DEFICIENT PLASTICITY IN THE PRIMARY VISUAL-CORTEX OF ALPHA-CALCIUM CALMODULIN-DEPENDENT PROTEIN-KINASE-II MUTANT MICE/

The recent characterization of plasticity in the mouse visual cortex p ermits the use of mutant mice to investigate the cellular mechanisms u nderlying activity-dependent development. As calcium-dependent signali ng pathways have been implicated in neuronal plasticity, we examined v isual cortical plasticity in mice lacking the alpha-isoform of calcium /calmodulin-dependent protein kinase II (alpha CaMKII). In wild-type m ice, brief occlusion of vision in one eye during a critical period red uces responses in the visual cortex. In half of the alpha CaMKII-defic ient mice, visual cortical responses developed normally, but visual co rtical plasticity was greatly diminished. After intensive training, sp atial learning in the Morris water maze was severely impaired in a sim ilar fraction of mutant animals. These data indicate that loss of alph a CaMKII results in a severe but variable defect in neuronal plasticit y.