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REVIEW

The Roles of CaMKII and F-Actin in the Structural Plasticity of Dendritic Spines: A Potential Molecular Identity of a Synaptic Tag?

Kenichi Okamoto^1,*, Miquel Bosch^2,* and Yasunori Hayashi^2,3

¹ Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada;
² RIKEN-MIT Neuroscience Research Center, The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts; and
³ Brain Science Institute, RIKEN, Wako, Saitama, Japan yhayashi{at}brain.riken.jp

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.

^* K. Okamoto and M. Bosch contributed equally to this review.