Yasuda Ryohei, Hayashi Yasunori, Hell Johannes W
Max Planck Florida Institute for Neuroscience, Jupiter, FL, USA.
Department of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Nat Rev Neurosci. 2022 Nov;23(11):666-682. doi: 10.1038/s41583-022-00624-2. Epub 2022 Sep 2.
Calcium-calmodulin (CaM)-dependent protein kinase II (CaMKII) is the most abundant protein in excitatory synapses and is central to synaptic plasticity, learning and memory. It is activated by intracellular increases in calcium ion levels and triggers molecular processes necessary for synaptic plasticity. CaMKII phosphorylates numerous synaptic proteins, thereby regulating their structure and functions. This leads to molecular events crucial for synaptic plasticity, such as receptor trafficking, localization and activity; actin cytoskeletal dynamics; translation; and even transcription through synapse-nucleus shuttling. Several new tools affording increasingly greater spatiotemporal resolution have revealed the link between CaMKII activity and downstream signalling processes in dendritic spines during synaptic and behavioural plasticity. These technologies have provided insights into the function of CaMKII in learning and memory.
钙调蛋白（CaM）依赖性蛋白激酶II（CaMKII）是兴奋性突触中含量最丰富的蛋白质，对突触可塑性、学习和记忆至关重要。它通过细胞内钙离子水平的升高而被激活，并触发突触可塑性所需的分子过程。CaMKII使众多突触蛋白磷酸化，从而调节其结构和功能。这导致了对突触可塑性至关重要的分子事件，如受体运输、定位和活性；肌动蛋白细胞骨架动力学；翻译；甚至通过突触-细胞核穿梭进行转录。几种具有越来越高时空分辨率的新工具揭示了在突触和行为可塑性期间，CaMKII活性与树突棘中下游信号传导过程之间的联系。这些技术为CaMKII在学习和记忆中的功能提供了深入了解。
