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PubMed1990

The effect of prolactin on murine in vitro fertilization and embryo development.

Elevated levels of serum and follicular fluid prolactin occur in women undergoing ovulation induction with both clomiphene citrate and gonadotropin therapy. Prolactin's effect on oocyte fertilization and embryo cleavage has not been fully characterized. Using a murine model, we investigated the effect of prolactin on in vitro fertilization and subsequent embryo cleavage in media containing 150, 400, and 600 ng/ml purified mouse prolactin. No difference was found in fertilization rates when compared with control rates. Culture of both in vivo and in vitro fertilized two-cell embryos in murine prolactin at 150, 400, and 600 ng/ml showed no significant difference in blastocyst, morula, or embryo degeneration rates when compared with control rates. An assay for binding of murine prolactin to spermatozoa, oocytes, and the embryo at various cleavage stages revealed no specific murine prolactin binding. These in vitro experimental results fail to show a role for murine prolactin in effecting mature oocyte fertilization or subsequent embryo cleavage. The lack of binding of murine prolactin to the gametes and early developing embryo supports the in vitro findings.

Animals↗
PubMed1988

Control of prolactin secretion in the teleost Oreochromis mossambicus: effects of water acidification.

Prolactin secretion is stimulated markedly in fish exposed to water of pH 4. This phenomenon was used to study the control of prolactin secretion. Activation occurs irrespective of changes in plasma osmolarity or plasma sodium and calcium concentrations. After acute acidification of the water, which leads to a substantial fall in plasma osmolarity and plasma electrolyte levels, the activation of the prolactin cells is less marked than after gradual acidification of the water, when plasma osmolarity, plasma sodium, and plasma total and ionic calcium levels are not noticeably affected. When fish bearing an implanted rostral pars distalis of the pituitary gland are exposed to water of pH 4, both the in situ prolactin cells and the prolactin cells of the implant become activated only when the drop in water pH is acute and followed by a reduction in plasma osmolarity and electrolyte levels. When the rate of reduction of the pH is slow and not changing plasma osmolarity or sodium and calcium levels, the in situ prolactin cells are stimulated, but not those of the implants. We conclude that the activation of the prolactin cells in situ in fish in acid water is not mediated by reductions in plasma osmolarity, plasma sodium, total calcium, or ionic calcium, but by hypothalamic mechanisms. The drop in plasma osmolarity and electrolytes probably reflects excessive osmoregulatory stress and this may hamper instead of stimulate the response of the prolactin cells to osmoregulatory disturbance. The physiological significance of the in vitro activation of prolactin cells by reduced ambient osmolarity is unclear.

Acids↗
PubMed1993

Serum prolactin levels in active multiple sclerosis and during cyclosporin treatment.

Prolactin is essential for immune function. Excess prolactin augments some immune reactions, whereas low serum levels of prolactin inhibit immune function and prevent experimental allergic encephalomyelitis, an animal model of multiple sclerosis (MS). Activated lymphocytes, characteristics of MS, release prolactin. In this study, serum prolactin levels were normal in 35 patients with chronic progressive MS and 19 patients with acute exacerbations. These results suggest it is unlikely that prolactin contributes to the enhanced immune reactivity characteristic of MS. Acute cyclosporin A (CsA) administration increases circulating prolactin levels in animals and might paradoxically augment some immune reactions. We find that chronic CsA therapy for MS does not cause elevations in serum prolactin and should not reverse any therapeutic effect of CsA. Disturbances of prolactin regulation are not characteristic of MS.

Adult↗
PubMed1987

The effects of the cholecystokinin antagonist, proglumide, on prolactin secretion in the rat.

