Autophosphorylation of αCaMKII Is Required for Ocular Dominance Plasticity

AbstractExperience is a powerful sculptor of developing neural connections. In the primary visual cortex (V1), cortical connections are particularly susceptible to the effects of sensory manipulation during a postnatal critical period. At the molecular level, this activity-dependent plasticity requires the transformation of synaptic depolarization into changes in synaptic weight. The molecule α calcium-calmodulin kinase type II (αCaMKII) is known to play a central role in this transformation. Importantly, αCaMKII function is modulated by autophosphorylation, which promotes Ca2+-independent kinase activity. Here we show that mice possessing a mutant form of αCaMKII that is unable to autophosphorylate show impairments in ocular dominance plasticity. These results confirm the importance of αCaMKII in visual cortical plasticity and suggest that synaptic changes induced by monocular deprivation are stored specifically in glutamatergic synapses made onto excitatory neurons