To investigate whether a pathological loss of EAAT4 and GLAST/EAAT1 protein has an effect on the spontaneous activity of PCs, and whether such a defect plays a key role in the pathogenesis of cerebellar ataxia, we performed whole-cell patch clamp recordings of PCs in vitro in EAAT4 (ET4–/–) and GLAST (GLAST–/–) knockout mice. The gene discussed is SLC1A3; the disease is cerebellar ataxia.