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PubMed1986

Observations on the interaction of prolactin and thyroxine in the tail of the bullfrog tadpole.

Explants of tail fin from tadpoles of Rana catesbeiana maintained in tissue culture underwent resorption when exposed to a medium containing 150 nM thyroxine (T4). Increases in the specific activity of hexosaminidase (Hex) and of acid phosphatase (AP) were associated with this response. Ovine prolactin inhibited resorption of explants in a dose-responsive manner; however, prolactin had no influence on the specific activity of either Hex or AP cultured explants. This result contrasted with the effect of prolactin in vivo, where it inhibited both the resorption of the tail and the increase in specific activity of hydrolytic enzymes induced by T4. The actions of both hormones, when applied in vivo, were more pronounced in the tail fin than in the muscular core of the tail at the stage of regression tested, indicating that the failure of prolactin to influence enzyme induction in vitro did not result from an incapacity of the fin to respond to prolactin in this fashion. It is suggested that the inhibition of T4-induced enzymic activity by prolactin which is observed in the intact animal may come about in response to some related but indirect systemic action of prolactin that is lacking when explants are cultured in vitro. It is concluded that inhibition of the induction of hydrolytic enzymes is not an essential factor in the inhibitory effect of prolactin on the resorption of the tail fin.

Acid Phosphatase↗

PubMed1986

Plasma concentrations of prolactin during the breeding cycle in the Cape gannet (Sula capensis): a foot incubator.

Plasma prolactin was measured in the Cape gannet (Sula capensis) which differs from most other avian species in that although both sexes share equally in incubation duties, neither sex possesses an incubation patch but rather incubates a single egg with its foot webbing. Five main categories of birds were studied: nonbreeders, unmated birds which were nevertheless defending a nest site, recently mated birds, incubators, and brooders with nestlings. Prolactin titers in the plasma were 8-9 ng/ml in nonbreeding gannets, increasing to 17.7 +/- 1.6 and 16.7 +/- 1.2 ng/ml in incubating females and males, respectively. Plasma concentrations of prolactin progressively increased in nonbreeding gannets from 5.5 +/- 0.4 ng/ml in 1-year-old birds to 8.7 +/- 1.6 ng/ml in birds defending a nest site but without an egg. Blood samples taken from both incubators and nonincubators every 3 hr over 27 hr did not reveal any significant daily cycling in prolactin titers. Plasma osmolarity did not vary significantly between nonincubators and incubators, being 300.1 +/- 3.2 and 298.2 +/- 3.0 mOsm/kg, respectively. No positive correlation was found between possible osmotic stress during incubating and plasma concentrations of prolactin. Plasma concentrations of luteinizing hormone and testosterone increased while prolactin decreased, significantly, 24 hr after clutch loss. The putative inhibition of the pituitary-gonadal axis by prolactin is discussed together with other possible roles of prolactin during the breeding season in gannets.

Aging↗

PubMed1986

Effect of thyrotropin-releasing hormone and dopamine on the in vitro secretion of prolactin by the bullfrog pituitary gland.

Pituitary glands of bullfrogs (Rana catesbeiana) were incubated in medium containing thyrotropin-releasing hormone (TRH) and/or dopamine in order to see their effects on the release and synthesis of prolactin, which was measured by a homologous radioimmunoassay. Prolactin synthesis was measured by monitoring the incorporation of [3H]leucine into prolactin. TRH (0.1-10 ng/ml) stimulated the release of immunoassayable prolactin and newly synthesized [3H]prolactin into the medium in a dose-dependent manner; however, it was ineffective in increasing total prolactin (medium plus pituitary) and the incorporation of [3H]leucine into the total prolactin during the experimental period (20 hr). The TRH-induced elevation of prolactin release was suppressed by the addition of dopamine (5 X 10(-7) M) to the medium.

Animals↗

PubMed1991

Effects of prolactin on chloride cells in opercular membrane of seawater-adapted tilapia.

