP) of excitatory synapse strength and memory formation. However, emerging evidence supports a direct role in information processing, while storage of synaptic information may instead be mediated by regulated interaction of CaMKII with the NMDA receptor (NMDAR) complex. These and other CaMKII regulation mechanisms are discussed here in the context of the kinase structure and their impact on postsynaptic functions. Recent findings also implicate CaMKII in long-term depression (LTD), as well as functional roles at inhibitory synapses, lending renewed emphasis on better understanding the spatiotemporal control of CaMKII regulation.
引用
收藏
页码：607 / 618
页数：12
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