4.5 Article

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

Journal

NEUROSCIENCE
Volume 151, Issue 3, Pages 750-757

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2007.11.012

Keywords

barrel cortex; alpha CaMKII autonomous activity; postsynaptic density protein; sensory pairing

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Calcium/calmodulin dependent protein kinase 11 (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 alpha CaMKII autophosphorylation abilities. Here we analyzed how learning-induced functional reorganization of cortical representations affected aCaMKII 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. aCaMKII 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 aCaMKII 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 aCaMKII 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 aCaMKII 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 aCaMKII involvement in the late phase of plastic change and suggests the participation of a presynaptic pool of kinase rather than postsynaptic at this point. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved.

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