Since cholecystokinin produced important effects on prolactin secretion following its intraventricular injection in ovariectomized rats, we have evaluated the effects of the cholecystokinin antagonist, proglumide, to assess the physiologic significance of CCK in the control of prolactin release. Conscious rats of either sex were used following implantation of third ventricular and/or intravenous cannulae for the administration of proglumide. Blood samples were drawn from conscious animals at various times after injection of the compound. Intraventricular injection of 1 or 10 micrograms of proglumide produced a dramatic decline in plasma prolactin levels in either castrate or intact male rats. Similar results were found following the intravenous injection of 10 or 100 micrograms of the drug. These results contrasted sharply with the findings in ovariectomized females in which the intraventricular injection of the same two doses of proglumide used in males produced a dose-related elevation of prolactin which was opposite to the delayed lowering of prolactin following the intravenous injection of the same doses of the compound used in males. These results indicate that proglumide can lower prolactin in male rats and suggests a physiologically significant role of CCK in the control of prolactin secretion in the male. There appears to be a sex difference in the response since the results contrasted sharply in ovariectomized female rats. The results in the females are puzzling and it is apparent that further studies are needed to determine whether or not CCK has a physiologically significant role to play in prolactin secretion in the female. Since previous results have shown that CCK has no effect on the release of prolactin by the pituitary directly these interactions are presumably taking place in the hypothalamus.

Animals↗
PubMed1992

PMA-sensitive protein kinase C is not necessary in TRH-stimulated prolactin release from female rat primary pituitary cells.

In GH3 cells and other clonal rat pituitary tumor cells, TRH has been shown to mediate its effects on prolactin release via a rise of cytosolic Ca2+ and activation of protein kinase C. In this study, we examined the role of protein kinase C in TRH-stimulated prolactin release from female rat primary pituitary cell culture. Both TRH and PMA stimulated prolactin release in a dose-dependent manner. When present together at maximal concentrations, TRH and PMA produced an effect which was slightly less than additive. Pretreatment of rat pituitary cells with 10(-6) M PMA for 24 hrs completely down-regulated protein kinase C, since such PMA-pretreated cells did not release prolactin in response to a second dose of PMA. Interestingly, protein kinase C down-regulation had no effect on TRH-induced prolactin release from rat pituitary cells. In contrast, PMA-pretreated GH3 cells did not respond to a subsequent stimulation by either PMA or TRH. Pretreatment of rat pituitary cells with TRH (10(-7) M, 24 hrs) inhibited the subsequent response to TRH, but not PMA. Forskolin, an adenylate cyclase activator, stimulated prolactin release by itself and in a synergistic manner when incubated together with TRH or PMA. The synergistic effects of forskolin on prolactin release was greater in the presence of PMA than TRH. Down-regulation of protein kinase C by PMA pretreatment abolished the synergistic effect produced by PMA and forskolin but had no effect on those generated by TRH and forskolin. sn-1,2-Dioctanylglycerol (DOG) pretreatment attenuated the subsequent response to DOG and PMA but not TRH. The effect of TRH, but not PMA, on prolactin release required the presence of extracellular Ca2+. In conclusion, the mechanism by which TRH causes prolactin release from rat primary pituitary cells is different from that of GH3 cells; the former is a protein kinase C-independent process whereas the latter is at least partially dependent upon the activation of protein kinase C.

Animals↗
PubMed1989

Effect of selective serotonin (5-HT) agonists and 5-HT2 antagonist on prolactin secretion.