Effects of prolactin on morphology and numbers of chloride cells in the opercular membrane of seawater-adapted tilapia (Oreochromis mossambicus) have been examined. Following five daily injections of ovine prolactin at a dose of 10 micrograms.g body wt-1, blood samples were taken and opercular membranes were removed and stained with a fluorescent mitochondrial dye (dimethylaminostyrylethylpyridiniumiodine), a fluorescent derivative of ouabain (anthroylouabain), and a histological stain specific for the extensive tubular system of chloride cells (zinc-osmium-iodine). Mean plasma osmolarity and sodium increased 23-24% following prolactin injection. An increase in the relative frequency of chloride cells between 20 and 180 microns2 in cross-sectional area and a decrease in the relative frequency of chloride cells greater than 180 microns2 were observed following prolactin injections. Average cell size decreased 46-70% and cell height decreased 26-38% following prolactin injections. There was no significant change in cell density. Anthroylouabain staining was observed in both prolactin- and saline-injected fish, and no significant effect on Na+,K(+)-adenosinetriphosphatase activity was seen in either opercular membrane or gill tissue. The results demonstrate an effect of prolactin on chloride cell size and provide a morphological correlate for decreased secretory activity of chloride cells following prolactin injections.

Acclimatization↗

PubMedDate not supplied

Comparative effects of prolactin, perphenazine and reserpine on non-arteriosclerotic (virgin) vs arteriosclerotic (breeder) rats.

Non-arteriosclerotic, virgin and arteriosclerotic breeder rats were subjected to chronic treatment with prolactin or prolactin-releasing drugs such as perphenazine and reserpine for 12 weeks. Males and females responded to the prolactin as evidenced by increased milk secretion, adrenal hyperplasia and thymus gland involution. Although the prolactin- and reserpine-treated animals gained weight and manifested pituitary gland basophilia, the perphenazine-treated animals showed considerable loss of body weight as well as involution of the pituitary gland, ovaries and testes, suggesting a condition of induced hypopituitarism. Chronic treatment with prolactin, both directly and indirectly, caused uniform increases in serum enzymes, e.g., CPK, SGOT, SGPT and LDH, lipids, e.g., triglycerides, free fatty acids and cholesterol, glucose and BUN. Corticosterone production was enhanced by prolactin, reduced by perphenazine and unaffected by reserpine. Prolactin did not induce any arterial disease in the arteriosclerosis-resistant, virgin rats but it did cause eracerbation of the usual severity of arteriosclerosis in the hilar renal arteries of the arteries sclerosis-prone, breeder rats as well as an increased incidence of "old" and "new" foci of myocardial necrosis, characteristically found in breeder rats. It is suggested that hypothalamic control of prolactin as well as ACTH release may play a role in the spontaneous arteriosclerosis which develops in repeatedly-bred, male and female rats.

Alanine Transaminase↗

PubMed1991

Serum postdexamethasone prolactin measures in depressive patients and control subjects.

Recently, some researchers noted significant positive relationships between postdexamethasone serum cortisol and prolactin levels, whilst endogenous depressives exhibited a significantly lower suppression of prolactin by dexamethasone than non-endogenous patients or normal controls. To ascertain the extent of prolactin responses to dexamethasone in severely depressed patients, we measured 8 a.m. pre- and postdexamethasone prolactin levels in 104 depressed and 42 normal subjects. Serum cortisol levels were also determined in depressed patients before and after dexamethasone administration. We found a significant suppressive effect of dexamethasone on prolactin levels. There were no significant differences either in pre- or postdexamethasone prolactin, or in actual dexamethasone-induced decrements in prolactin between normal controls, melancholics, simple major or minor depressed subjects. We have not found any significant relationships between cortisol and prolactin, either under baseline or postdexamethasone conditions.

Adjustment Disorders↗

PubMed1986

Increased dietary leucine changes the rhythm of prolactin secretion.

As we have recently shown that prolactin secretion in vitro is regulated by extracellular leucine, we wanted to determine whether leucine had a similar regulatory action on prolactin secretion in the intact animal. Leucine was administered to cycling female rats by way of their drinking water (0.5%) for a period of 24 days. At daily intervals during this time, six control and six leucine-treated rats were killed and their trunk blood subsequently assayed for prolactin content. On days 7, 14, and 21 during this period, pituitaries from the sacrificed rats were fixed and processed for electron microscopy. Leucine treatment resulted in an alteration in the normal four-day cyclicity in serum prolactin levels and a stimulation of prolactin synthesis as evidenced by ultrastructural changes in the pituitary mammotrophs. In a parallel set of experiments, daily vaginal smears were taken from nonsynchronized animals for 24 days before and 24 days during leucine administration. Leucine treatment resulted in variable alterations in the estrus cycle depending upon the stage of the cycle when the leucine was first administered. The changes in serum prolactin and the disturbances of the estrus cycle in the leucine-treated animals persisted for approximately 20 of the 24 days. In a shorter control experiment (seven days), alanine treatment (0.5%) was found to have no effect on prolactin levels. It is concluded that a mild elevation in dietary leucine can affect prolactin synthesis and release and the normal progression of the estrus cycle.

