Its possible role became only indirectly apparent, when we observed that, in contrast to the single GluA1-KO mice, the double GluA1/GluA3-KO mice virtually completely lacked glutamatergic currents in PCs, and the double L7-GluA1/GluA3-KO mice showed significant signs of ataxia and deficits in motor learning. This evidence concerns the gene GRIA1 and Ataxia.