First Author | Strutz-Seebohm N | Year | 2005 |
Journal | J Physiol | Volume | 565 |
Issue | Pt 2 | Pages | 381-90 |
PubMed ID | 15774536 | Mgi Jnum | J:112487 |
Mgi Id | MGI:3656411 | Doi | 10.1113/jphysiol.2004.079582 |
Citation | Strutz-Seebohm N, et al. (2005) Regulation of GluR1 abundance in murine hippocampal neurones by serum- and glucocorticoid-inducible kinase 3. J Physiol 565(Pt 2):381-90 |
abstractText | 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. |