Cerebellar Bergmann glial cells (BG) enwrap synapses on Purkinje-cell spines formed by parallel or climbing fibers. On their membranes, BG expresses localized glutamate transporters (GLAST close to the synaptic cleft) and AMPA-type glutamate receptors (GluR 1 and GluR 4 close to the shaft of presynaptic terminals). While the role of GLAST in controlling extracellular glutamate levels is rather obvious, we have only a limited knowledge of glial AMPA receptor function. To investigate the impact of glial transmitter receptors in vivo, we implemented a conditional knockout approach by crossbreeding mice in which astrocytes express the tamoxifen inducible variant of the Cre recombinase CreERT2 under the control of the human GFAP promoter or from the murine GLAST gene, respectively, with genetically modified mice in which exons 11 of the GluR 1 and GluR 4 genes, respectively, were flanked by loxP sites. Here, we demonstrate the successful ablation of GluR 1 and 4 from BG processes in an inducible and timely controlled manner. The lack of GluR 1 and 4 induces ultrastructural changes in the cerebellum: the BG retract their lamellae from Purkinje-cell synapses. As a physiological consequence of these ultrastructural changes we observe altered excitatory postsynaptic currents (EPSCs) in Purkinje cells upon parallel fiber stimulation. EPSCs exhibit larger amplitudes and slower decay kinetics. These alterations of the cerebellar network lead to deficits in complex motor performance. This study shows that astroglial AMPA receptors are important mediators of neuron-glia interactions that are essential for in vivo behavior.