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The knock-out of -calcium/calmodulin-dependent protein ki- nase II (CaMKII) was the kickoff for a new subfield in neuro- science, in which mouse mutants are used as a tool to gain insight into the molecular basis of cognition and brain plasticity. In our review, we give an overview of the CaMKII mutants that have since been developed, and we summarize the key findings that these studies have provided on the function of CaMKII in hip- pocampal plasticity, cortical plasticity, and learning and memory. Furthermore, we discuss recent results that misregulation of CaMKII function may cause the neurological symptoms in An- gelman's syndrome (AS).

Mouse Genetic Approaches to Investigating Calcium/Calmodulin-Dependent Protein Kinase II Function in Plasticity and Cognition: Table 1.