351. Participation of CaMKII in neuronal plasticity and memory formation.
- Author
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Cammarota M, Bevilaqua LR, Viola H, Kerr DS, Reichmann B, Teixeira V, Bulla M, Izquierdo I, and Medina JH
- Subjects
- Animals, Calcium Signaling physiology, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Hippocampus cytology, Humans, Presynaptic Terminals ultrastructure, Receptors, Glutamate metabolism, Synaptic Membranes metabolism, Calcium-Calmodulin-Dependent Protein Kinases metabolism, Hippocampus enzymology, Memory physiology, Neuronal Plasticity physiology, Presynaptic Terminals enzymology, Synaptic Transmission physiology
- Abstract
1. The unique biochemical properties of Ca(2+)/calmodulin (CaM)-dependent protein kinase II have made this enzyme one of the paradigmatic models of the forever searched "memory molecule." 2. In particular, the central participation of CaMKII as a sensor of the Ca(2+) signals generated by activation of NMDA receptors after the induction of long-term plastic changes, has encouraged the use of pharmacological, genetic, biochemical, and imaging tools to unveil the role of this kinase in the acquisition, consolidation, and expression of different types of memories. 3. Here we review some of the more exciting discoveries related to the mechanisms involved in CaMKII activation and synaptic plasticity.
- Published
- 2002
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