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PubMed1983

Inhibition of ovarian aromatase by prolactin in vivo.

Ovarian aromatase activity was inhibited by prolactin treatment in both cycling rats and immature gonadotropin-primed animals. Cycling rats were injected s.c. with prolactin (4 mg/kg BW) beginning on diestrus 1. Aromatase activity in the largest follicles on diestrus 2 and on proestrus was reduced relative to controls. None of the prolactin-treated animals had ovulated when examined on the expected estrus morning. In other experiments, the immature pregnant mare's serum gonadotropin (PMSG)-primed rat was used as a model for the cycling rat. Microsomal aromatase activity but not the activity of the C17-21 lyase was reduced in ovaries of animals injected with prolactin [6 IU (200 micrograms)/rat] 48 h after PMSG administration and sacrificed 4 h later. Furthermore, aromatase activity was significantly increased when endogenous prolactin was inhibited by bromocryptine (CB-154). The effect of LH treatment, on the other hand, was to increase both aromatase and lyase activities. However, prolactin pretreatment did not consistently prevent the LH-induced increase in aromatase activity. The results suggest that inhibition of ovulation by prolactin is mediated, at least in part, by direct inhibition of aromatase activity.

Animals↗
PubMed1983

Regulation of prolactin secretion in the pregnant pig: effect of fetal hypophysectomy and fetal death in small litters.

Fetal effects on prolactin secretion in late pregnancy and at term were studied in gilts with small litters of intact, hypophysectomized, partially hypophysectomized or dead fetuses. Litter size was reduced at surgery at Days 30-40 of gestation and fetal hypophysectomy or sham procedure attempted on Days 90-95 of gestation using an electrocoagulating probe. Plasma prolactin concentrations rose markedly before parturition in three gilts with normal litters (P = 0.05) and to lower peak concentrations in two gilts with a single fetus. Plasma prolactin did not change from basal concentrations in 4 gilts with small litters (1-2 fetuses) of hypophysectomized fetuses or, in 2 gilts with dead fetuses. Basal plasma prolactin concentrations were significantly lower in gilts carrying hypophysectomized or dead fetuses, compared to normal gilts (P = 0.01). A surge of prolactin secretion preceded delivery in 2 gilts with fetuses with incomplete hypophysectomy and in 1 gilt with 1 of 3 hypophysectomized fetuses. Abnormal patterns of prolactin secretion were seen in 1 gilt with 3 of 5 hypophysectomized fetuses and in 1 gilt with 1 partially hypophysectomized fetus. The results suggest that the fetus may be associated with a mechanism regulating plasma prolactin concentration at term. It is possible that this association may be by way of the fetal pituitary endocrine axes, and/or a function of conceptual mass.

Animals↗
PubMed1984

Evidence for an inhibitory influence of rat placental lactogen on prolactin release in vitro.

Incubation of placental tissue from Day 11 pregnant rats for increasing periods of time resulted in proportionately more rat placental lactogen (rPL) release. The amount of placental tissue incubated correlated directly with the amount of rPL released into the medium. When placentas were coincubated with anterior pituitaries from ovariectomized rats, prolactin release was significantly inhibited. When media from incubations which had contained varying numbers of Day 11 placentas for 24 h were added to vials containing anterior pituitaries, prolactin release was inhibited, proportionate to the amount of rPL in the media. Media from incubations of Day 9 placentas, which contained very little rPL, had no effect on prolactin release. When medium containing anterior pituitary tissue was incubated for 24 h, pituitaries removed, and the medium incubated with placental tissue for an additional 24 h, there was no difference in prolactin levels compared to incubation medium not containing placental tissue. Addition of a trypsin inhibitor to the medium containing placental tissue did not augment the amount of prolactin remaining after a 24-h incubation. Thus it would appear that the placenta does not release a substance into the medium that destroys prolactin. This suggests that secretions from the placenta, presumably rPL, can exert a negative feedback on prolactin secretion at the level of the anterior pituitary.

Animals↗
PubMed1986

Prolactin modulates steroidogenesis by rat granulosa cells: I. Effects on progesterone.

