Deficient plasticity in the primary visual cortex of alpha-calcium/calmodulin-dependent protein kinase II mutant mice

Neuron. 1996 Sep;17(3):491-9. doi: 10.1016/s0896-6273(00)80181-6.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Calcium-Calmodulin-Dependent Protein Kinases / deficiency
  • Calcium-Calmodulin-Dependent Protein Kinases / genetics*
  • Electrophysiology
  • Maze Learning / physiology
  • Mice
  • Mice, Mutant Strains
  • Mutation / physiology
  • Neuronal Plasticity / physiology*
  • Phenotype
  • Spatial Behavior / physiology
  • Visual Cortex / enzymology*
  • Visual Cortex / growth & development
  • Visual Cortex / physiology*

Substances

  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Camk2a protein, mouse