CaMKII: the Swiss army knife of synaptic plasticity.
CaMKII: the Swiss army knife of synaptic plasticity.
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CaMKII：突触可塑性的瑞士军刀。
DOI：
10.1113/jphysiol.2014.284414
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发表时间：
2014
期刊：
影响因子：
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通讯作者：
Hayashi Y.
中科院分区：
文献类型：
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作者：
Kim K;Hayashi Y.
Ca2+/钙调蛋白依赖性蛋白激酶 II (CaMKII) 已知在突触可塑性中发挥关键作用。它具有由四种不同亚型α-δ组成的十二聚结构。在过去十年左右的时间里，研究人员已经证明，抑制 CaMKII 活性或消除/下调 CaMKII 水平会导致长时程增强 (LTP)、学习和记忆缺陷。 CaMKII 的研究主要集中在 CaMKIIα 在调节海马和皮层兴奋性突触 LTP 中的作用。然而，最近的报告表明，CaMKII 不仅参与 LTP 的调节，而且也是海马长期抑郁 (LTD) 所必需的，其中对底物的特异性根据诱导方案而变化。在小脑中，CaMKII 还调节平行纤维浦肯野细胞突触的 LTP 和 LTD。此外，越来越多的证据表明 CaMKII 具有功能异质性，这是由不同亚型赋予的。
Ca2+/calmodulin-dependent protein kinase II (CaMKII) is known to play key roles in synaptic plasticity. It has a dodecameric structure composed of four different isoforms α–δ. Over the past decade or so, researchers have demonstrated that inhibition of CaMKII activity or ablation/down-regulation of CaMKII levels results in deficits in long-term potentiation (LTP), learning and memory. The study of CaMKII has primarily focused on the role of CaMKIIα in modulating LTP at excitatory synapses of the hippocampus and cortex. However, recent reports indicate that CaMKII is not only involved in the regulation of LTP, but that it is also required for hippocampal long-term depression (LTD) in a manner in which the specificity towards substrate changes depending on the induction protocol. In the cerebellum, CaMKII also regulates both LTP and LTD at parallel fibre–Purkinje cell synapses. In addition, growing evidence suggests that CaMKII is functionally heterogeneous, which is conferred by different isoforms.