摘要:

Effects of microinjection of neurotensin (NT) into the medial preoptic area on luteinizing hormone (LH) release were examined in unanesthetized ovariectomized rats with or without estrogen priming. Microinjection of NT (100 ng) into the medial preoptic area of ovariectomized estrogen-primed rats significantly facilitated the circadian afternoon rise of LH secretion as compared to the hormone values in control animals microinjected with physiological saline. The timing of the afternoon LH rise was not altered by the peptide. In ovariectomized estrogen-unprimed rats, on the other hand, NT did not affect the existing pulsatile LH secretion nor induced an afternoon rise of the hormone secretion. These results show that NT can stimulate the preoptic LH release mechanism which undergoes the circadian clock under the influence of estrogen.

ISSN:0028-3835    

DOI:10.1159/000124843

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

To assess whether gonadotropin-releasing hormone (GnRH) release from the hypothalamus might be altered by hyperprolactinemia in the male rat, we measured in chronically hyperprolactinemic rats the pituitary GnRH receptor content and described the pattern of luteinizing hormone (LH) release during the postcastration rise in gonadotropin secretion 24 and 72 h after gonadectomy. In intact rats, the effect of hyperprolactinemia was determined by describing the pattern of LH secretion, pituitary GnRH receptor content and assessment of pituitary responsiveness to small doses of GnRH (1.0 ng). In addition, to determine the role endogenous opioids might play in inhibiting GnRH release in hyperprolactinemic rats, we examined the effect of both a continuous infusion and a bolus injection of the opioid antagonist naloxone on the pattern of LH release. Chronic hyperprolactinemia was achieved by implanting 4 pituitaries under the kidney capsules 3–4 weeks before study. Acute hyperprolactinemia was achieved by injecting rats with 1 mg ovine prolactin every 12 h for 3 days. Control animals were untreated or were chronically hyperprolactinemic rats in which the hyperprolactinemia was transiently reversed by treatment for 3 days with the dopamine agonist 2-α-bromoergocryptine. The mean LH concentration was greatly decreased at 24 postcastration in chronically hyperprolactinemic rats relative to controls. This decrease was associated with a decrease in LH pulse height and pulse amplitude and pituitary GnRH receptor content, but not with an increase in the LH interpulse interval. In contrast, the decrease in mean LH concentrations in hyperprolactinemic animals at 72 h postcastration was primarily associated with a significantly longer LH interpulse interval than that observed in control animals. Chronic hyperprolactinemia in intact rats decreased the pituitary GnRH receptor content, in addition to decreasing the mean LH concentrations during pulsatile GnRH administration. Chronic hyperprolactinemia also inhibited LH release relative to controls during the continuous 4-hour infusion of naloxone and in response to a bolus injection of naloxone. However, in acutely hyperprolactinemic intact male rats a bolus injection of naloxone increased LH secretion 20 min later to levels similar to those obtained in control rats. In summary, these results indicate that chronic hyperprolactinemia decreased LH secretion by primarily decreasing GnRH secretion as suggested by a decrease in pituitary GnRH receptor content and a decrease in LH pulse frequency and pulse amplitude. It is also possible that a decrease in pituitary responsiveness to GnRH may have contributed to the decrease in LH pulse amplitude. The effects of chronic hyperprolactinemia do not appear to be mediated by an opioid whose actions are antagonized by naloxo

ISSN:0028-3835    

DOI:10.1159/000124844

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Bradykinin (BK), a nonapeptide, originally discovered in blood, is also present in neurons and fibers of the hypothalamus. We tested the putative releasing factor properties of BK on prolactin (PRL) release from anterior pituitary cells in vitro. BK stimulated the release of PRL in a dose-dependent manner, the threshold concentration being in the range. 0.1–1.0 nM. The release of PRL induced by BKat 1 nM concentration was about 2-fold, delayed and sustained over many minutes. Higher concentrations of BK stimulated PRL release in two phases. The shape of the BK-induced PRL release was superficially similar to that induced by thyrotropin-releasing hormone (TRH). 10 nM BK and 10 nM TRH induced about a 4-fold increase in PRL release within 5 min, followed by a gradual recovery to basal secretion. These results indicate that this peptide can act directly at the anterior pituitary gland to release PRL. Phorbol ester also promoted PRL release over the range of 1–10 nM, but the time course of the release was somewhat differ

ISSN:0028-3835    

DOI:10.1159/000124845

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The effect of glucocorticoids on corticotropin-releasing factor (CRF) gene expression was studied by combination of in situ hybridization histochemistry and steroid implantation. Dexamethasone micropellets, implanted around the hypothalamic paraventricular nucleus (PVN), caused total inhibition of the hybridizable CRF mRNA signal above the parvocellular neurons of the PVN. Unilateral implantation of dexamethasone around the PVN resulted in a decrease of hybridizable CRF mRNA at the dexamethasone-implanted side. Dexamethasone implants into the cerebral cortex, dorsal hippocampus, ventral subiculum, lateral septum or amygdala were without any effect on the CRF expression in the PVN. Corticosterone did not result in any significant change in CRF mRNA, when implanted into the paraventricular region, dorsal hippocampus or ventral subiculum. When it was placed into the amygdala however, in a few cases it slightly inhibited the CRF mRNA levels in the ipsilateral PVN.

ISSN:0028-3835    

DOI:10.1159/000124846

出版商:S. Karger AG    

年代:1987

数据来源: Karger