REGULATION OF PITUITARY CORTICOTROPIN-RELEASING HORMONE-BINDING PROTEIN MESSENGER-RIBONUCLEIC-ACID LEVELS BY RESTRAINT STRESS AND ADRENALECTOMY

Citation
Sj. Mcclennen et al., REGULATION OF PITUITARY CORTICOTROPIN-RELEASING HORMONE-BINDING PROTEIN MESSENGER-RIBONUCLEIC-ACID LEVELS BY RESTRAINT STRESS AND ADRENALECTOMY, Endocrinology, 139(11), 1998, pp. 4435-4441
Citations number
32
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
139
Issue
11
Year of publication
1998
Pages
4435 - 4441
Database
ISI
SICI code
0013-7227(1998)139:11<4435:ROPCHP>2.0.ZU;2-4
Abstract
CRH is the primary hypothalamic regulator of the stress response in hi gher organisms, where it acts as the key mediator of ACTH release in t he hypothalamus-pituitary-adrenal axis. The 37-kDa CRH-binding protein (CRH-BP) is known to bind CRH and antagonize CRH-induced ACTH release in vitro. The expression of this protein in anterior pituitary cortic otrophs suggests a role for CRH-BP in modulation of the stress respons e. To investigate the in vivo role of rat CRH-BP, the regulation of pi tuitary CRH-BP gene expression by acute restraint stress and/or adrena lectomy was examined using ribonuclease protection assays. After restr aint stress, steady-state levels of CRH-BP transcripts increase two to three times over basal level and remain significantly higher than bas al levels for 120 min after the start of restraint. Adrenalectomy decr eases CRH-BP messenger RNA steady-state levels to 8% of control levels . These results demonstrate that pituitary CRH-BP messenger RNA levels are increased in response to acute restraint stress and that glucocor ticoids play a significant role in this positive regulation. These dat a also suggest that increased CRH-BP levels, in response to stress, ma y modulate the endocrine stress response by providing an additional fe edback mechanism to maintain homeostasis of the hypothalamus-pituitary -adrenal axis.