Animals↗

PubMed1990

Amniotic fluid prolactin in the third trimester of pregnancies complicated by gestational or pregestational diabetes mellitus.

Amniotic fluid concentrations of immunoreactive prolactin were measured during the third trimester in 184 diabetic gravidas and correlated with concurrent levels of prolactin in maternal plasma. Prolactin measurements concorded with previously published estimates in normal gravid women and averaged 825 +/- 32 ng/mL (mean +/- SEM) in amniotic fluid and 168 +/- 6.5 ng/mL in simultaneously sampled plasma. Cross-sectional and longitudinal analyses indicated that the prolactin levels in amniotic fluid of pregnant diabetics declined significantly between weeks 32 and 40 of gestation, whereas plasma levels did not change consistently during the same interval. Mean values for amniotic fluid prolactin did not correlate with simultaneous prolactin concentrations in plasma, nor with maternal age, clinical estimates of polyhydramnios, amniotic fluid creatinine content, or lecithin/sphingomyelin (L/S) ratios or subsequent birth weight of the offspring. Clear-cut correlations with overall maternal glucose regulation could not be demonstrated. However, subtle effects may be operative since amniotic fluid prolactin displayed weak but significant correlations with concurrent levels of maternal plasma glucose, and mean values for hemoglobin A1c (HbA1c) but not with mean values for fasting plasma glucose (FPG). Amniotic fluid prolactin concentrations were significantly greater in patients with pregestational diabetes (White classes C, D, and F) than in women with gestational diabetes mellitus (GDM) (our classes A1, A2, and B1). The differences could not be accounted for by differences in metabolic regulation, maternal age, or weights of these two populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗

PubMed1994

Hypothalamic injection of prolactin or its antibody alters the rat sleep-wake cycle.

Several studies have suggested an interaction between prolactin and the sleep-wake cycle. In this study ovine prolactin (oPRL) and anti-prolactin antibody were microinjected into the rat dorsolateral hypothalamus, which contains prolactin-like immunoreactive neurons. Results indicate that during the light period, prolactin injection induced an increase in paradoxical sleep duration, whereas it caused a decrease when injected during the dark period. Anti-prolactin antibody injection during the dark period also decreased paradoxical sleep duration. There was no effect of oPRL or antibody on slow wave sleep duration irrespective of injection time. These results suggest that prolactin injection may have an inhibitory effect on hypothalamic prolactin neurons.

Animals↗

PubMed1989

Prolactin and sodium lactate-induced panic.

Sodium lactate infusions reliably induce panic attacks in panic disorder patients but not in normal controls, but the mechanism underlying this response is unknown. We studied the plasma prolactin response to infusion of 0.5 molar sodium lactate in 38 patients with panic disorder or agoraphobia with panic attacks, and 16 normal controls. As expected, baseline plasma prolactin was significantly higher in female subjects than in male subjects. However, the males who experienced lactate-induced panic had significantly elevated baseline prolactin levels compared to male nonpanickers and controls. Prolactin levels increased in all groups during lactate infusion, which may reflect osmotic effects, but were blunted in the late panickers compared to nonpanickers and controls. The elevated baseline prolactin for male panickers supports a relationship between prolactin and anticipatory anxiety. The blunted prolactin response for late panickers suggests a net diminution, rather than a sensitization, of prolactin response in panic anxiety.

Adult↗

PubMed1995

Pindolol pretreatment blocks stimulation by meta-chlorophenylpiperazine of prolactin but not cortisol secretion in normal men.

Previous reports from this laboratory have shown that pindolol, a partial serotonin1A receptor agonist, inhibited prolactin, but not cortisol secretion induced by administration of the serotonin (5-HT) precursor L-5-hydroxytryptophan or the direct-acting 5-HT2A/5HT2C receptor agonist MK-212. The findings suggest additive or interactive effects of 5-HT1A and 5-HT2A/5-HT2C receptors in modulating 5-HT-related prolactin, but not cortisol, responsivity. To examine further the role of 5-HT1A and 5-HT2A/5-HT2C receptors in prolactin and cortisol secretion in healthy men, the effects of meta-chlorophenylpiperazine (mCPP), a potent 5-HT receptor agonist, on the above hormones were studied in eight healthy men with and without pindolol pretreatment. It has previously been demonstrated that ketanserin, a 5-HT2A antagonist, and ritanserin, a 5-HT2A/5-HT2C antagonist, block the prolactin and attenuate the hypothalamic-pituitary-adrenal axis responses to mCPP in man or rodents. Administration of mCPP induced a significant increase in plasma concentrations of prolactin and cortisol. The mCPP-induced prolactin concentrations were significantly blocked by pretreatment with pindolol, whereas mCPP-stimulated cortisol levels were not diminished by pindolol pretreatment. Thus, mCPP-induced prolactin secretion appears to require the availability of both 5-HT2C and 5-HT1A receptor activation, since blockade of either of these receptors may diminish the mCPP-induced prolactin response. Cortisol secretion stimulated by mCPP may occur following 5-HT2C receptor stimulation in the presence of 5-HT1A receptor blockade.

