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PubMed1977

Mechanism of increased prolactin secretion by sulpiride.

The effect of sulpiride, a neuroleptic agent, on the secretion of prolactin by the anterior pituitary gland of the rat was studied. A significant increase in serum prolactin was observed after subcutaneous administration of the drug. Although sulpiride (0-10 micronmol/1 or 0-14 mmol/1) had no effect on the secretion of newly synthesized or radioimmunoassayable prolactin in vitro, the drug significantly overcame the inhibitory action that dopamine (0-50 micronmol/1) exerted on prolactin secretion. Rats implanted with a prolactin-secreting pituitary tumour MtTW15 showed an inhibition of prolactin biosynthesis and release. Injection of these rats with sulpiride restored prolactin biosynthesis and release of the hormone toward normal levels. These results demonstrate that sulpiride has a direct effect on the pituitary antagonizing the inhibitory effects exerted by dopaminergic mechanisms, although the drug itself does not stimulate the secretion of prolactin in vitro. Sulpiride may have a direct action on the pituitary lactotrophs in vivo, but effects at higher centres have not been excluded.

Animals↗
PubMed1977

Prolactin and luteinizing hormone levels before and after parturition in rats bearing either single or multiple embryos.

Levels of prolactin and LH were determined in serum and pituitary during the last days of pregnancy and post partum in rats bearing single and multiple embryos. In rats with a single embryo serum prolactin and LH levels were significantly lower during the last 2 days of pregnancy and post partum than in rats bearing multiple embryos. While large increases were recorded in serum prolactin and LH levels in the rats with multiple embryos between days 21 and 22 of gestation, in the group with single embryos changes occurred in LH level only. Throughout the experiment pituitary prolactin was lower in rats with a single embryo than in those with multiple embryos in spite of the sharp drop in prolactin level in the group with multiple embryos from day 21 to 22. No differences were observed in the pituitary LH levels of either group during the days preceding parturition, but in the rats with multiple embryos there was a sharp drop in LH level post partum. It seems that the reduced serum prolactin level in the rats with a single embryo was associated with inhibition of pituitary prolactin synthesis and release, whereas the decreased serum LH level resulted from impaired release but not synthesis. These results support the hypothesis of a regulatory role for the placenta in pituitary prolactin and LH synthesis and release, either by hypothalamus-pituitary stimulation, or perhaps by way of the ovaries, through regulation of ovarian steroid production.

Animals↗
PubMed1977

Relationships among bioassay, radioimmunoassay and disc electrophoretic assay methods of measuring rat prolactin in pituitary tissue and incubation medium.

Relationships among bioassay, radioimmunoassay (RIA) and disc electrophoretic assay methods of estimating rat prolactin in pituitary tissue and incubation medium were determined. Highly significant correlations were obtained between disc electrophoretic and RIA estimates of prolactin in tissue and between bioassay and RIA estimates of prolactin in medium. Less significant relationships were obtained between disc electrophoresis and RIA (medium) and between bioassay and disc electrophoresis (tissue and medium). The relationship between bioassay and RIA of prolactin in the incubated tissue was not significant. Regression analysis disclosed the following: the RIA measured slightly more, and the bioassay detected substantially more prolactin in tissue and medium than did disc electrophoresis; the bioassay detected about five times more prolactin in medium than did the RIA. No significant relationships were found within or among the assays for depletion and release of prolactin. The results indicate that secreted prolactin has increased bioassay activity relative to its detectability by disc electrophoresis and RIA.

Animals↗
PubMed1977

Homologous radioimmunoassay for canine prolactin and its application in various physiological states.