The present study was undertaken to determine the involvement of serotonergic 5-HT1 and 5-HT2 receptor subtypes in stimulation of the secretion of prolactin. Several 5-HT agonists were administered, in a dose-response fashion, to conscious rats and the effect on the levels of prolactin in plasma was measured. The 5-HT1A + 5-HT1B agonist RU 24969 (5-methoxy-3[1,2,3,6-tetrahydropyridin-4-yl]-1H-indole succinate) and the 5-HT1 + 5-HT2 agonist MK-212 (6-chloro-2-[1-piperazinyl]pirazine) increased levels of prolactin in plasma in a dose-dependent manner. In contrast, the selective 5-HT1A agonists 8-OH-DPAT (8-hydroxy-2-[di-n-propylamino]tetralin) and ipsapirone (2-[4-[4-(2-pyrimidinyl)-1-piperazinyl]butyl]-1,2-benzisothiazol-3 -(2H) one-1,1-dioxidehydrochloride) did not increase levels of prolactin in plasma at any dose. The 5-HT-releasing drug, fenfluramine, also increased the concentration of prolactin in plasma. Pretreatment with the selective 5-HT2 antagonist, LY53857 (6-methyl-1-[1-methylethyl]ergoline-8-carboxylic acid, 2-hydroxy-1-methyl propyl ester (Z)-2-butenedioate [1:1]), did not significantly diminish an increase in levels of prolactin in plasma, induced by injection of fenfluramine. The antagonist LY53857 inhibited, but did not block the MK-212- and RU 24969-induced increase in the levels of prolactin in plasma. By deduction, these data suggest that 5-HT1B receptors, or as yet undefined 5-HT receptor subtypes may be involved in the stimulation of the secretion of prolactin by endogenously released 5-HT, and that 5-HT2 receptors may play a minor role in the serotonergic regulation of the secretion of prolactin.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1993

Effects of systemic and central prolactin injections on food intake, weight gain, and estrous cyclicity in female rats.

It has been suggested that prolactin may contribute to the hyperphagia of lactation. Studies examining the effects of the systemic administration of prolactin on food intake, however, have produced varying results. In species other than the rat, central prolactin administration has been found to increase food intake, but it is not known if central prolactin administration increases food intake in rats. In the current study the effects of peripheral and central prolactin administration on food intake, weight gain, and estrous cyclicity in female rats were compared. Prolactin was administered twice daily at 0800 and at 1900 h either subcutaneously at 3 mg/kg or 1 mg/kg b.wt. or by intracerebroventricular (ICV) infusion (2 micrograms/0.5 microliter) for 10 days to female rats. Control animals received similar injections of vehicle. Food intake, body weight, and vaginal smears were taken daily. Results showed that peripheral administration of prolactin increased food intake and weight gain and disrupted vaginal cyclicity. In contrast, ICV administration increased food intake to the same extent as did systemic prolactin administration but had no effect on weight gain or cyclicity. These data suggest that prolactin acts both peripherally and centrally to regulate energy balance in the female rat.

Animals↗
PubMed1993

Differential effects of prolactin upon activation and differentiation of human B lymphocytes.

The effects of human prolactin on enriched peripheral B lymphocytes obtained from healthy males were examined. Immunoregulation by prolactin was studied in B cells activated with either anti-IgM alone, or anti-IgM antibodies and recombinant interleukin-2 (r-IL-2), as well as control resting B cells. Expression of IL-2 receptors (IL-2R), and IgM and IgG in the culture supernatants were used as a measure of B cell activation and differentiation. Prolactin significantly synergized with IL-2 in the enhancement of surface expression of IL-2R on anti-IgM treated B cells. Although no differentiating effect was observed on resting B cells, prolactin (0.2-100 ng/ml) exhibited a dose-dependent enhancement upon both IgM and IgG secretion from B cells treated with anti-IgM and IL-2. In the absence of exogenously added IL-2 similar differentiating effect were observed in B cells treated with anti-IgM at prolactin concentrations of 0.2-10 ng/ml, but not 100 ng/ml. Thus, the present results demonstrate the modulatory effect of prolactin on activation and differentiation of anti-IgM triggered human B cells, and emphasize the importance of co-stimulatory signal mediated by IL-2 in B cell responses to high prolactin levels. These findings extend the immunoregulatory effects of prolactin, previously confirmed for T cells, to the B cell arm of the immune response, and suggest an important role of prolactin in mediating adaptation and communication between the nerve and immune systems.

Adult↗
PubMed1996

Effects of cyclosporin treatment on prolactin pulsatility in chronic hyperprolactinemic male rats.

