Phosphatidylinositol 3 kinase (PI3‐kinase) is activated during and is required for hippocampal glutamate receptor‐dependent long‐term potentiation. It mediates the delivery of AMPA receptors to the neuronal surface. Among the downstream targets of PI3‐kinase are three members of the serum‐ and glucocorticoid‐inducible kinase family, SGK1, SGK2 and SGK3. In Xenopus oocytes expressing the AMPA subunit GluR1, we show that SGK3, and to a lesser extent SGK2, but not SGK1, increase glutamate‐induced currents by increasing the abundance of GluR1 protein in the cell membrane. We further show Sgk3 mRNA expression in the hippocampus by RT‐PCR and in situ hybridization. According to Western blotting, the hippocampal abundance of GluR1 is significantly lower in gene‐targeted mice lacking SGK3 (Sgk3−/−) than in their wild‐type littermates (Sgk3+/+). The present observations disclose a novel mechanism in the regulation of GluR1.