Department of Pharmacology, University of California, Davis, Davis, CA 95615, USA.
Neuron. 2014 Jan 22;81(2):249-65. doi: 10.1016/j.neuron.2013.12.024.
While CaMKII has long been known to be essential for synaptic plasticity and learning, recent work points to new dimensions of CaMKII function in the nervous system, revealing that CaMKII also plays an important role in synaptic organization. Ca(2+)-triggered autophosphorylation of CaMKII not only provides molecular memory by prolonging CaMKII activity during long-term plasticity (LTP) and learning but also represents a mechanism for autoactivation of CaMKII's multifaceted protein-docking functions. New details are also emerging about the distinct roles of CaMKIIα and CaMKIIβ in synaptic homeostasis, further illustrating the multilayered and complex nature of CaMKII's involvement in synaptic regulation. Here, I review novel molecular and functional insight into how CaMKII supports synaptic function.
虽然 CaMKII 长期以来一直被认为对突触可塑性和学习至关重要,但最近的工作揭示了 CaMKII 在神经系统中的新功能维度,表明 CaMKII 也在突触组织中发挥重要作用。Ca(2+)触发的 CaMKII 自磷酸化不仅通过在长期可塑性 (LTP) 和学习过程中延长 CaMKII 活性来提供分子记忆,而且还代表了 CaMKII 多方面蛋白对接功能的自动激活机制。CaMKIIα 和 CaMKIIβ 在突触稳态中的独特作用的新细节也在不断涌现,进一步说明了 CaMKII 参与突触调节的多层次和复杂性质。在这里,我回顾了关于 CaMKII 如何支持突触功能的新的分子和功能见解。