Acute stress and corticosterone enhance 5- HT1A receptor- mediated responses in rat hippocampal CA1 cells within 1 - 2 h, through a process involving transcriptional regulation of unknown genes. Earlier studies showed that regulation of the 5- HT1A receptor gene cannot explain the functional effects. We here tested the hypothesis that corticosterone targets genes encoding RGS4 or SGK1, which can both affect the 5- HT1A receptor associated K-ir channel, thus affecting 5- HT1A receptor function. To this end, the effect of a single corticosterone injection on hippocampal expression of RGS4 and SGK1 mRNAs, measured by in situ hybridization, was studied. Expression of RGS4 or SGK1 mRNA was not affected by the corticosterone injection, neither in the CA1 area nor in other hippocampal subregions. Strikingly, SGK1 mRNA expression was strongly up- regulated in the corpus callosum. We reject, however, the hypothesis that the effect of corticosterone on 5- HT1A responsiveness is mediated via altered RGS4 or SGK1 mRNA expression.
|Number of pages||6|
|Journal||Stress-The international journal on the biology of stress|
|Publication status||Published - Sep-2006|
- corpus callosum
- regulator of G-protein signaling 4
- serum- and glucocorticoid-regulated kinase 1
- KINASE GENE FAMILY