Alpha calcium/calmodulin dependent protein kinase II in learning-dependent plasticity of mouse somatosensory cortex

Calcium/calmodulin dependent protein kinase II (CaMKII), and more specifically its alpha subunit, is widely believed to be fundamental for hippocampal synaptic plasticity. In the cerebral cortex, deprivation-evoked plasticity was shown to depend on αCaMKII autophosphorylation abilities. Here we analyzed how learning-induced functional reorganization of cortical representations affected αCaMKII in adult Swiss mice. Mice were subjected to short-lasting sensory training in which stimulation of whiskers was paired with tail shock. The pairing results in enlargement of functional representation of vibrissae activated during the training. αCaMKII protein and its autophosphorylation level were determined by Western-blotting in somatosensory cortex crude synaptosomal fraction (P2) and postsynaptic protein-enriched, Triton X-100 insoluble fraction (TIF). The first training session resulted in an increase in αCaMKII autophosphorylation at autonomy site observed in TIF. A similar increase was also observed after the first session of just whiskers stimulation, which alone does not induce rearrangement of cortical representations. These data indicate that increased autophosphorylation of postsynaptic αCaMKII is not a correlate of induction phase of plasticity related reorganization of cortical representation of vibrissae. The increase observed in both experimental groups was transient and did not persist in the maintenance phase of the plastic change. Furthermore, we found that the training caused a delayed upregulation of αCaMKII protein level in crude synaptosomal fraction, but not in TIF, and the upregulation was not accompanied by an increase in autophosphorylation level of the kinase. The result indicates αCaMKII involvement in the late phase of plastic change and suggests the participation of a presynaptic pool of kinase rather than postsynaptic at this point.