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 permits the use of mutant mice to investigate the cellular mechanisms underlying activity-dependent development. As calcium-dependent signaling pathways have been implicated in neuronal plasticity, we examined visual cortical plasticity in mice lacking the alpha-isoform of calcium/calmodulin-dependent protein kinase II (alpha CaMKII). In wild-type mice, brief occlusion of vision in one eye during a critical period reduces responses in the visual cortex. In half of the alpha CaMKII-deficient mice, visual cortical responses developed normally, but visual cortical plasticity was greatly diminished. After intensive training, spatial learning in the Morris water maze was severely impaired in a similar fraction of mutant animals. These data indicate that loss of alpha CaMKII results in a severe but variable defect in neuronal plasticity.
Gordon
J A
JA
Department of Physiology, University of california, San Francisco 94143-0444, USA.
Cioffi
D
D
Silva
A J
AJ
Stryker
M P
MP
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000172:deficiency / Q000235:genetics*; D004594:Electrophysiology; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D008817:Mice, Mutant Strains; D009154:Mutation / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D010641:Phenotype; D013037:Spatial Behavior / Q000502:physiology; D014793:Visual Cortex / Q000201:enzymology* / Q000254:growth & development / Q000502:physiology*
D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases; C517671:Camk2a protein, mouse