In the current study, proteins binding calmodulin (Basp1, Akap5; A-kinase anchor protein 5), as well as proteins playing a role in long term synaptic potentiation (Picalm; Phosphatidylinositol-binding clathrin assembly protein, Akap5) or synaptic transmission (Picalm) and formation (Dbnl; Drebrin-like protein), were up-regulated in the temporal cortices of WD rats. This evidence concerns the gene DBNL and Wilson disease.