Neuroendocrine effects of cyclosporin (CsA) have been demonstrated, but the mechanisms involved are poorly understood. This work was designed to analyse (i) if chronic CsA administration could influence the episodic secretion of prolactin in adult male rats; and (ii) the effects of the chronic administration of the drug, in adult animals with elevated plasma prolactin levels. Male rats were implanted with one anterior pituitary gland under the kidney capsule or were sham-operated, at 30 days of age. Both pituitary-grafted and sham-operated rats were injected subcutaneously with vehicle or CsA (5 micrograms/kg/day) for 9 days beginning at the 60th day of age. In pituitary-grafted male rats, mean prolactin levels, absolute prolactin pulse amplitude and mean half-life of the hormone increased, while the pulse frequency and relative amplitude of the peaks decreased, as compared with sham-operated rats. CsA administration to sham-operated rats decreased the relative pulse amplitude of prolactin but increased the mean half-life of the hormone, the pulse duration and the mean hormone levels, as compared with rats of the same group treated with vehicle. However, CsA treatment to pituitary-grafted rats decreased mean prolactin levels and the absolute amplitude of its peaks and increased the relative amplitude of its pulses, whereas all the other parameters showed no change. When considering circulating values of prolactin in plasma from the trunk blood, CsA administration was followed by changes similar to those described when mean values of the serial samples were considered. These data suggest the existence of an interrelationship between elevated circulating prolactin levels and CsA, which probably takes place at the hypothalamic level, to regulate the pulsatile pattern of prolactin secretion in male rats, although a direct effect of the drug on the ectopic gland in pituitary-grafted male rats cannot be excluded.

Animals↗
PubMed1982

Evidence for a coupling of prolactin secretion and synthesis by rat pituitary cells in culture.

The relationship between the release and the synthesis of prolactin by rat pituitary cells in culture was studied using a microtubule-disrupting drug, vinblastine. (1) Prolactin secretion was inhibited by vinblastine in short-term incubations. Vinblastine did not act via the dopamine pathway, since a potent anti-dopaminergic drug, fluphenazine, was unable to reverse the inhibiting action of the antimicrotubular agent. (2) Continuous treatment by vinblastine induced a progressive decrease of the rate of incorporation of [3H]leucine in prolactin. The half-inhibition time was about 2 days. This inhibition of prolactin synthesis was selective, since total protein synthesis remained unaffected. (3) Measurements of radioimmunoassayable prolactin showed that the inhibition of hormone release by vinblastine led to a transient increase of the intracellular content of prolactin. The phase of over-accumulation was followed by a progressive reduction of the total (cell + medium) prolactin. This result is in agreement with the observed inhibition of de novo synthesis of prolactin and indicates that a degradation process takes place in pituitary cells in culture. In conclusion, the use of vinblastine allows us to demonstrate that the rate of prolactin synthesis is dependent upon the secretory status of the cell.

Animals↗
PubMed1989

Studies on the mechanism by which prolactin regulates protein, RNA, and DNA synthesis in Nb2 node lymphoma cells.

Specific aspects of the prolactin stimulation of RNA, DNA and protein synthesis in the Nb2 node lymphoma cell line were determined. In time sequence studies the onset of the prolactin stimulation of the incorporation of radiolabeled precursors into these macromolecules was found to be 0.5-1 h for [3H]uridine incorporation into RNA, 1-2 h for [3H]leucine incorporation into protein, and 4-8 h for [3H]thymidine incorporation into DNA. The total DNA content of the cell cultures was increased by 12-18 hours after addition of prolactin. Amiloride, an inhibitor of the plasma-membrane-bound Na+/H+ antiporter, was found to inhibit the mitogenic effects of prolactin. Amiloride was also found to inhibit the prolactin stimulation of DNA, RNA and protein synthesis, thus suggesting that the initial regulation of the Na+/H+ antiporter may initiate these responses as well as the mitogenic effect of prolactin. In contrast, H-7, a drug which inhibits protein kinase C, had no effect on the magnitude of the prolactin stimulation of DNA, RNA or protein synthesis at a drug concentration (100 muM) that abolished the mitogenic effect of prolactin. The early effects of prolactin on RNA, DNA and protein synthesis would therefore appear not to involve an activation of protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Evidence for immunomodulatory properties of prolactin in selected in vitro and in vivo situations.

