Delta-catenin is required for the maintenance of neural structure and function in mature cortex in vivo

摘要

Delta (™)-catenin is a brain specific member of the adherens junction complex that localizes to the post-synaptic and dendritic compartments. This protein is likely critical for normal cognitive function; its hemizygous loss is linked to the severe mental retardation syndrome, Cri-du-Chat, and it directly interacts with Presenilin-1 (PS1), the protein most frequently mutated in familial Alzheimer's disease. Mice lacking normal ™-catenin display severe impairments in learning and memory tasks and synaptic plasticity. Here we examine dendritic structure and cortical function in vivo in mice lacking ™-catenin. We find that in cerebral cortex of 5-week-old mice dendritic complexity, spine density, and cortical responsiveness are similar between mutant and littermate controls; thereafter, mutant mice experience progressive dendritic retraction, a reduction in spine density and stability, and concomitant reductions in cortical responsiveness. Our results indicate that ™-catenin regulates the maintenance of dendrites and dendritic spines in mature cortex but does not appear to be necessary for the initial establishment of these structures during development.