Ocular dominance plasticity is stably maintained in the absence of calcium calmodulin kinase II ( CaMKII) autophosphorylation

The molecule calcium calmodulin kinase II ( CaMKII) is known to play a fundamental role in the induction of many forms of synaptic plasticity. A major theory of CaMKII function proposes that autophosphorylation of the molecule mediates not only the induction but also the maintenance of synaptic plasticity. To test this hypothesis, we assessed ocular dominance plasticity in genetically engineered mice that carry a mutation preventing autophosphorylation of CaMKII. These mutant mice are deficient in plasticity after monocular deprivation, but a sufficiently long period of monocular deprivation will induce ocular dominance plasticity. After induction of ocular dominance plasticity, the stability of the induced changes was assayed after binocular deprivation. Plasticity in homozygous mutant animals was as stable as that measured in WT littermates; also, response characteristics did not differ between the two groups. Our results suggest that CaMKII autophosphorylation is required for the induction of ocular dominance plasticity but is not needed for its stable maintenance thereafter.