Prolactin

About: Prolactin is a research topic. Over the lifetime, 22356 publications have been published within this topic receiving 609537 citations. The topic is also known as: lactotropin, & PRL,.

Leptin directly acts within the hypothalamus to stimulate gonadotropin-releasing hormone secretion in vivo in rats.

Abstract: It is still not known whether leptin, an adipocyte-derived hormone, acts directly within the hypothalamus to stimulate the gonadotropin-releasing hormone (GnRH)-luteinizing hormone (LH) system. In order to address this question, the present study examined the effects of direct intrahypothalamic perfusions with leptin on the in vivo release of GnRH in ovarian steroid-primed ovariectomized rats utilizing the push-pull perfusion technique. Both α-melanocyte-stimulating hormone (α-MSH) and neuropeptide Y were also measured in the hypothalamic perfusates. In normally fed animals, the leptin infusion was without effect on the release of these three hypothalamic peptides and also without effect on plasma LH and prolactin (PRL), whether leptin was infused into the medial preoptic area (where the majority of GnRH neuronal cell bodies exist) or the median eminence-arcuate nucleus complex (where axon terminals of GnRH neurons are located). In contrast, in 3-day fasted rats leptin was effective in stimulating the secretion of GnRH, α-MSH, and LH, regardless of the site of perfusion. These three hormones were increased in a temporal order of α-MSH, GnRH and LH. Irrespective of the site of perfusion, leptin was without effect on the release of neuropeptide Y. Only when leptin was infused into the median eminence-arcuate nucleus complex was PRL secretion also stimulated, although its onset was 1 h behind that of LH. The leptin-induced elevations of GnRH, α-MSH, LH and PRL were all dose-dependently stimulated by subnormal (1.0 ng ml−1) and normal (3.0 ng ml−1) concentrations of leptin, but at higher concentrations (10 ng ml−1) it did not produce additional effects. Leptin infusion into the anterior hypothalamic area, a control site equidistant from both the medial preoptic area and the median eminence-arcuate nucleus complex, did not produce a significant change in any of the hormones in either the fed or fasted rats. These results demonstrate for the first time that leptin can act at both the cell bodies and axon terminals of GnRH neurons to stimulate the release of the neurohormone in vivo, and they also suggest that α-MSH may play a significant intermediary role in linking leptin and GnRH secretion.

Prolactin of apparent large molecular size: the major immunoactive prolactin component in plasma of a patient with a pituitary tumor.

Abstract: Multiple immunoactive components of circulating human prolactin were detected in each of six plasma samples analyzed by assay of fractions from Sephadex G–100 chromatography. Prolactin of apparent large molecular size (Kav ≃ 0.2) was the major (70%) circulating immunoactive prolactin in a patient with a pituitary tumor and acromegaly. Much less (<10-20%) Kav 0.2 prolactin was detected in the other 5 plasma samples, drawn from volunteers before and after administration of synthetic TRF, during pregnancy and postpartum lactation, and from a patient with a chromophobe adenoma and galactorrhea. In these 5 plasmas, the major (80–90%) immunoactive prolactin component (Kav ≃ 0.4) was not distinguishable chromatographically from monomeric pituitary prolactin.

Localization of prolactin binding in prostate and testis: the role of serum prolactin concentration on the testicular lh receptor

Abstract: Specific binding sites for prolactin (PRL) and gonadotrophins on ventral and dorsolateral prostate as well as on Leydig cells and tubules of testes of rats at different ages were examined. The binding sites for PRL were found in greatest number in ventral prostate and in Leydig cells. LH binding sites were also more numerous than FSH binding sites in the latter. FSH sites were greater than LH sites in tubular preparations obtained from the testis. Specific binding (SB) of PRL in the Leydig cells reached a maximum at 45 days (4%) and in the case of LH a maximum of 12% was obtained at 70 days. In both preparations SB of FSH exhibited a plateau between 20 and 40 days (11%) followed by a gradual decline to 6% at 100 days. Following 20 dyas of treatment with Bromocriptin beginning at 20 days serum PRL was suppressed and SB of LH to the Leydig cells was significantly decreased, whereas SB of PRL and FSH was unaffected. These studies suggest that despite decreases in serum PRL, the number of PRL and FSH receptors remain unaltered. On the contrary, LH receptors in the rat testis are modulated by changes in serum PRL.