Abstract
Fos B, one of the immediate early genes, belongs to the Fos family of transcription factors. Fos B has been regarded as a marker for chronic cellular activation since its activity lasts for more than days in contrast to Fos activity which lasts for hours. We reported that bilateral adrenalectomy (ADX) increased markedly the FosB/delta FosB immunoreactivity in the corticotropin-releasing hormone neurons in the PVN and vasopression neurons in the SON. In order to demonstrate that glucocorticoid suppresses expression of FosB/delta FosB immunoreactivity, the effect of glucocorticoid supplementation was examined in these nuclei following ADX. Male Wistar rats were used. The number of FosB/delta FosB immunoreactive neurons increased significantly in the PVN and SON following ADX in comparison with the sham-operated controls. The increase in the FosB/delta FosB immunoreactivity was observed at 24 h after ADX in the PVN and SON. In the PVN, the increase lasted till day 4 and subsided by day 7 following ADX, whereas in the SON, it lasted till day 2 and subsided by day 4. Dexamethasone (0.1 mg/kg/day) supplementation suppressed the enhanced FosB/delta FosB immunoreactivity in both the PVN and SON. Thus it was demonstrated that glucocorticoid suppresses FosB/delta FosB immunoreactivity in the PVN and SON in rats. Physiological meaning of the phenomena is under investigation. [J Physiol Sci. 2008;58 Suppl:S136]
