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1 Department of Physiology I, University of Tuebingen, D-72076 Tuebingen, Germany
2 Department of Anatomy, University of Tuebingen, D-72074 Tuebingen, Germany
3 Department of Psychiatry, Charité Medicine, D-14050 Berlin, Germany
4 Department of Biochemistry I – Receptor Biochemistry, Ruhr University Bochum, D-44780 Bochum, Germany
5 Departments of Cellular and Molecular Pharmacology and Physiology, University of, California, San Francisco, CA 94143, USA
6 Division of Nephrology, Departments of Medicine and of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143-0532, USA
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.
(Received 19 November 2004;
accepted after revision 17 March 2005;
first published online 17 March 2005)
Corresponding author F. Lang: Department of Physiology I, University of Tuebingen, 72076 Tuebingen, Germany. Email: florian.lang{at}uni-tuebingen.de
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