CaMKII: a molecular substrate for synaptic plasticity and memory.
Learning and memory is widely believed to result from changes in connectivity within neuronal circuits due to synaptic plasticity. Work over the past two decades has shown that Ca(2+) influx during LTP induction triggers the activation of CaMKII in dendritic spines. CaMKII activation results in autophosphorylation of the kinase rendering it constitutively active long after the Ca(2+) dissipates within the spine. This "molecular switch"(1) mechanism is essential for LTP and learning and memory. Here, we discuss this key regulatory mechanism and the diversity of downstream targets that can be modulated by CaMKII to exert dynamic control of synaptic structure and function.
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Brian C
BC
Shonesy
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Nidhi
N
Jalan-Sakrikar
Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Victoria S
VS
Cavener
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA; Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, Tennessee, USA; Vanderbilt-Kennedy Center for Research on Human Development, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Roger J
RJ
Colbran
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D006801:Humans; D008568:Memory / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*
D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2
AMPA receptors; CaMKII; Calcium/calmodulin-dependent protein kinase II; Hippocampus; LTD; LTP; Long-term depression; Long-term potentiation; Memory; NMDA receptors; Synaptic plasticity