The purification of canine prolactin and the development of an homologous radioimmunoassay including several physiological studies in the Beagle dog are described. The assay measured immunoreactive canine prolactin with a sensitivity limit of 0-6 ng/ml. Purified canine luteinizing hormone gave no significant inhibition in the assay whereas purified canine growth hormone inhibited the binding of 125I-labelled canine prolactin to antiserum only at very high dose levels. In Beagle dogs. basal serum prolactin concentrations were in the range 1-2 ng/ml in normal male, normal female (metoestrus and anoestrus) and oophorectomized-hysterectomized female dogs. The prolactin concentration in one sample of amniotic fluid was in the same range, while in hypophysectomized male dogs no serum prolactin could be detected by our assay system. Serum prolactin concentrations tended to increase during late pregnancy and parturition, remaining high during the first 9 days of lactation. In consequence, a negative correlation was suggested between serum prolactin and serum progesterone concentrations.

Animals↗
PubMed1979

Secretion rate and metabolic clearance rate of prolactin in the rat during mid- and late lactation.

The prolactin concentration in the plasma of lactating rats rose less rapidly and attained a significantly lower plateau level in response to suckling on day 20--21 of lactation than it did on day 13--14 of lactation. Neither differences in suckling stimulation of the older pups nor a higher metabolic clearance rate (MCR) of prolactin were implicated in the reduced prolactin concentration seen in the late-lactating rats. The MCR was, in fact, slightly reduced in both conscious and late-lactating rats anaesthetized with urethane when compared with those in mid-lactation. The MCR of prolactin was not significantly altered by urethane anaesthesia in rats on either day of lactation. However, the secretion rate of prolactin, computed from the MCR multiplied by the equilibrium concentration of prolactin during suckling, was considerably reduced (665 to 392 ng/min) from mid- to late lactation. We conclude from these data that the reduced plasma concentration of prolactin in response to suckling in late lactation is the result of an impairment within the prolactin secretory mechanism.

Anesthesia, General↗
PubMed1979

Annual rhythms of luteinizing hormone, follicle-stimulating hormone, prolactin and testosterone in the serum of male rhesus monkeys.

Six male rhesus monkeys were kept under rigidly controlled conditions for 1-2 years. During August of the first year a thyrotrophin releasing hormone (TRH) test was performed on each of the monkeys by giving 10 microgram TRH as a bolus injection. Significantly increased serum prolactin levels occurred 15 min after the injection. After a training period of 2 months, during which blood samples were collected every other day by puncture of the saphenous vein, blood was collected three times a week for 14 months. Serum levels of prolactin, LH, FSH and testosterone were measured by radioimmunoassay. Mean serum prolactin levels increased significantly during June, July and August in all six animals. Peak levels were observed in August and September and then levels declined gradually to reach a minimum in April and May. Mean serum testosterone levels closely paralleled the annual pattern of prolactin. Mean serum LH levels significantly decreased during the time when mean serum prolactin and testosterone levels were increasing and they increased again at the time of decreasing mean prolactin levels, i.e. mean serum LH and prolactin were negatively correlated. In individual monkeys, however, a rigid negative correlation between serum prolactin and LH could not be demonstrated. Mean serum FSH levels did not change significantly.

Animals↗
PubMed1981

Prolactin in maintenance of the corpus luteum of early pseudopregnancy in the golden hamster.

The role of prolactin in the maintenance of the corpus luteum of pseudopregnancy was studied in the golden hamster. Nine groups of seven to fourteen animals each received 1 mg bromocriptine at 11.00 h on days 1, 2 or 3 of pseudopregnancy (three groups for each day). On each day of treatment with bromocriptine, one group of hamsters was injected with bovine prolactin 4 h before bromocriptine, and one group received prolactin 4 h before bromocriptine for three consecutive days following treatment with bromocriptine. One group received bromocriptine only. These nine groups were compared with a control group of animals given 0.85% saline instead of bromocriptine and prolactin. Peripheral blood samples were taken from all hamsters at 11.00 h on days 3, 4, 5 and 6 of pseudopregnancy and plasma levels of progesterone were determined by radioimmunoassay. Luteolysis, indicated by a decline in progesterone level by 24 or 48 h after treatment with bromocriptine, occurred in all hamsters given bromocriptine alone, whether it was administered on day 1, 2 or 3. Pretreatment with a single dose of prolactin did not mitigate the bromocriptine-induced fall in progesterone. In the majority of cases, pretreatment with prolactin plus daily doses of prolactin maintained the progesterone at levels not different from saline-treated hamsters. These data suggest that prolactin is a necessary luteotrophin during early pseudopregnancy without which luteolysis ensues.