Adrenergic beta-Antagonists↗

PubMed1990

Acute effect of prolactin on the intestinal calcium absorption in normal, pregnant and lactating rats.

Acute effect of prolactin on intestinal calcium absorption was studied in Wistar rats. Prolactin when given subcutaneously 24 h, or intraperitoneally 1 h, before intragastric administration of 45Ca-containing CaCl2 solution markedly increased the plasma 45Ca content. Of interest was the enhancing effect of prolactin on calcium transport seen in 1 h which suggested that prolactin could act directly on the intestine. Physiological significance of prolactin was evaluated in pregnant and lactating rats. Pretreatment with bromocriptine, an inhibitor of prolactin release, had no effect in rats on day 20 of pregnancy but significantly reduced calcium absorption in lactating rats. This reduced calcium absorption was only partially restored by prolactin treatment. The present investigation thus showed that prolactin, besides stimulating 1,25(OH2)D3 production, may also enhance calcium absorption directly. This effect was absent in pregnant rats but was of physiological significance in lactating rats.

Animals↗

PubMed1991

Further studies on acute effect of prolactin on intestinal calcium absorption in rat.

The present investigation aimed to (1) reconfirm the acute effect of prolactin on intestinal calcium absorption in the rat, (2) evaluate the influence of age on prolactin action, and (3) further investigate the mechanisms of prolactin action on calcium absorption. The intestinal calcium absorption in mature rats was evaluated by measuring the plasma 45Ca content at intervals during a 1-h period following intragastric administration of a 45Ca-containing test solution and by measuring tibial 45Ca content in weaned rats. By using weaned (50-70 g), sexually mature (180-200g) or aged (greater than 250 g) female Wistar rats, we demonstrated that calcium absorption was inversely related to age. Prolactin at a dose of 0.02 mg/100 g body weight, administered intraperitoneally 1 h before Ca administration, significantly enhanced calcium absorption in sexually mature and weaned rats but not in aged rats. At a luminal calcium concentration of 5 mM, prolactin had no effect when the luminal solution was either CaCl2 alone or an Na-free electrolyte solution. On the other hand, prolactin significantly increased the plasma 45Ca content by 57, 42 and 28% at 5, 15 and 30 min respectively, when the electrolyte solution contained sodium. In contrast, in the presence of 0.5 mM calcium, the enhancing effect of prolactin on calcium absorption was not dependent on the presence of sodium. Compared with the saline control, the plasma 45Ca content in prolactin treated animals was significantly elevated by 63% at 5 min when the test solution was a sodium-free electrolyte solution.

Aging↗

PubMed1988

The permanent effect of reproductive events on blood prolactin levels and its relation to breast cancer risk: a population study of postmenopausal women.

In each of two population-based studies conducted on the Island of Guernsey between 1967-1976 and 1977-1984, respectively, single specimens of blood were taken from over 5000 normal women. From these two studies there were 1173 and 946 postmenopausal women in whom blood prolactin was determined and multivariate analysis was used to establish the association between blood prolactin concentration and possible determinants of risk of breast cancer. Since prolactin levels were log-normally distributed these analyses were done on log-transformed data. The age at menarche or menopause, age at first or last childbirth, length of reproductive life (i.e. time from menarche to menopause) or post-menopausal life (i.e. time from menopause to time of blood sampling), contraceptive use and history of breast cancer were not significantly associated with blood prolactin concentration. Of significance were age, parity, time of blood sampling and assay drift. Ponderosity (Quetelet's Index) was positively associated with prolactin concentration and this was significant using a one-tail criterion. Women with a mammographic pattern designated DY by Wolfe had significantly higher prolactin levels than those with N1 patterns. However, the main finding to emerge was that after standardizing for all the other variables increasing parity was related to a step-wise reduction in blood prolactin levels. Since this had occurred in women who had had their last child up to 35 years previously it implies this effect is permanent. It could therefore be that the protective effect on breast cancer risk of multiparity and early first pregnancy could be mediated by such a life-long reduction in blood prolactin levels.

