Glucocorticoid Dependency of Surgical Stress-Induced FosB/ΔFosB Expression in the Paraventricular and Supraoptic Nuclei of the Rat Hypothalamus

FosB is a member of the Fos family transcription factors. To determine whether FosB expression is regulated by glucocorticoids (GCs) in the hypothalamus, rats underwent sham adrenalectomy (sham‐ADX) or bilateral ADX, and FosB/ΔFosB (ΔFosB, a truncated splice variant of FosB)‐immunoreactivity (ir) was determined in the paraventricular nucleus (PVN) and supraoptic nucleus (SON). In the parvocellular division of the PVN (paPVN) and SON, FosB/ΔFosB‐immunoreactivity (ir) increased significantly following sham‐ADX compared to naive rats, which was suppressed with either corticosterone (CORT) or dexamethasone (DEX). Following ADX, the increase in FosB/ΔFosB‐ir was much more prominent than that in the sham‐ADX group, and the ADX‐induced robust increase was suppressed by CORT or DEX, but not by aldosterone. Stressless removal of CORT from drinking water did not induce FosB/ΔFosB‐ir in either the PVN or SON, and thus the up‐regulation of FosB/ΔFosB‐ir following ADX was dependent on the systemic stress associated with surgery. In the paPVN, the majority of corticotrophin‐releasing hormone (CRH) neurones co‐expressed FosB/ΔFosB‐ir following ADX, whereas, in the magnocellular division of the PVN, vasopressin (AVP) and oxytocin (OXT) neurones did not express FosB/ΔFosB‐ir. In the SON, approximately 40% of the AVP neurones co‐expressed FosB/ΔFosB‐ir following ADX, but the OXT neurones were devoid of FosB/ΔFosB‐ir. In concert with these results obtained in vivo, DEX suppressed the forskolin‐induced increase in FosB gene promoter activity in a homologous hypothalamic cell line. These results suggest that GCs may be a potent regulator of FosB/ΔFosB expression, which is induced by stress, in hypothalamic neuroendocrine neurones.