Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Physiology (Bethesda). 2009 Dec;24:357-66. doi: 10.1152/physiol.00029.2009.
Ca2+/calmodulin-dependent protein kinase II (CaMKII) and actin are two crucial molecules involved in long-term potentiation (LTP). In addition to its signaling function, CaMKII plays a structural role via direct interaction with actin filaments, thus coupling functional and structural plasticity in dendritic spines. The status of F-actin, regulated by CaMKII, determines the postsynaptic protein binding capacity and thus may act as a synaptic tag that consolidates LTP.
钙/钙调蛋白依赖性蛋白激酶 II(CaMKII)和肌动蛋白是参与长时程增强(LTP)的两个关键分子。除了其信号功能外,CaMKII 通过与肌动蛋白丝的直接相互作用发挥结构作用,从而在树突棘中连接功能和结构可塑性。CaMKII 调节的 F-肌动蛋白决定了突触后蛋白的结合能力,因此可以作为巩固 LTP 的突触标记。