Animals↗
PubMed1981

Effects of mating on levels of oxytocin and prolactin in the plasma of male and female rabbits.

The effects of mating on plasma levels of oxytocin and prolactin in male and females rabbits have been investigated. Blood was collected through indwelling cardiac catheters at intervals of 1, 2, 4, 6, 12, 24, 36 and 60 min after mating. In female rabbits additional samples were taken 5h after mating, as well as daily during the ensuing pregnancy or pseudopregnancy. They were also fitted with intrauterine balloons for recording uterine activity. Copulation induced a rapid, transient rise in plasma oxytocin in female rabbits at the same time as a fall in plasma prolactin. Mating or sexual excitement had no significant effect on plasma concentrations of oxytocin or prolactin in bucks. Relatively large fluctuations of plasma oxytocin were seen in male rabbits under normal conditions and after mating, suggesting episodic release of oxytocin in a random fashion. The uterine recordings indicated that, in spite of the modest release of oxytocin, a strong sympathetic adrenal activation occurred in response to mating and this provided the overriding influence on uterine activity. During pregnancy plasma levels of prolactin rose significantly on day 4, and remained raised throughout most of gestation. Plasma prolactin fluctuated widely during the first half of pregnancy but the mean levels were higher than those found during the second half of gestation. When pseudopregnancy was induced with injection of an ovulating dose of LH, plasma prolactin rose in a similar manner as during early gestation or mating-induced pseudopregnancy. Thus, in contrast to rats, stimuli associated with mating have no direct influence on the subsequent release of prolactin in rabbits. The secretion of prolactin during gestation seems to be controlled entirely by ovarian steroids, probably progesterone.

Animals↗
PubMed1981

Interaction between prolactin and androgens in the accessory sex organs of male mice.

Treatment of adult male mice with varying doses of prolactin increased the weights of the seminal vesicles and the anterior prostate gland. Only in the seminal vesicles were these increases in organ weights associated with increased levels of DNA. In castrated mice, prolactin alone failed to alter the weights of the accessory sex organs or DNA content. However, the simultaneous administration of prolactin and testosterone resulted in enhanced androgenic stimulation of seminal vesicle weights and their DNA content. Prostatic weights, but not DNA content, were augmented by treatment with prolactin and testosterone. Although the kidneys exhibited androgen sensitivity, prolactin failed to enhance the effect of testosterone upon the kidney. Augmentation of androgen action in the accessory sex organs was observed only after treatment with prolactin or growth hormone. Prolactin also enhanced the effects of dihydrotestosterone and 5 alpha-androstane-3 alpha, 17 beta-diol, but not of 5 alpha-androstane-3 beta, 17 beta-diol. These studies revealed that prolactin enhances the proliferative actions of androgens in mouse seminal vesicles, but not in the anterior prostate glands or the kidneys.

Animals↗
PubMed1982

Neurotransmitter effects on release of prolactin and growth hormone in vitro from pituitary glands of the pigeon, Columba livia.

Single pigeon anterior pituitary glands were incubated with or without a hypothalamus in media containing various drugs. Release of prolactin and growth hormone was quantified by an electrophoretic-densitometric method. The hypothalamus stimulated release of both prolactin and growth hormone from the pituitary gland. Dopamine did not affect hormone release from pituitary glands incubated alone, but inhibited hypothalamus-stimulated release of prolactin and augmented hypothalamus-stimulated release of growth hormone in a dose-related manner. The effects of dopamine were reversed by its antagonist, pimozide. Serotonin stimulated release of prolactin and inhibited release of growth hormone from pituitary-hypothalamus co-incubations, and these effects were blocked by its antagonist, methysergide. Thyrotrophin releasing hormone (TRH) stimulated release of both hormones directly from pituitary glands incubated alone. Dopamine now inhibited TRH-stimulated release of prolactin, without affecting TRH-stimulated release of growth hormone. These results indicate that the neurotransmitters, dopamine and serotonin, affect the in-vitro release of factors from the hypothalamus which control the secretion of prolactin and growth hormone. In addition, dopamine may inhibit release of prolactin directly from the pituitary gland, but only when secretion of prolactin is high initially.