Either testosterone or follicle-stimulating hormone (FSH) stimulates progesterone secretion by granulosa cells from rats but the combination of the two hormones increases progesterone production in a synergistic manner. We have investigated the effects of graded doses of prolactin (0, 0.02, 0.2, 2, or 10 micrograms/ml) alone or in combination with testosterone (0.5 microM), FSH (300 ng/ml), or FSH + testosterone on progesterone secretion by granulosa cells at two stages of differentiation. Relatively undifferentiated granulosa cells from immature, diethylstilbestrol-treated, hypophysectomized (HPX) rats were cultured in defined (serum-free) medium for 3 days. More highly differentiated granulosa cells were obtained on the morning of proestrus from the preovulatory follicles of 30-day-old rats induced to undergo an estrous cycle by injection with 4 IU pregnant mare's serum gonadotropin; these cells were cultured in medium containing 10% fetal bovine serum. Prolactin alone did not enhance the negligible secretion of progesterone by cells from HPX rats, but increased progesterone secretion by cells from proestrous rats. Prolactin significantly enhanced the stimulatory effects of testosterone or FSH alone on cells from both HPX and proestrous rats. When cultures containing both FSH + testosterone were treated with prolactin, progesterone secretion by cells from proestrous rats was significantly enhanced, whereas secretion by cells from HPX rats was significantly depressed. Therefore when cells from HPX rats were cultured with both FSH and testosterone, the direction of the effect of prolactin was reversed from that observed with prolactin + FSH or testosterone alone, and from that observed when cells from proestrous rats were cultured with prolactin + FSH + testosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Antagonism of estrogen-induced prolactin release by dihydrotestosterone.

Previous work from our laboratory has demonstrated that progesterone can inhibit estrogen-induced prolactin release in female rats. Since androgens have been reported to mimic progesterone actions in certain systems, and to antagonize estrogen action in rat uteri, the purpose of this study was to determine whether androgens, like progestins, can inhibit estrogen-induced prolactin release. The ovariectomized (26 days of age) immature rat was used as the model for analysis of this question. Dihydrotestosterone (DHT) was chosen to be used throughout the study since it does not undergo aromatization to estrogens. In response to estradiol exposure (2 micrograms/rat), prolactin release reached peak values at 12 h and returned to control levels by 24 h. A second injection of estradiol 13 h after its initial injection stimulated a second increase in serum prolactin at 25 h. A single injection of DHT (0.8 mg/kg BW) 1 h before the second estradiol injection blocked the increase in serum prolactin. DHT had no effect on basal serum prolactin levels. The DHT inhibition of estrogen-induced prolactin release required estrogen priming. A dose dependency for the DHT effect was demonstrated, with low doses effective and high doses ineffective, in inhibiting estrogen action. This effect of DHT seemed to be androgen receptor-mediated, since flutamide blocked the effect. However, the possibility of progestin receptor mediation could not be ruled out since RU486 also blocked DHT's effect. Flutamide was also effective in blocking progesterone's inhibition of estrogen-induced action. This is perhaps consistent with an overlap of activities in androgens and progestins reported by several investigators.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Prolactin-induced regression of the rat corpus luteum: expression of monocyte chemoattractant protein-1 and invasion of macrophages.

Monocyte chemoattractant protein-1 (MCP-1) is a potential mediator of the recruitment of monocytes/macrophages into the regressing corpus luteum (CL). We investigated whether the luteolytic effect of prolactin in the rat is associated with the expression of MCP-1 and an invasion of monocytes/macrophages. Ovulation was induced in immature female rats by injection of eCG (5 IU, s.c.) at 30 days of age. All rats were hypophysectomized 3 days later. Rats received injections of ovine prolactin (250 micrograms, s.c.) at 12-h intervals on Day 9, 10, and 11 posthypophysectomy; controls received injection of vehicle. Rats were killed by decapitation 24, 48, or 72 h after the first injection of prolactin or vehicle. In rats treated with prolactin, immunoreactive MCP-1 was detected in the CL at 24 h after the first injection, and a consistent level of staining was reached by 72 h with immunodetectable MCP-1 diffused throughout individual CL. The number of monocytes/macrophages in the CL (mean +/- SEM) increased significantly after prolactin treatment, from 3.1 +/- 1.8 at 24 h to 49.3 +/- 8.2 at 72 h (p < 0.05), and the number of monocytes/macrophages was different from that in control, vehicle-treated rats at 72 h (10.3 +/- 4.1; p < 24 and 72 h in prolactin-treated rats (p < 0.05). It is concluded that a potentially important component of the luteolytic effect of prolactin in the rat is the expression of MCP-1 and invasion of monocytes/macrophages into the CL.

20-alpha-Dihydroprogesterone↗
PubMed1990

Polymers of prolactin and their clinical significance.

Elevated levels of prolactin are known to cause a range of disturbances of ovarian function. However, in a small number of women, sustained hyperprolactinemia has been found by chance in association with apparently normal ovarian function and normal fertility. In these women the dominant form of circulating prolactin has been found by gel chromatography to be a polymeric form of large molecular size, 'big-big' prolactin (BBPRL), with similar immunoreactivity to monomeric prolactin (PRL) but much lower biological activity. In a few cases an intermediate polymeric form, 'big' prolactin (BPRL), has also been described. The exact nature and biological significance of polymeric forms of prolactin remain unclear. It has been shown that concentrations of BBPRL in the circulation in individual women change more slowly and less profoundly than concentrations of PRL in various physiological and pharmacological situations. Minor changes occur during the menstrual cycle, while increases of PRL and BBPRL occur progressively during pregnancy. In pregnancy PRL rises much more than BBPRL. Acute stimulation with metoclopramide, TRH, or suckling favors the production of PRL, although BBPRL also rises to a small extent. During treatment with bromocriptine the proportion of PRL in the circulation is markedly reduced, while BBPRL falls to a much lesser extent. Further study is required before it can be proved that BBPRL and BPRL have no biological significance. There is much controversy regarding the structure and mechanism of production of polymeric forms of prolactin. There is no evidence of a circulating factor in serum which binds several molecules to form BBPRL.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1989

Cell-specific expression of the prolactin gene in transgenic mice is controlled by synergistic interactions between promoter and enhancer elements.

Prolactin gene expression is restricted to the lactotrophic and somatomammotrophic cells of the anterior pituitary. In transgenic mice, a fusion gene consisting of 3 kb of prolactin 5'-flanking region fused to a firefly luciferase or human growth hormone (hGH) reporter gene is expressed at high levels with the strict tissue and cell-type specificity that is characteristic of the endogenous prolactin gene. High levels of expression require two cis-acting regions: a distal enhancer (-1.8 to -1.5 kb) and a proximal region (-422 to +33 bp). Each of these regions alone can direct low levels of fusion gene expression to prolactin-producing cell types in transgenic mice, but a synergistic interaction between these regions is necessary for high levels of expression. The ontogeny of the prolactin transgene expression closely follows the appearance of high levels of a POU homeo-domain transcription factor, Pit-1, that has been shown previously to bind structurally related sequences in both the distal enhancer and proximal regions and to activate the expression of the prolactin gene in vitro. Unexpectedly, transgenes containing the distal enhancer removed from its normal context are expressed in both the prolactin-producing lactotrophs and the thyroid-stimulating hormone (TSH)-producing thyrotrophs, thereby suggesting that sequences flanking this enhancer are necessary to restrict expression to the correct cell type within the pituitary. These data indicate that distinct processes of gene activation and restriction are necessary for the fidelity of cell-type-specific expression within an organ.

Animals↗
PubMed1977

Alterations in serum prolactin heterogeneity by provocative tests in a patient with a pituitary tumour.

The proportion of serum prolactin heterogeneity were investigated in a patient with a pituitary adenoma producing both prolactin and growth hormone. Glucose tolerance (GTT) and insulin tolerance (ITT) tests were performed alone and in combination with chlorpromazine both before and after hypophysectomy. Serum prolactin multiple forms were separated by Sephadex G-100 column chromatography at 3 degrees C. None of the provocative tests altered the already elevated serum prolactin either before (300 ng/ml) or after (100 ng/ml)hypophysectomy. Chlorpromazine or ITT did not alter the proportion of prolactin heterogeneity; GTT, whether in conjunction with chlorpromazine or alone and both before and after hypophysectomy, increased the proportions of the larger molecular species. In five tests in which the GTT was not performed the prolactin heterogeneity was as follows: 'void volume', 4.9%; 'big', 13.1%; 'little', 82.1%; in those experiments in which the GTT was performed the proportions of prolactin heterogeneity were: 'void volume', 13.5%, 'big', 19.2%; 'little', 67.3%.

Adenoma, Acidophil↗
PubMed1982

Size heterogeneity of immunoreactive prolactin in hyperprolactinaemic serum.

Thirty-five samples of serum with levels of immunoreactive prolactin greater than 500 mu/l have been fractionated by gel filtration. In samples from seven normal subjects with elevated prolactin levels following TRH or insulin stimulation and samples from twelve patients with prolactin levels greater than 1500 mu/l, over 8% of the immunoreactive material eluted in the position of native or 'little' prolactin. In eleven out of sixteen samples containing 500 to 1500 mu/l the proportion of 'little' prolactin was less than 80% and more than 20% eluted as 'big-big' prolactin. It appears therefore that patients with moderately elevated levels of immunoreactive prolactin may not have genuine hyperprolactinaemia.

Chemical Phenomena↗
PubMed1984

The effect of endogenous and exogenous gonadotrophin-releasing hormone on the prolactin response to TRH.

The prolactin response to TRH in a group of patients with Kallmann's syndrome was found to be significantly lower compared to a group of hypergonadotrophic hypogonadal patients. Since levels of testicular products are comparably low in both groups, we hypothesize that high endogenous LHRH production might be associated with an increased prolactin response to TRH. In support of this, we were, indeed, able to establish a positive correlation between the magnitude of the prolactin response to TRH and basal and LHRH-stimulated LH/FSH levels (the latter serving as an index of endogenous LHRH production) in: (1) eugonadal men, (2) men with Kallmann's syndrome, (3) oestrogen-treated agonadal men, (4) men with severely impaired spermatogenesis and, (5) agonadal men. A direct relation between LHRH and the prolactin response to TRH was demonstrated in a group of eugonadal men, the prolactin response to TRH being greater after prolonged LHRH pretreatment. We speculate that an increase of endogenous or exogenous LHRH might be associated with decreased hypothalamic dopamine secretion which could directly increase prolactin synthesis. Indirectly, decreased dopamine secretion could augment the potency of TRH in releasing prolactin.

Adult↗
PubMed1990

Impaired prolactin secretion and body fat distribution in obesity.

Human obesity shows clustering within families. The hypothesis for the presence of a major gene or genes acting in human obesity is supported by recent evidence from studies of obesity in adoptees and their biological parents and siblings. The heterogeneity of obesity may be demonstrated by the shape of fat distribution and the prolactin response to insulin hypoglycaemia. Fat distribution has been shown to have a genetic background whereas a primary disorder of hypothalamic function is suspected in obese women who show an impaired prolactin response to insulin-induced hypoglycaemia. We have investigated the possible association between fat distribution and hypothalamic function in 23 extremely obese, nondiabetic premenopausal women who have been characterized using their absolute body weight, body mass index (BMI), fat distribution (expressed as waist to hip ratio), fasting insulin, basal prolactin and prolactin response to hypoglycaemia. Fasting insulin values showed a significant correlation (P less than 0.05, R = 0.604) with increasing waist to hip ratio (upper body segment obesity), whereas the graded prolactin response to hypoglycaemia of the obese women showed a negative association with increasing upper body segment obesity (P less than 0.05; R = -0.446). No relationship was observed between fasting insulin and the prolactin response to hypoglycaemia. We suggest that this previously unrecognized association of an impaired prolactin response to hypoglycaemia and upper body segment fatness may be useful for the investigation of the genetics of obesity.

Adipose Tissue↗
PubMed1982

The value of plasma prolactin levels in the prediction of the responsiveness of growth hormone secretion to bromocriptine and TRH in acromegaly.

UNLABELLED: The mechanism of the inhibition of growth hormone secretion in response to bromocriptine and the ability of thyrotropin releasing hormone to stimulate growth secretion in acromegaly is unknown. In the present study the relationship between the plasma prolactin concentration of untreated acromegalic patients and the reaction of growth hormone to thyrotropin releasing hormone and bromocriptine was investigated. Plasma prolactin levels were elevated in thirty-three (42%) of seventy-nine untreated acromegalic patients. Seventeen patients had mildly elevated prolactin levels, but in sixteen the plasma prolactin concentration was higher than 30 ng/ml. Bromocriptine (2.5 mg) inhibited growth hormone secretion by more than 50% in 22% of the normoprolactinaemic, in 53% of the mild hyperprolactinaemic and in 88% of the patients with a prolactin level above 30 ng/ml (P less than 0.01 v. normoprolactinaemic; P less than 0.01 v. mildly elevated prolactin levels). An increase of growth hormone secretion by more than 100% of the basal value in response to thyrotropin releasing hormone was observed in 44% of the normoprolactinaemic, in 59% of the mildly hyperprolactinaemic and in 75% of the clearly hyperprolactinaemic patients; (P less than 0.01 v. normo- and mildly hyperprolactinaemic patients). CONCLUSION: An increased plasma prolactin concentration in patients with acromegaly is accompanied in most patients by a higher sensitivity of growth hormone secretion to bromocriptine.

Acromegaly↗
PubMed1994

Prolactin receptor mRNA localization in the hypothalamus by in situ hybridization.

Prolactin receptors may mediate the action of prolactin in the brain to influence behavior and neuroendocrine secretions. We recently demonstrated prolactin receptor gene expression in the anterior and medial basal hypothalamus and not in the cortex by the reverse transcription-polymerase chain reaction. In this paper, we localize the prolactin receptor gene expression to individual cells with in situ hybridization. Several steps in the in situ hybridization method were modified to increase sensitivity by using (i) probes complementary to the coding sequence of the extracellular binding domain common to both long and short prolactin receptor, (ii) more stringent hybridization and wash conditions to reduce background and (iii) higher specific activity, more complex and saturating amounts of probe. We detected prolactin receptor gene expression in cells of the periventricular area of the preoptic nucleus, medial preoptic nucleus, supraoptic nucleus, rostral arcuate nucleus and choroid plexus. Cortical brain tissue, which has been demonstrated previously by reverse-transcription polymerase chain reaction to be lacking in prolactin receptor mRNA, did not have any detectable signal for the receptor mRNA and was used as an indication of background levels of signal. The mean area of silver grains over labeled cells in periventricular area of the preoptic nucleus, medial preoptic nucleus, supraoptic nucleus, arcuate nucleus, lateral ventromedial nucleus was at least 10 times greater than the background in the cortex of the same brain section.

Animals↗
PubMed1992

Serum prolactin concentration in normal and small for gestational age fetuses.

OBJECTIVES: To study fetal and maternal serum prolactin concentrations in appropriately-grown (AGA) fetuses and in small for gestational age (SGA) fetuses. DESIGN: A cross-sectional study of 27 AGA and 27 SGA fetuses undergoing cordocentesis for prenatal diagnosis or for determination of fetal karyotype and acid-base balance. Serum prolactin concentration was measured by radioimmunoassay. SETTING: Harris Birthright Research Centre for Fetal Medicine. RESULTS: In the AGA group, both fetal and maternal serum prolactin concentration increased significantly with gestation (P < 0.001 and P < 0.01, respectively). In the SGA group, the fetal concentration of prolactin was significantly higher (P < 0.05), but the maternal serum prolactin concentration was not different from that of the AGA group. CONCLUSIONS: The finding of prolactin in the fetal circulation suggests that the anterior lobe of the pituitary is functioning from at least 12 weeks gestation. The increased serum prolactin concentration in SGA fetuses may be the consequence of hypoglycemic stress on the pituitary or the relative immaturity of the inhibitory hypothalamic-pituitary pathways.

Cross-Sectional Studies↗
PubMed1995

D-fenfluramine-induced prolactin responses in postwithdrawal alcoholics and controls.

Serum prolactin response to the serotonin agonist D-fenfluramine were measured in 19 DSM-111-R male alcoholics, 2.5 or more weeks postalcohol withdrawal. Prolactin responses were compared with nine healthy nonalcoholic male controls. After an overnight fast, each subject received 30 mg of D-fenfluramine orally, and serial samples of serum prolactin were taken over a 4-hr period. D-fenfluramine caused a significantly attenuated peak delta-prolactin response in the alcoholics relative to the controls (p = 0.05). A repeated-measures ANOVA of delta-prolactin yielded a significant within-subjects effect of time (p < 0.05), a within-subjects effect of group that reached significance (p = 0.05), and a nonsignificant group by time interaction. The delta-prolactin value at time points 60 and 240 min postadministration of the probe was significantly attenuated in the alcoholic group, with p < 0.05. There was also some evidence for a diminished serotonergic response in those alcoholics with a negative family history. The delta-prolactin response did not correlate with subjects' age, duration of alcohol use, duration of abstinence from alcohol, severity of alcohol dependence, or age of onset. Results imply a relative subsensitivity of the serotonin system in postwithdrawal alcoholics, and this may be primarily of the 5-HT2 receptor.

Adult↗
PubMed1977

Inhibition of prolactin secretion and synthesis by dopamine, noradrenaline and pilocarpine in cultured rat pituitary tumour cells.

Clonal strains of rat pituitary tumour cells (GH3-cells) synthesize and secrete prolactin into a chemically defined culture medium. Short time treatment (0.5-2 hrs) of cell cultures with noradrenaline (10(-3) M) and dopamine (10(-3 M) reduced the spontaneous secretion of prolactin by 50% and 30%, respectively, while pilocarpine (10(-3) M) had no effect. Long-term treatment (20 hrs) with noradrenaline (10(-3)M) or with pilocarpine (10(-3) M) inhibited prolactin synthesis by 45% and 65% of control cultures, respectively. Neither compounds affected cell growth. The inhibitory effect of noradrenaline, but not that of pilocarpine, was completely reversed 4 hrs after cessation of treatment. Adrenaline, dopamine and acetylcholine in concentrations up to 10(-3) M did not change prolactin synthesis. In contrast thyroliberin treatment (2 X 10(-8)M) caused a 45% increase in prolactin secretion, and resulted in a 40% increase in hormone synthesis after treatment for 20 hrs. It is concluded that both noradrenaline and dopamine are able to inhibit prolactin section. Prolactin synthesis could be inhibited by noradrenaline and pilocarpine. How, only the effect of noradrenaline is easily reversible on cessation of treatment.

Animals↗
PubMed1986

A central serotonin receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin, has different effects on prolactin secretion in male and female rats.

Male and female rats were compared with respect to alterations in prolactin secretion induced by the serotonin receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). The dose-response curves after 8-OH-DPAT were irregular and had different shapes in the two sexes. In males, 0.1 and 0.3 mg/kg enhanced serum prolactin concentrations to about 200% of control values, whereas higher doses (1 and 3 mg/kg) had no effect on prolactin release. In females, in contrast, 0.1 mg/kg of 8-OH-DPAT tended to decrease serum levels of prolactin, while 0.3, 1, and 3 mg/kg elevated them in a dose dependent manner to maximally 700% of control values. The serotonergic agonist 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) (5 mg/kg), too, caused increased prolactin release in both sexes, and, again, females responded more forcefully. In males, but not in females, pretreatment with 8-OH-DPAT (1 mg/kg) reduced the 5-MeODMT-induced elevation of serum prolactin levels. The mechanism underlying the sexually differentiated effects of 8-OH-DPAT on prolactin secretion is discussed.

8-Hydroxy-2-(di-n-propylamino)tetralin↗