GSK3β overexpression driven by GFAP promoter improves rotarod performance

We have studied the consequences of in vivo GSK3 beta overexpression in the cerebellum using transgenic mice with conditional expression where the transactivator tTA protein expression is driven by GFAP promoter. We demonstrate an increase in GSK3 beta in Bergmann cells. To study cerebellar dysfunctions and evaluate motor coordination we analysed the latency to fall in the accelerating rotarod test. GSK3 beta transgenic mice performed significantly better than wild-type mice and transgene shutdown with doxycycline normalizes the values in latency to fall in rotarod test. We had previously demonstrated using the same transgenic model, that over expression of GSK3 beta in the hippocampus results in an increase in neural precursor cells. However, we did not observe that increase in the number of Sox2 + cells in the cerebellum. All the same, we observed an increase in cerebellar glutamate transporters GLT1 and GLAST. These data show that GSK3 beta can be a crucial kinase in cerebellum and especially in Bergmann glial cells.