Animals↗
PubMed1983

Concentrations of prolactin in the plasma of fetal sheep and in amniotic fluid in late gestation and during dexamethasone-induced parturition.

The concentration of prolactin in samples of fetal plasma and amniotic fluid collected from sheep with indwelling catheters has been measured by radioimmunoassay. There was considerable variation between animals in the concentration of prolactin in fetal plasma which ranged from less than 2 micrograms/l to greater than 50 micrograms/l. In five out of eight fetuses which were sampled at intervals throughout the last 30 days of pregnancy, there was an increase in the concentration of prolactin in the plasma before parturition. The concentration of prolactin in amniotic fluid was consistently low (approximately 1 microgram/l). Induction of premature parturition by intrafetal infusion of dexamethasone was accompanied by an increase in the concentration of prolactin in only one of three fetuses infused. These results indicated that prolactin is present in fetal plasma but that an increase in prolactin in fetal plasma before the onset of parturition does not always occur. The low concentration of prolactin in amniotic fluid contrasts with the high concentrations of this hormone found in the amniotic fluid of the primate.

Amniotic Fluid↗
PubMed1984

Inhibition by testosterone of prolactin and growth hormone release from chicken anterior pituitary glands in vitro.

Pituitary glands and hypothalami from broiler fowl were incubated in medium containing testosterone, and prolactin and GH release were determined. Pituitary glands were also preincubated for 20 h in medium containing testosterone, and then in medium containing various secretagogues. Testosterone inhibited the release of prolactin directly from the pituitary gland in a concentration-related manner. The hypothalamus stimulated the release of prolactin, but by a lesser amount in the presence of testosterone. When pituitary glands were preincubated with testosterone, subsequent release of prolactin was inhibited, except with the highest concentration which stimulated prolactin release. Hypothalamic extract (HE) markedly stimulated prolactin release from control pituitary glands although testosterone-primed glands were less responsive. The stimulation of prolactin release by thyrotrophin releasing hormone (TRH) and prostaglandin E2 (PGE2) was also reduced by preincubation of the pituitary glands with testosterone. Priming with testosterone did not affect the release of GH from pituitary glands alone, but reduced the TRH-, HE- and PGE2-stimulated release of GH. These results demonstrate that testosterone directly inhibits prolactin secretion and reduces the sensitivity of pituitary lactotrophs and somatotrophs to provocative stimuli.

Animals↗
PubMed1984

Role of prolactin in the photoperiodic control of moulting in the mink (Mustela vison).

Beginning at the summer solstice adult female mink were maintained in long- or short-day photoperiods and treated with bromocriptine or prolactin. In control females kept under natural lighting conditions the moult coincided with the seasonal decrease in prolactin and resulted in the growth of a dense winter coat which was completed by the end of November. Long days, which slowed the decrease in plasma prolactin relative to animals in the natural photoperiod, induced a more or less complete moult followed by growth of a thin summer coat. On the contrary we observed an accelerated decrease in plasma prolactin concentrations followed by an early and brief moult in females kept under long days but treated with bromocriptine and in females under short days. The growth of a dense winter coat was completed by the end of September in all the females of the short-day group and in six of eleven females treated with bromocriptine. In the other five females, moult was followed by the growth of a summer coat. These results may suggest that the decline of prolactin after the summer solstice is responsible for the onset of the autumn moult, but the early, abbreviated moult and the growth of a winter coat observed in females kept under short days and treated with prolactin do not seem to support this hypothesis. However, the huge non-physiological levels of prolactin measured in the plasma of these females and the appearance of abnormal white under-hairs might suggest that the hormonal balance in this group was completely disturbed by the treatment. The physiological role of prolactin in the seasonal moulting cycle in mink is discussed.

