Calcium/calmodulin-dependent protein kinase II and synaptic plasticity.
A prominent role for calcium/calmodulin-dependent protein kinase II (CaMKII) in regulation of excitatory synaptic transmission was proposed two decades ago when it was identified as a major postsynaptic density protein. Since then, fascinating mechanisms optimized to fine-tune the magnitude and locations of CaMKII activity have been revealed. The importance of CaMKII activity and autophosphorylation to synaptic plasticity in vitro, and to a variety of learning and memory paradigms in vivo has been demonstrated. Recent progress brings us closer to understanding the regulation of dendritic CaMKII activity, localization, and expression, and its role in modulating synaptic transmission and cell morphology.
Colbran
Roger J
RJ
Vanderbilt University Medical Center, Nashville, Tennessee 37232-0615, USA. roger.colbran@vanderbilt.edu
Brown
Abigail M
AM
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D002454:Cell Differentiation / Q000502:physiology; D002490:Central Nervous System / Q000166:cytology / Q000201:enzymology*; D003712:Dendrites / Q000201:enzymology / Q000648:ultrastructure; D006801:Humans; D008568:Memory / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D013569:Synapses / Q000201:enzymology* / Q000648:ultrastructure; D013570:Synaptic Membranes / Q000201:enzymology / Q000648:ultrastructure; D009435:Synaptic Transmission / Q000502:physiology*
D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases