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PubMed2002

IGF-2 is a mediator of prolactin-induced morphogenesis in the breast.

The mechanisms by which prolactin controls proliferation of mammary epithelial cells (MECs) and morphogenesis of the breast epithelium are poorly understood. We show that cyclin D1(-/-) MECs fail to proliferate in response to prolactin and identify IGF-2 as a downstream target of prolactin signaling that lies upstream of cyclin D1 transcription. Ectopic IGF-2 expression restores alveologenesis in prolactin receptor(-/-) epithelium. Alveologenesis is retarded in IGF-2-deficient MECs. IGF-2 and prolactin receptor mRNAs colocalize in the mammary epithelium. Prolactin induces IGF-2 mRNA and IGF-2 induces cyclin D1 protein in primary MECs. Thus, IGF-2 is a mediator of prolactin-induced alveologenesis; prolactin, IGF-2, and cyclin D1, all of which are overexpressed in breast cancers, are components of a developmental pathway in the mammary gland.

Animals↗
PubMed2003

Delusions of pregnancy associated with increased prolactin concentrations produced by antipsychotic treatment.

Treatment of psychotic symptoms has traditionally involved conventional antipsychotics. While efficacious, their side-effects have been problematic and the approval by the Food and Drug Administration of the newer antipsychotics with improved side-effects profiles heralded important advances in treating psychoses. Prolactin elevation has been associated with all classical and some atypical antipsychotics. We present cases where elevation of prolactin concentrations secondary to antipsychotic treatment was associated with delusions of pregnancy. Risperidone was the antipsychotic employed and elevation of prolactin concentrations were noted each time. The delusions abated and prolactin concentrations decreased when the drug was discontinued. Rechallenge with risperidone resulted in re-elevation of prolactin levels along with recurrent delusions. Substituting risperidone with another antipsychotic (either olanzapine or quetiapine) also led to abatement of the delusions and lowering of prolactin. Although no direct psychotogenic effects of prolactin are known, it is contended that delusions of pregnancy reported during antipsychotic treatment might be associated with rising prolactin concentrations.

Adult↗
PubMed2004

Prolactin response to d-fenfluramine in combat-related post-traumatic stress disorder.

Central serotonergic function can be investigated by measuring the prolactin response to the serotonin releasing/uptake agent, d-fenfluramine. This study investigated the effect of diagnosis, depressive symptoms and history of alcohol or tobacco abuse or dependence on the d-fenfluramine test in combat-related post-traumatic stress disorder (PTSD). Male, non-hospitalized combat-exposed veterans diagnosed with PTSD (DSM-III-R) and a similarly aged combat-exposed control group were assessed for both PTSD and depressive symptoms and prolactin responses to a 30-mg d-fenfluramine challenge test. Ninety-five subjects were studied; 23 were controls, 46 subjects met the criteria for current PTSD and 26 for past PTSD. There were no significant differences between the three groups for baseline prolactin, peak prolactin, and time to reach peak, delta prolactin or area under the curve of the prolactin vs. time curve. Depressive symptoms and history of alcohol or tobacco abuse or dependence did not have a confounding effect on the prolactin responses to d-fenfluramine. This study suggests that a blunted prolactin response to d-fenfluramine may be a consequence of combat exposure rather than PTSD. To confirm this, further studies involving both healthy and combat-exposed control groups in addition to subjects with PTSD of similar ages are required.

Adult↗
PubMed1982

Conformational studies of secreted mouse pituitary prolactin.

A secreted form of mouse pituitary prolactin has been shown to contain only a single tryptophan residue. All previously reported prolactins contain two tryptophans. Circular dichroism spectra indicate that secreted mouse prolactin is conformationally similar to stored forms of prolactin previously isolated from several other species, including its alpha-helix content (65%). However, like secreted rat prolactin, secreted mouse prolactin shows no tryptophan signal in its circular dichroism spectrum. All stored forms of prolactin studied to date display distinct tryptophan signals. This suggests the possibility that secretion of prolactin may be accompanied by modification of the protein's tertiary structure.

Animals↗
PubMed2003

Prolactin and paternal care: comparison of three species of monogamous new world monkeys (Callicebus cupreus, Callithrix jacchus, and Callimico goeldii).

The authors explored whether prolactin is associated with paternal care in 3 monkey species: titi monkey (Callicebus cupreus), common marmoset (Callithrix jacchus), and Goeldi's monkey (Callimico goeldii). They compared prolactin levels in fathers before and after infant birth as well as between fathers and nonfathers. C. cupreus fathers carry infants almost exclusively, have higher prolactin levels than nonfathers, but show no prolactin increase after infant birth. C. goeldii fathers carry infants only after 3 weeks, show an increase in prolactin levels during the precarrying period, but do not have higher levels than nonfathers. C jacchus fathers are the primary carriers, have higher prolactin levels than nonfathers, and show a trend for a prolactin increase after the birth of infants. In conclusion, species differences in the patterns of prolactin secretion were evident and reflect the different paternal roles.

Animals↗
PubMed1980

Oestrogens regulate divergent effects of prolactin in the ovary.

Prolactin exerts well established stimulatory effects both in vitro and in vivo in the rat ovary. However, in the ovary of higher mammals, prolactin action is not well characterised, and may differ from that observed in rodents. For example, in human clinical conditions of physiological or pathological prolactin excess, ovarian function is depressed, and in isolated, human granulosa cells in vitro, prolactin seems to inhibit progesterone production. To examine direct prolactin effects in the higher mammalian ovary, we have used an in vitro porcine granulosa-cell model. In this system, prolactin action is bipotential, depending critically on the degree of granulosa-cell differentiation attained in vivo. Prolactin suppresses steroid production by cultured granulosa cells isolated from small (1-2 mm), immature follicles, but stimulates progesterone secretion by granulosa cells collected from large (greater than 6 mm) mature follicles. The present studies show that oestrogens may play an important part in regulating these divergent actions of prolactin in the ovary.

Animals↗
PubMed1976

Osmotic control of prolactin release and its effect on renal water excretion in man.

Prolactin appears to play a role in osmoregulation of fishes and birds and a possible contribution of this hormone to the regulation of salt and water excretion in mammals has been suggested as well. The present studies were undertaken to investigate the role of osmotic pressure on the secretion of prolactin and the effect of the hormone on renal water excretion in man. The i.v. administration of synthetic thyrotropin releasing hormone (TRH) (7 mug/kg) to five subjects undergoing a maximal sustained water diuresis increased serum prolactin to supraphysiologic levels in all as mean concentration rose from 30.2 +/- 2.9 to 60.2 +/- 5.0 ng/ml (P less than 0.005). This increase was not associated with either significant alterations in renal hemodynamics or sodium excretion and water excretion. The osmoregulation of prolactin release was then investigated by the oral administration of 20 ml/kg of water to seven subjects in 11 studies. While the water load decreased serum osmolality from 293 +/- 285 +/- 1.5 mOsm/kg H2O (P less than 0.001), there was no significant change in prolactin level, 28+/- 1.8 to 30 +/- 2.4 ng/ml. Serum hypertonicity was achieved in six subjects with the infusion of 5% NaCl which increased serum osmolality from 287 +/- 1.8 to 298 +/- 1.4 mOsm/kg (P less than 0.001). While the hypertonic state caused a marked antidiuresis as urinary osmolality rose from 62 +/- 5.9 to 480 +/- 48 mOsm/kg (P less than 0.001), the concentration of prolactin remained unchanged at 28 ng/ml. We conclude that supraphysiologic levels of prolactin have no antidiuretic properties in a vasopressin-free state and that acute alterations in serum tonicity within the range observed do not affect the release of prolactin in man.

Adolescent↗
PubMed2000

Physiopathology of prolactin secretion in obesity.

In many species prolactin is of biological importance and has a major role in determining the deposition and mobilization of fat. In human physiology, outside pregnancy, prolactin secretion is altered by increasing body weight in both children and adults. Prolactin in this circumstance appears to be marker of hypothalamic-pituitary function: the prolactin response to insulin-hypoglycaemia, thyrotrophin releasing hormone stimulation and other stimulatory factors may be diminished. In addition, obesity alters the 24h spontaneous release of prolactin with a generalised dampening of release. A number of explanations have been given as possible causes for these alterations, but it seems likely that they reflect obesity per se and are associated with hyperinsulinaemia. Weight reduction, with accompanying decrease in plasma insulin levels, leads to a normalization of prolactin responses in most, but not all, circumstances. To date, no molecular basis has been identified which links prolactin with increasing body fatness, weight and appetite: new data suggests a possible link in obese men between fasting plasma prolactin and leptin concentrations.

Adrenal Glands↗
PubMed1979

Biosynthesis and degradation of prolactin in the rat anterior pituitary gland. Time course of incorporation of label in vitro and evidence for rapid degradation.

Biosynthesis of prolactin was studied in anterior pituitary glands from female rats, incubated in vitro. In this system [3H]leucine was incorporated into pituitary proteins, including somatotropin (growth hormone) and prolactin. The rate of uptake of label into prolactin (and to a lesser extent into total protein) slowed considerably during the first 2 h of incubation, although the rate of uptake into somatotropin was constant for 8 h. The most probable explanation for this apparent decrease in the rate of prolactin synthesis is degradation of prolactin in the gland. Degradation of this hormone was also demonstrated by incubating prelabelled pituitaries in unlabelled medium and following the content of labelled prolactin, and by studying the hormonal content of pituitary glands (by radioimmunoassay) before and after incubation. Degradation of prolactin appears to be much more rapid than that of somatotropin, and may represent a physiological mechanism whereby over-accumulation of prolactin is prevented when secretion of the hormone has been rapidly switched off.

Animals↗
PubMed1981

Effects of dopamine on prolactin secretion and cyclic AMP accumulation in the rat anterior pituitary gland.

The effects of dopamine on pituitary prolactin secretion and pituitary cyclic AMP accumulation were studied by using anterior pituitary glands from adult female rats, incubated in vitro. During 2h incubations, significant inhibition of prolactin secretion was achieved at concentrations between 1 and 10nm-dopamine. However, 0.1-1mum-dopamine was required before a significant decrease in pituitary cyclic AMP content was observed. In the presence of 1mum-dopamine, pituitary cyclic AMP content decreased rapidly to reach about 75% of the control value within 20min and there was no further decrease for at least 2h. Incubation with the phosphodiesterase inhibitors theophylline (8mm) or isobutylmethylxanthine (2mm) increased pituitary cyclic AMP concentrations 3- and 6-fold respectively. Dopamine (1mum) had no effect on the cyclic AMP accumulation measured in the presence of theophylline, but inhibited the isobutylmethylxanthine-induced increase by 50%. The dopamine inhibition of prolactin secretion was not affected by either inhibitor. Two derivatives of cyclic AMP (dibutyryl cyclic AMP and 8-bromo cyclic AMP) were unable to block the dopamine (1mum) inhibition of prolactin secretion, although 8-bromo cyclic AMP (2mm) significantly stimulated prolactin secretion and both compounds increased somatotropin (growth hormone) release. Cholera toxin (3mug/ml for 4h) increased pituitary cyclic AMP concentrations 4-5-fold, but had no effect on prolactin secretion. The inhibition of prolactin secretion by dopamine was unaffected by cholera toxin, despite the fact that dopamine had no effect on the raised pituitary cyclic AMP concentration caused by this factor. Dopamine had no significant effect on either basal or stimulated somatotropin secretion under any of the conditions tested. We conclude that the inhibitory effects of dopamine on prolactin secretion are probably not mediated by lowering of cyclic AMP concentration, although modulation of the concentration of this nucleotide in some other circumstances may alter the secretion of the hormone.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Isolation and characterization of phosphorylated bovine prolactin.

Quantitative isolation of bovine prolactin was accomplished by immunoaffinity chromatography using clonal antibody as the stationary ligand. The phosphorylated and non-phosphorylated (native) prolactins contained in the immunopurified preparations were separated by chromatofocusing. Isolates from individual pituitaries revealed that phosphorylated prolactin represented between 20 and 80% of the total prolactin. The stoichiometry of phosphate in phosphorylated prolactin was 1.4:1 when determined by amino acid analysis after preparation of the S-ethylcysteine derivative. One major phosphorylation site, serine-90, and two minor sites, serine-26 and -34, were determined by mapping and sequencing studies. Serine-90 was conserved in prolactins, growth hormones and placental lactogens. Serine-26 and -34 were conserved in prolactins, but were not found in growth hormones or placental lactogens. Absorption spectroscopy of the aromatic amino acid residues indicated that phosphorylation of prolactin was associated with a unique structural conformation.

Amino Acid Sequence↗
PubMed2001

Excitotoxic lesions of the medial amygdala differentially disrupt prolactin secretory responses in cycling and mated female rats.

This study examined the role of the posterodorsal medial amygdala (MePD) in the control of prolactin secretion in gonadally intact female rats 20 min after mating, during the oestrous cycle, and during early pregnancy/pseudopregnancy (P/PSP). Cycling females received bilateral infusions of an excitotoxic dose of N-methyl-D-aspartate (NMDA) or vehicle into the MePD. Two to 4 weeks later, they were surgically implanted with intra-atrial catheters for repeated blood sampling and were mated on the evening of proestrus until receiving 5, 10, 15 or 20 intromissions or 15 mounts-without-intromission (MO) from males. The percentages of rats becoming P/PSP increased as a function of numbers of intromissions received. All groups receiving intromissions showed similar approximately four-fold increases in plasma prolactin concentrations 20 min after mating, while MO rats showed no increase at this time. There was no effect of NMDA lesion on this acute secretory response. Among rats that continued cycling, bilateral MePD lesion completely abolished the diurnal preovulatory prolactin surge, while incomplete and sham lesions did not. In rats that subsequently became P/PSP, bilateral lesion of the MePD resulted in dampening of prolactin concentrations at all sampling times 6-7 days after mating, while incomplete or sham lesions did not alter prolactin secretion at these times. These results demonstrate that the MePD is selectively important for the secretion of prolactin on the afternoon of proestrus and that this structure may also modulate prolactin release in P/PSP rats. Activity within MePD neurones does not appear to be required for the acute prolactin response to vaginocervical stimulation which occurs within minutes after mating.

Amygdala↗
PubMed2003

Opioid receptor subtypes involved in the regulation of prolactin secretion during pregnancy and lactation.

Afferent endogenous opioid neuronal systems facilitate prolactin secretion in a number of physiological conditions including pregnancy and lactation, by decreasing tuberoinfundibular dopamine (TIDA) inhibitory tone. The aim of this study was to investigate the opioid receptor subtypes involved in regulating TIDA neuronal activity and therefore facilitating prolactin secretion during early pregnancy, late pregnancy and lactation in rats. Selective opioid receptor antagonists nor-binaltorphimine (kappa-receptor antagonist, 15 micro g/5 micro l), beta funaltrexamine (mu-receptor antagonist, 5 microg/5 microl) and naltrindole (delta-receptor antagonist, 5 microg/5 microl) or saline were administered intracerebroventricularly (i.c.v.) on day 8 of pregnancy during a nocturnal prolactin surge, on day 21 of pregnancy during the ante partum prolactin surge or on day 7 of lactation before the onset of a suckling stimulus. Serial blood samples were collected at regular time intervals, via chronic indwelling jugular cannulae, before and after drug administration and plasma prolactin was determined by radioimmunoassay. TIDA neuronal activity was measured using the 3,4-dihydroxyphenylacetic acid (DOPAC) : dopamine ratio in the median eminence 2 h 30 min after i.c.v. drug injection. In each experimental condition, plasma prolactin was significantly inhibited by both kappa- and mu-receptor antagonists, whereas the delta-receptor antagonist had no effect compared to saline-injected controls. Similarly, nor-binaltorphimine and beta funaltrexamine significantly increased the median eminence DOPAC : dopamine ratio during early and late pregnancy, and lactation whereas naltrindole had no effect compared to saline-injected controls. These data suggest that TIDA neuronal activity, and subsequent prolactin secretion, is regulated by endogenous opioid peptides acting at both kappa- and mu-opioid receptors during prolactin surges of early pregnancy, late pregnancy and lactation.

Animals↗
PubMed2003

Prolactin and oxytocin interaction in the paraventricular and supraoptic nuclei: effects on oxytocin mRNA and nitric oxide synthase.

We investigated the contribution of prolactin and oxytocin to the increase in staining for NADPH-d and oxytocin mRNA in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) observed at the end of pregnancy, or following a steroid-priming regimen that mimics the hormonal profile of late pregnant females. Ovariectomized rats received chronic implants of silastic capsules containing oestrogen and progesterone followed by progesterone removal. In experiment 1, oxytocin antagonist (OTA) was administered to rats to investigate whether intranuclear oxytocin release was necessary for NADPH-d staining. In experiments 2a and b, rats received concurrent treatment with bromocryptine (0.5 mg/day) to suppress endogenous prolactin release, and either systemic prolactin (0.5 mg once daily), or prolactin (2 micro g/ micro l), or vehicle infused twice a day into the third ventricle, or chronic oxytocin infusion (24 ng/day) for 3 days following progesterone removal. Brains were then processed for NADPH-d histochemistry. In experiment 3, the interaction of prolactin and oxytocin on oxytocin mRNA within the SON and PVN was examined. NADPH-d staining in the SON and PVN was reduced by the highest dose of the OTA, and by bromocryptine treatment. Central prolactin and oxytocin replacement completely restored NADPH-d staining in bromocryptine-treated rats. Finally, both bromocryptine and the OTA suppressed oxytocin mRNA expression and prolactin replacement restored expression levels to that of controls. Together, these data suggest that the increased capacity to produce nitric oxide in the SON and PVN during late pregnancy is dependent on prolactin stimulating oxytocin gene mRNA and hence intranuclear oxytocin release.

Animals↗
PubMed1999

Serum prolactin in neonatal seizures.

BACKGROUND: Prolactin is the most specific neurohormone that is elevated after seizures. This study was undertaken to determine the clinical usefulness of plasma prolactin as a diagnostic aid in differential diagnosis of neonatal convulsions. METHODS: Forty-five patients followed for seizures were included in the study. Postictal serum prolactin levels were obtained 30 min after the onset of the seizures. A second sample obtained 24 h later was used to measure an unstimulated serum prolactin level. RESULTS: The most common cause of seizure was hypoxic ischemic encephalopathy (HIE) followed by sepsis. In patients with HIE, postictal serum prolactin levels were significantly higher than the unstimulated levels (P < 0.0002). Additionally, postictal prolactin levels were significantly higher than the unstimulated levels in clonic (P < 0.02) and tonic convulsions (P < 0.001). CONCLUSIONS: We conclude that the postictal serum prolactin level may be a marker in the differentiation of seizures as well as providing important information about their etiology. Further studies are needed to assess the normal range of serum prolactin levels in unstressed newborns.

Biomarkers↗
PubMed1990

Prolactin secretion in myotonic dystrophy.

In order to evaluate prolactin secretion in females with myotonic dystrophy (MD) prolactin responses to TRH, metoclopramide and bromocriptine were studied in 13 women with myotonic dystrophy (10 normoprolactinaemic and 3 hyperprolactinaemic) and 8 healthy women. Following TRH administration mean maximal net increase was significantly higher in a group of normoprolactinaemic patients with MD in comparison to controls (p less than 0.05). In three patients with increased basal prolactin levels an exaggerated prolactin response to TRH has been observed. Normal prolactin response in a group of normoprolactinaemic as well as in hyperprolactinaemic patients have been observed following metoclopramide bolus injection. Following bromocriptine administration, maximal net decrease in prolactin levels has been found to be greater in normoprolactinaemic patients compared to healthy subjects, although the difference was statistically insignificant. The suppressive action of bromocriptine was more pronounced in patients with hyperprolactinaemia. Those results showed that there is some derangement in prolactin secretion in myotonic dystrophy leading to increased prolactin levels in some patients. Although the mechanism of this derangement has not been clarified yet it seems that it is not mediated via dopaminergic receptors.

Adult↗
PubMed1994

Temporal effects of prolactin on casein kinase activity, casein synthesis and casein mRNA accumulation in mouse mammary gland explants.

Studies were carried out to investigate the mechanism by which prolactin stimulates casein synthesis in cultured mouse mammary tissues. The onset of the prolactin stimulation of casein synthesis occurs 8-10 hours after prolactin addition to cultured tissues; a maximum effect is evoked by 16 hours. A similar time-course of response to prolactin was observed when the tissue accumulation of the mRNA for beta-casein was determined. At 16 hours, however, prolactin had no effect on tissue-specific casein kinase activity which is associated with the Golgi apparatus. These studies suggest that the tissue content of casein mRNA is causally related to the onset of the prolactin stimulation of casein synthesis in cultured mouse tissues. In contrast, the activity of the kinase that catalyzes the phosphorylation of the caseins is not altered by prolactin and thus apparently is not a contributing factor to the early prolactin effect on casein synthesis.

Animals↗
PubMed1985

Ovine prolactin potentiates the action of adrenocorticotropic hormone on the secretion of dehydroepiandrosterone sulfate and dehydroepiandrosterone from cultured bovine adrenal cells.

To determine the direct effect of prolactin on adrenal androgen secretion, the daily secretions of dehydroepiandrosterone sulfate (DHEA-S), dehydroepiandrosterone (DHEA), androstenedione and cortisol were determined in monolayer culture of bovine adrenal cells in the presence or absence of adrenocorticotropic hormone (ACTH) and/or prolactin. In the absence of ACTH ovine prolactin alone had no effect on steroid secretion during seven-day culture. Ovine prolactin, when administered in combination with ACTH, significantly potentiated the stimulatory effect of ACTH on DHEA-S and DHEA but not androstenedione secretion on the seventh day in culture. On the first day in culture prolactin showed no synergistic effect with ACTH on DHEA and DHEA-S secretion, although ACTH significantly increased DHEA and cortisol secretion. DHEA-S secretion increased as a function of prolactin concentration in the presence of ACTH. These results indicated that long-term treatment by ovine prolactin with ACTH caused the increase in adrenal androgen secretion from bovine adrenal cells. The site of action of prolactin was suggested to be the partial inhibition of adrenal 3 beta-hydroxysteroid dehydrogenase by the result of increases in DHEA-S and DHEA but not androstenedione secretion.

Adrenal Glands↗