Age Factors↗

PubMed1975

Effect of thyreotrope-releasing hormone (TRH) on prolactin turnover in culture.

A kinetic study of the influence of thyreotrope-releasing hormone (TRH) on prolactin turnover and synthesis by a new rat pituitary prolactin cell line (SD1) has been performed by means of pulse-chase experiments. After a 10-min [3H]leucine pulse, the chase was carried out in the presence or absence of TRH (54 nM), cycloheximide (3.6 X 10(-5)M) and/or [14C]-proline. The prolactin content of the cells in the medium was estimated using a radioimmunoassay technique. The specific radioactivity of prolactin in the medium was estimated after its isolation by disc gel electrophoresis. This kinetic study demonstrated, firstly, a rapid intracellular transit of newly synthesized prolactin (15 + 10 min or less); secondly, the existence of at least two intracellular prolactin pools; thirdly, a rapid effect of TRH on release of stored prolactin, which is independent of de novo protein synthesis, and fourthly, a delayed stimulating effect of TRH on prolactin synthesis.

Cell Line↗

PubMed1978

Prolactin receptor on dissociated mammary epithelial cells at different stages of development.

Properties of prolactin receptors were measured by monitoring [125I]prolactin binding to specific receptor sites on collagenase-dissociated mammary epithelial cells of virgin, pregnant and lactating mice. On a Scatchard plot the data generated a straight line and the estimated dissociation constant (Kd) and number of receptor sites on lactating cells were 0.9 x 10(-9) and 1540 per cell. The [125I]prolactin binding was inhibited in presence of unlabeled prolactin and other lactogenic polypeptide hormones, but not by nonlactogenic polypeptide hormones. The [125I]prolactin binding was sensitive to pronase and trypsin but not to DNAase, RNAase and hyaluronidase. Scatchard plot analysis further showed that while the number of receptors on mammary cells was variable at different stages of endocrine regulated developmental changes of the gland, Kd of the hormone--receptor complex generally remained similar. The high level of prolactin receptors on mammary cells of virgins was reduced during pregnancy and the lactating mammary cells showed a highly elevated level of prolactin receptors. The results demonstrate that specific prolactin receptors can be measured on collagenase dissociated mammary epithelial cells and this method permits a direct assessment of the number of receptors on a per cell basis rather than indirect estimates, based on average DNA or protein content of the tissue, composed of heterogeneous cell types.

Animals↗

PubMed1978

Influence of bromoergocryptine on estrogen-modulated prolactin receptors of mouse mammary gland.

Modulation of specific binding of prolactin to murine mammary gland as a response to treatment with various doses of estradiol benzoate (EB) was studied. Measurements of serum and pituitary levels of prolactin were also carried out simultaneously. Estradiol benzoate at a dose of 5 microgram significantly increased the binding of 125I-labelled rat prolactin (rPRL) to mammary gland concomitant with increased serum prolactin levels in ovariectomized mice. Administration of bromoergocryptine along with EB resulted in decreased serum prolactin levels as well as binding of prolactin to breast tissue. It thus appears that the influence of estradiol on binding of prolactin to mammary gland is mediated primarily via its property of enhancing serum prolactin concentration apart from its possible direct effect at the target tissue level.

Animals↗

PubMed1982

Prolactin synthesis in primary cultures of pituitary cells: regulation by estradiol.

Pituitary cells cultured with estradiol respond by a specific increase in prolactin synthesis. Extensive inhibition of DNA synthesis (61-78%) with hydroxyurea or cytosine arabinoside resulted in only 28-33% decrease in estrogen-induced prolactin synthesis. To assess the role of prolactin cell proliferation in the estrogen-induced response, mammotrophs were identified by immunocytochemistry. Cultures treated with estradiol for 1, 2 or 5 days contained 101 +/- 1, 113 +/- 2 and 132 +/- 1% of the number of mammotrophs in controls. Estradiol treatment for corresponding periods resulted in prolactin synthesis representing 94 +/- 5, 144 +/- 11 and 270 +/- 22% of controls and prolactin mRNA levels representing 115 +/- 7, 160 +/- 7 and 322 +/- 22% of controls. Thus estrogen caused a considerable increase in prolactin synthesis which paralleled the increase in prolactin mRNA levels and a much smaller relative increase in the number of mammotrophs. We conclude that regulation of prolactin synthesis by estrogen is mediated predominantly but not exclusively through stimulation of gene expression in existing pituitary cells.

Animals↗