Persistent modification of cortical neuronal responses upon alternations in sensory experience is believed to be the neural correlate of memory and learning. Ocular dominance (OD) plasticity, a process in which changes in visual input cause a shift in cortical responsiveness, is a paradigmatic model for studying experience-dependent plasticity. To understand the rapid processes of OD plasticity, we combined chronic in vivo two-photon microscopy and intrinsic signal optical imaging to monitor the activity of CaMKII-alpha, a protein kinase critically involved in the induction of long-term potentiation (LTP), in the visual cortex of ferrets. We found that in layer II/III pyramidal neurons located in the deprived eye domain, CaMKII-alpha activity in the spines and the adjacent dendritic regions increased significantly after 4 hr of monocular deprivation (MD). This increase was also seen in the binocular eye domain. However, the overall increase in CaMKII-alpha activity was not observed in the open eye domain. These observations were specific to MD as control experiments did not show such changes. Furthermore, in spines that were eliminated after 4 hr MD, the basal level of CaMKII-alpha activity was low. These results lend support to the model that both Hebbian, as well as homeostatic compensatory mechanism subserve OD plasticity.

Society for Neuroscience Abstract, 2009.