Glucocorticoid dependency of surgical stress-induced FosB/DeltaFosB 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/DeltaFosB (DeltaFosB, 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/DeltaFosB-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/DeltaFosB-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/DeltaFosB-ir in either the PVN or SON, and thus the up-regulation of FosB/DeltaFosB-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/DeltaFosB-ir following ADX, whereas, in the magnocellular division of the PVN, vasopressin (AVP) and oxytocin (OXT) neurones did not express FosB/DeltaFosB-ir. In the SON, approximately 40% of the AVP neurones co-expressed FosB/DeltaFosB-ir following ADX, but the OXT neurones were devoid of FosB/DeltaFosB-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/DeltaFosB expression, which is induced by stress, in hypothalamic neuroendocrine neurones.
Das
G
G
Laboratory of Information Biology, Graduate School of Information Sciences, Tohoku University, Sendai, Japan. itoik@m.tains.tohoku.ac.jp
Uchida
K
K
Kageyama
K
K
Iwasaki
Y
Y
Suda
T
T
Itoi
K
K
D000311:Adrenal Glands / Q000601:surgery*; D000315:Adrenalectomy / Q000009:adverse effects; D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism; D005576:Colforsin / Q000378:metabolism; D003345:Corticosterone / Q000378:metabolism; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism; D005938:Glucocorticoids / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000502:physiology; D010121:Oxytocin / Q000378:metabolism; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology*; D020033:Protein Isoforms / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000502:physiology*; D013495:Supraoptic Nucleus / Q000502:physiology*
C483820:Fosb protein, rat; D005938:Glucocorticoids; D020033:Protein Isoforms; D016760:Proto-Oncogene Proteins c-fos; D001127:Arginine Vasopressin; D005576:Colforsin; D000450:Aldosterone; D010121:Oxytocin; D003907:Dexamethasone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone