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      Stress-Induced Alterations in Corticotropin-Releasing Hormone and Vasopressin Gene Expression in the Paraventricular Nucleus during Ontogeny

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          From postnatal day (PND) 4 to 14, neonates display a minimal pituitary-adrenal response to mild stress, the so-called ‘stress hyporesponsive period’ (SHRP). During the SHRP, maternal deprivation (MD) alters the pituitary-adrenal system, enabling neonates to become endocrine responsive to specific stimuli. We have previously reported that during the SHRP, mild stress enhances corticotropin-releasing hormone (CRH) messenger RNA (mRNA) expression in the paraventricular nucleus (PVN). Insofar as elevated CRH mRNA was observed both in the presence and absence of adrenocorticotropin (ACTH) release, we hypothesized that other ACTH secretagogues may participate in the pituitary stress response. During the SHRP, does arginine vasopressin (AVP) complement the actions of CRH which might be reflected centrally by the enhanced biosynthesis of both neuropeptides? To test this hypothesis we examined the time course of stress-induced CRH and AVP mRNA in the PVN at PND 6, 12, and 18. As an index of neural activity, c-fos mRNA in the PVN was also examined. Restraint was used as the stressor and MD was employed to enable an endocrine response during the SHRP. Despite the absence of stress-induced ACTH, in nondeprived pups during the SHRP, CRH mRNA was rapidly enhanced. In their maternally deprived (DEP) counterparts, ACTH levels were increased, and a significant induction of CRH mRNA was only observed at day 12. AVP mRNA levels were elevated in DEP 12-day-old pups at 15, 30 and 60 min. In rats beyond the SHRP, plasma ACTH levels, CRH and AVP mRNA were all enhanced following restraint. At PND 18, elevated CRH mRNA was not observed until 4 h after stimulus. Following restraint, c-fos mRNA was increased at all three ages, although the magnitude of c-fos response was less during the SHRP. These results demonstrate that when restraint elicits prototypical ACTH release, the neonatal central response is to enhance the biosynthesis of both AVP and CRH. If nucleic acid changes correlate with release, the increased synthesis of both neuropeptides may indicate the potential for AVP to synergize with CRH during the neonatal stress response.

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          Regulation of the hypothalamic pituitary adrenal axis during chronic stress: responses to repeated intraperitoneal hypertonic saline injection.

          Chronic osmotic stress inhibits, while repeated physical stress can increase pituitary ACTH responsiveness to a novel stress. The interaction between these effects was studied in rats subjected to repeated i.p. injection of hypertonic saline, a strong aversive stimulus with osmotic and painful and psychological stress components, for 14 days. Hypertonic saline injection caused marked drinking responses, transient increases in plasma vasopressin (VP), and marked increases in VP mRNA and irVP in magnocellular cell bodies in the hypothalamus. Parvicellular activity was also enhanced as indicated by increases in VP immunostaining in the external zone of the median eminence and CRH mRNA and irCRH in the PVN. Plasma ACTH levels increased 10-fold after 30 min hypertonic saline injection, returning to basal levels in 4 h, and there was no desensitization of the ACTH responses after repeated injections (from basal values of 76 +/- 10 to 782 +/- 57, 788 +/- 83 and 779 +/- 31 pg/ml 30 min after the first, 4th and 14th injection, respectively). Basal ACTH levels were normal 24 h after the last injection, but pituitary POMC mRNA levels were increased by 95%, and ACTH responses to a novel stress (15 min immobilization) were significantly larger than in controls (P < 0.01) despite increases in morning plasma corticosterone levels (1.5 +/- 0.4 and 9.2 +/- 3.1 micrograms/dl in controls and stressed rats, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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            Stressor-specific increase of vasopressin mRNA in paraventricular hypophysiotrophic neurons

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              Effects of a specific glucocorticoid receptor antagonist on corticotropin releasing hormone gene expression in the paraventricular nucleus of the neonatal rat


                Author and article information

                S. Karger AG
                June 2000
                23 June 2000
                : 71
                : 6
                : 333-342
                aDepartment of Biological Sciences, University of Delaware, Newark, Del., and bExperimental Station, DuPont Pharmaceutical Company, Wilmington, Del., USA
                54554 Neuroendocrinology 2000;71:333–342
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 7, References: 30, Pages: 10
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