The relationship between neuroendocrine regulation and the immune system has recently become the subject of intense investigations. The pituitary secretes both immunostimulatory (growth hormone and prolactin) and immunosuppressive (ACTH) hormones, and is thus involved in the control of immune functions. The present work was aimed at the study of the immunoregulatory properties of prolactin in selected in vitro and in vivo model situations. Prolactin was found to enhance recovery of the receptor for sheep red blood cells (in vitro). Compared with control cells, incubation with prolactin and/or prolactin containing sera significantly enhanced the capacity of trypsin treated lymphocytes from the peripheral blood of healthy volunteers to form E-rosettes. Chlorpromazine stimulated prolactin release in males, and lactation stimulated prolactin release in females raised the number of large granular lymphocytes in peripheral circulation. Sera containing elevated prolactin levels stimulated the metabolic activity of peripheral neutrophilic leukocytes. These results suggest that prolactin may stimulate selective functions of cellular immunity, and that it is involved in interactions between the nervous, the hormonal and the immune systems.

Adult↗
PubMed1981

Age related changes in the control of prolactin secretion in the female rat.

The purpose of this investigation was to evaluate the effects of advancing age on the control of pituitary prolactin secretion. The effects of dopaminergic inhibition and estrogen stimulation of pituitary prolactin secretion were tested both in vivo and in vitro. Estrogen stimulated prolactin secretion in both old and young animals, and elevated estrogen levels in old rats may be partially responsible for elevated prolactin levels. Oral L-DOPA administration induced cycles in old rats but had no effect on prolactin levels in either old or young rats. Injections of L-DOPA lowered prolactin in young but not in old rats, while apomorphine reduced prolactin levels in both groups. The pituitaries of young rats secrete more prolactin in vitro than old pituitaries, further supporting a decrease in hypothalamic DA turnover as a cause for elevated prolactin levels in old rats.

Aging↗
PubMed1984

Different subcellular storage sites for decidual- and pituitary-derived prolactin: possible explanation for differences in regulation.

The intracellular sites of storage for human decidual- and pituitary-derived prolactins have been determined by measuring the hormones in subcellular fractions following differential and density gradient centrifugations. In decidual tissue, 78 +/- 4% (mean +/- SE, n = 5) of the prolactin was detected in the post-microsomal supernatant, while 98% of the prolactin in the pituitary was detected in mitochondrial and microsomal particulate fractions. Following centrifugation on sucrose density gradients, decidual prolactin was distributed diffusely throughout the gradients, while greater than 90% of the pituitary prolactin sedimented as a single peak with a mean density of 1.22 g/cm3. These studies indicate that, unlike pituitary prolactin, decidual prolactin is not stored in secretory granules. Differences in the intracellular storage sites of decidual and pituitary prolactins may explain observed differences in the regulation of prolactin secretion by decidual and pituitary tissues.

Animals↗
PubMed1985

Calcium mobilization potentiates prolactin release induced by protein kinase C activators.

The in vitro effect of synthetic diacylglycerol (DG) and phorbol myristate acetate (PMA), potent stimulators of protein kinase C, was studied on prolactin release. These substances increased, in a concentration-dependent manner, prolactin release from primary cultures of anterior pituitary cells. Similarly, exposure of pituitary cells to phospholipase C, which liberates endogenous DG from various substrates, also enhanced prolactin release. The effect of Ca2+ mobilization on PMA-, synthetic DG- or phospholipase C-induced prolactin release was examined. A23187 at 400 nM or 2 ng/ml maitotoxin, a Ca2+ channel activator, did not affect prolactin release by themselves, but enhanced the release of prolactin induced by DG, PMA or phospholipase C. The stimulatory effects of DG, PMA and phospholipase C on prolactin release were reduced by co-incubation with dopamine. These results suggest that the presumed activation of protein kinase C by DG and mobilization of Ca2+ may be synergistically involved in the regulation of prolactin release. Dopamine appears to inhibit prolactin release at a point distal to the DG-enhanced stimulation of the process.

