The roles of CaMKII and F-actin in the structural plasticity of dendritic spines: a potential molecular identity of a synaptic tag?
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.
Okamoto
Kenichi
K
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Bosch
Miquel
M
Hayashi
Yasunori
Y
D008841:Actin Cytoskeleton / Q000502:physiology; D000199:Actins / Q000502:physiology*; D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000502:physiology*; D049229:Dendritic Spines / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology
D000199:Actins; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2