Animals↗
PubMed1985

Effect of a single injection of prolactin on the serum concentrations of thyroid hormones and corticosterone and liver monodeiodinase in the domestic fowl before and after hatching.

The influence of an intravenous injection of ovine prolactin on the liver monodeiodinase activity and serum concentrations of thyroid hormones and corticosterone was studied in Hisex embryos and chicks after hatching. An injection of 1 and 10 micrograms ovine prolactin into 18-day-old chick embryos increased serum concentrations of tri-iodothyronine (T3) five- and eightfold respectively after 2 h. At the same time serum concentrations of thyroxine (T4) and reverse T3 (rT3) were decreased in the chick embryo, but only with 10 micrograms prolactin. This was accompanied by a doubling of the liver monodeiodinase activity. Serum concentrations of corticosterone, however, were not influenced by the prolactin injections. In the 5-day-old chicken, serum concentrations of T3, rT3, T4 and liver T4-5'-monodeiodinase activity were not influenced by 1 or 10 micrograms prolactin. Serum concentrations of corticosterone after injection of 1 or 10 micrograms prolactin were doubled compared with controls. These results are compatible with a prolactin-induced shift from a T4-5-monodeiodination into a T4-5'-monodeiodination in the liver at the end of incubation. This effect, however, is not mediated through a prolactin-induced corticosterone release.

Animals↗
PubMed1991

Role of the placenta in the control of the ante-partum surge of prolactin in the rat.

A nocturnal surge of prolactin secretion occurs in the dark period preceding parturition in the rat. The aim of this study was to examine the role of the placenta in the control of this prolactin surge. Plasma prolactin and progesterone were measured by radioimmunoassay in serial blood samples collected after surgical removal of conceptuses during late pregnancy, and after intracerebroventricular (i.c.v.) injection of placental lactogen (PL) before the prolactin surge. In intact control animals, prolactin secretion remained low until a nocturnal surge of secretion occurred in the dark period preceding parturition, peaking at 269 +/- 51 (S.E.M.) micrograms/l at 03.00 h on day 21. Progesterone levels fell from greater than 200 nmol/l on day 19 to less than 40 nmol/l by 12.00 h on day 20 of pregnancy. PL levels during late pregnancy were modified by partial or complete removal of conceptuses at 10.00 h on day 19 of pregnancy. Removal of all but one or two conceptuses did not change the normal pattern of prolactin or progesterone secretion. Removal of all conceptuses, however, induced a large nocturnal surge of prolactin secretion, peaking at 211.7 +/- 78 micrograms/l at 03.00 h on day 20, 24 h earlier than the surge in intact animals. Progesterone levels after removal of all conceptuses fell to less than 40 nmol/l by 23.00 h on day 19, approximately 12 h before the decline in intact animals. Maintenance of increased progesterone levels after conceptus removal using silicone tubing implants significantly (P less than 0.05) reduced the peak of the premature prolactin surge to 79.7 +/- 18 micrograms/l at 05.00 h on day 20.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Protein kinase C activation and calcium mobilization decrease prolactin release from human decidual cells in early pregnancy.

The present study was undertaken to investigate the effects of protein kinase C (PKC) activation and calcium mobilization on the release of prolactin from human decidual cells in early pregnancy. Decidua obtained from patients in early pregnancy was enzymatically dispersed and cultured with phorbol myristate acetate (PMA) and calcium ionophore A23187 in a cell culture system. Prolactin in the medium was measured by enzyme-immunoassay. PMA, a PKC activator, dose-dependently attenuated the release of prolactin from cultured decidual cells, while a PKC inhibitor, H7, significantly (P < 0.001) diminished the effect of PMA on prolactin release. PMA had no effect on cell numbers or DNA synthesis in the decidual cells during culture. It did not significantly increase the generation of inositol phosphate in decidual cells prelabelled with myo-[3H]inositol and it had no effect on intracellular calcium concentration ([Ca2+]i). Calcium ionophore A23187, a Ca(2+)-mobilizing agent, also significantly (P < 0.001) attenuated the release of prolactin and potentiated the PMA-induced suppression of prolactin release from decidual cells. These findings suggest that activation of PKC and mobilization of Ca2+ may be involved in regulating prolactin release from human decidual cells. The PMA-induced suppression of prolactin release is not triggered by phosphoinositide hydrolysis nor by the increase in [Ca2+]i in decidual cells.

