CaMKII: claiming center stage in postsynaptic function and organization.
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.
Department of Pharmacology, University of California, Davis, Davis, CA 95615, USA. Electronic address: jwhell@ucdavis.edu.
Johannes W
JW
Hell
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D008958:Models, Molecular; D009420:Nervous System / Q000166:cytology; D009473:Neuronal Plasticity / Q000502:physiology*; D013569:Synapses / Q000502:physiology*
D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2