Animals↗
PubMed1990

A high concentration of dopamine preferentially permitted release of newly synthesized prolactin.

We used continuous labelling ([3H]leucine) of cultured adenohypophysial cells to investigate the relationship between the storage and release of newly synthesized and stored prolactin in response to dopamine (1 mumol/l) and thyrotropin-releasing hormone (TRH) (0.1 mumol/l) challenge. Newly synthesized prolactin was identified by the tritium radiation activity incorporated in prolactin. A maximal dose of dopamine (1 mumol/l) could not completely block prolactin release from a primary culture of lactotrophs. During 3 h of continuous labelling under maximal dopaminergic inhibition, newly synthesized prolactin was released which was of a significantly higher specific activity than control groups. In contrast, TRH stimulation produced results consistent with previous observations of the release of predominantly old, stored hormone. However, the absolute amount of the newly synthesized prolactin was increased by the TRH administration, and the increased release of the newly synthesized prolactin could be accounted for by increased levels of synthesis. Our results are consistent with the concept of the existence of a regulated route and a dopamine-insensitive constitutive route of prolactin release which predominantly encompasses newly synthesized hormone. However, the possibility that cellular heterogeneity or that non-dopaminergic prolactin-release inhibiting factor(s) (PIF) is responsible for this observed release cannot be ruled out.

Animals↗
PubMed1994

Sequence and regulation of European eel prolactin mRNA.

cDNA clones encoding the European eel (Anguilla anguilla L.) prolactin were isolated from a pituitary cDNA library constructed in gamma gt10, using a rainbow trout Prl cDNA fragment as a probe. Four different inserts were subcloned into the pGEM 3Z plasmid after PCR amplification. The 1082 bp-long nucleotide sequence revealed an open reading frame of 627 bp encoding a 24 amino acid-long signal peptide followed by a 185 amino acid-long mature protein. Comparison studies showed 60-70% homology with other known teleost fish prolactins and 30-45% with non-teleost fish, amphibian, reptilian, avian and mammalian prolactins. In situ hybridization studies using labelled prolactin RNA probe showed a strong signal in the rostral pars distalis of the pituitary gland. We next examined the physiological regulation of this prolactin synthesis in vivo using Northern blot analysis and prolactin cDNA probe labelled by random priming. The pituitary prolactin mRNA level was markedly decreased 3 weeks after transfer of eels from freshwater to sea water. Implants of thyroid hormones left for up to three weeks were ineffective on prolactin mRNA. Estradiol administered as implant, alone or in combination with 500 micrograms testosterone, was also unable to significantly alter the pituitary mRNA level for prolactin in the freshwater silver eels whatever the dose used (20-500 micrograms) and whatever the duration of treatment (from 4 days to 10 weeks).

Amino Acid Sequence↗
PubMed1987

Effects of age, season and active immunization against estrogen on serum prolactin concentrations in stallions.

Prolactin concentrations in stallion serum were measured by radioimmunoassay based on antiserum generated against equine prolactin and radioiodinated canine prolactin. Prolactin concentrations in serum collected from 152 stallions at a slaughterhouse were higher (P less than .01) in summer than in winter (5.7 +/- .15 vs 2.0 +/- .17 ng/ml). Moreover, there was an effect of age (P less than .02) in the analysis of variance; there was no interaction between age and season. In general, prolactin concentrations increased with age up to 3 to 5 years. Samples of serum collected from five control and five estrogen-immunized stallions from 6 to 26 months of age also were assessed for prolactin concentration. Active immunization against estrogen had no effect (P greater than .10) on prolactin concentrations. In contrast, whether analyzed by age or by month of the year, prolactin concentrations varied with time (P less than .01) in these stallions. Averaged over both groups, concentrations were high during summer and low during winter and were also gradually increasing with time as indicated by a linear trend (P less than .01) in the data. It is concluded that serum prolactin concentrations in stallions 1) are seasonal, as in many other seasonally breeding species, 2) in general are highest in older stallions and lowest in young stallions and 3) are not affected by active immunization against estrogens.

Aging↗