Endocrine
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Randomized Controlled Trial Clinical Trial
Gonadal steroid modulation of the limbic-hypothalamic- pituitary-adrenal (LHPA) axis is influenced by social status in female rhesus monkeys.
Chronic stress can have a deleterious effect on the re-productive axis that, for females, is manifested in an increased incidence of infertility. However, gonadal steroids may, in turn, affect a female's response to stress as measured by activity within the limbic-hypothalamic-pituitary-adrenal (LHPA) axis. What is not clear is whether a history of exposure to stress modifies the effect of gonadal steroids on LHPA responsivity. ⋯ The response to a combined DEX suppression-CRF stimulation test was assessed using a counterbalanced design during a placebo (control) treatment condition and during E2, P4, and E2 + P4 re-placement therapy. Females who were members of a large breeding group of 140 adults and juveniles of both sexes, were classified as dominant (n = 4) or subordinate (n = 3) based on the relative social dominance positions within the group. Plasma levels of cortisol were significantly higher during E2 replacement compared to the other treatment conditions following DEX suppression and stimulation with CRF.
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We have found that exogenous prolactin (PRL) stimulates all three populations of hypothalamic neuroendocrine dopaminergic neurons. In this study, we investigated the effects of immunoneutralization of endogenous PRL on the activity of these neurons. Injection of 17beta-estradiol (E2) (20 microg subcutaneously) 10 d after ovariectomy induced a proestrus-like increase in PRL in peripheral plasma the following afternoon. ⋯ However, administration of PRL-AS minimally suppressed the turnover of DA in the neural lobe. Moreover, administration of PRL-AS attenuated the rise of DA in the anterior lobe associated with the waning phase of the E2-induced PRL surge. These results clearly indicate that endogenous PRL regulates its own secretion by activating hypothalamic neuroendocrine dopaminergic neurons.
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Comparative Study
CRH and AVP-induced changes in synthesis and release of ACTH from the ovine fetal pituitary in vitro: negative influences of cortisol.
During late gestation in sheep, fetal plasma adreno-corticotrophin (ACTH) and cortisol levels increase, and these are associated with increased pro-opiomelanocortin (POMC) mRNA levels in the anterior pituitary. Corticotrophin-releasing hormone (CRH) and vasopressin (AVP) are the primary hypophysiotrophic factors regulating ACTH secretion from the fetal sheep pituitary corticotroph, but previous reports with term fetal tissue have failed to show effects on levels of POMC mRNA. The objectives of the present study were to establish the effects of CRH and AVP on both synthesis and secretion of ACTH before term, and to determine how cortisol affects these responses. ⋯ Cortisol attenuated (p < 0.05) the neuropeptide-induced increases in POMC mRNA, though AVP-stimulated POMC mRNA levels were significantly higher than in cells treated with cortisol alone. Cortisol failed to alter non-stimulated POMC mRNA levels. We conclude that in late gestation: 1) Fetal pituitary corticotrophs respond to CRH and AVP by increasing POMC mRNA levels and ACTH secretion 2) AVP is more potent than CRH at the level of ACTH secretion, but not POMC transcription 3) Cortisol attenuates the synthetic and secretory responses to CRH and AVP, but has little effect in the non-stimulated state.