Calcimycin↗
PubMed1994

Functional heterogeneity with respect to oestrogen treatment in prolactin cell subpopulations separated by Percoll gradient centrifugation.

The effects of oestradiol on prolactin gene expression were studied by quantitative in situ hybridization histochemistry in different prolactin pituitary cell (sub)populations, which had been obtained by separation on a discontinuous Percoll gradient. When cells were incubated in vitro in the presence of oestradiol (10(-8) M) for a period of 4, 24, 48 and 72 h, there was an increase in the amount of prolactin mRNA, from 24 h on, only in high-density prolactin cells and lactotrophs of the total cell suspension. In contrast, the amount of prolactin mRNA in lactotrophs of low density did not change upon treatment with oestradiol. Pharmacological treatment with 50 micrograms oestradiol/day (s.c.) of random cycling female rats in vivo for 14 days increased the total number of prolactin gene-expressing cells and more lactotrophs were recovered at high density after Percoll gradient centrifugation. These results suggest a preferential stimulatory effect of oestradiol on prolactin gene transcription on a subpopulation of lactotrophs. Changes observed in prolactin cell layers after oestradiol treatment in vivo may represent a preferential effect in situ on a particular mammotroph cell subpopulation.

Animals↗
PubMed2002

Regulation by endogenous opioids of suckling-induced prolactin secretion in pregnant and lactating rats: role of ovarian steroids.

Evidence suggests that endogenous opioid peptides are implicated in the suckling-induced prolactin rise. We explored the role of the opioid system and the participation of ovarian hormones in the regulation of prolactin induced by the suckling stimulus at the end of pregnancy in rats with developed maternal behavior, and during lactation. Suckling for 24 h induced a significant increase in serum prolactin on day 19 of pregnancy, which was increased more than three times when naloxone (2 mg/kg s.c.) or mifepristone (2 mg/kg) was administered. The combination of naloxone and mifepristone did not increase serum prolactin more than either compound alone. Administration of tamoxifen (500 microg/kg orally) on days 14 and 15 of pregnancy completely abolished the effect of naloxone, indicating a role for estrogens in establishing this inhibitory role of opioids. To examine the participation of the opioid system during lactation, we used groups of rats on days 1, 3, 5, 12 and 19 postpartum either (i) isolated from the pups for 4 h, or (ii) isolated from the pups for 3.5 h and reunited with them and suckled for 30 min. Naloxone, given just before replacing the pups, prevented the increase in serum prolactin levels observed in the suckled group of rats but had no effect on the basal levels of the isolated rats. To examine whether the participation of the opioid system in the release of prolactin is dependent on the variation of progesterone levels, rats on day 20 of pregnancy were implanted with two cannulae containing progesterone (that blocked postpartum ovulation) or cholesterol, and cesarean surgery was performed on day 21. To maintain lactation, pups (1-3 days old) were replaced every 24 h, and 4 days after the cesarean eight pups were placed in the cage at 1800 h to maintain a strong suckling stimulus during the following 24 h. Naloxone administration significantly reduced serum prolactin levels in control (cholesterol) rats but progesterone implants prevented the inhibitory effect of naloxone and this effect was not modified by treatment with estrogen. These results indicate that the opioid system modulates suckling-induced prolactin secretion, passing from an inhibitory action before delivery to a stimulatory action during lactation. This regulatory shift seems to be dependent on the fall in progesterone concentration at the end of pregnancy and the subsequent increase after the postpartum ovulation and luteal phase.

Animals↗