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PubMed1979

Inherent ranges of seminal prolactin in pre- and postvasectomy subjects.

Seminal immunoreactive prolactin (i prolactin) was studied in 14 healthy subjects, ages 31 +/- 2 SEM, before and after undergoing elective vassectomy for birth control. Seminal plasma was separated within 2 hours of ejaculation, and prolactin was measured in duplicate by radioimmunoassay. The difference between the prevasectomy (mean +/- SEM 11.1 +/- 0.8 ng/ml) and postvasectomy seminal i prolactin (mean +/- 9.9 +/- 0.7 ng/ml) was statistically significant (mean +/- SEM 1.21 +/- 0.53 ng/ml, paired t-test, t = 2.36, P < 0.05). The mean prevasectomy seminal prolactin correlated with the corresponding mean postvasectomy value of the same subject (linear regression analyses, r = 0.77, P < 0.001). This study suggested that the accessory sex organs were the major source of seminal immunoreactive prolactin, and that a minor contribution might come from the in vivo presence of spermatozoa and/or testicular secretions. It also suggested that the magnitude of seminal immunoreactive prolactin was characteristic for each individual.

Adult↗
PubMed1983

[Comparison of the mechanism of action of insulin and prolactin].

One of the major actions of prolactin in the mammary cell is to activate the expression of casein genes by enhancing the transcription rate of the genes. Anti-prolactin receptor antibodies can mimic prolactin action when added to mammary cells, suggesting that a relay is formed at the membrane level and transferred to the target genes. None of the classical hormone intracellular relays can account for the transfer of the prolactin message. The incubation of membranes from various tissues containing prolactin receptor with prolactin provokes the release of a factor which specifically accelerates the transcription of the beta-casein gene in isolated mammary nuclei. The factor is thermostable, inactivated by trypsin and is eluted from G-10 Sephadex as a molecule smaller than 1000 daltons. The action of the factor is prevented by phosphatase inhibitors. These results are strikingly reminiscent of those obtained with insulin which activates enzymes via a factor released from the membranes and which dephosphorylates the enzymes. The analogy between the action mechanism of prolactin and insulin is discussed.

Animals↗
PubMed1978

Prolactin responses to neuroleptics in normal and schizophrenic subjects.

The prolactin response to neuroleptics can serve as an index of dopamine blockade in humans. Plasma prolactin increments to single doses of chlorpromazine, and prolactin decrements to single doses of levodopa, were similar in normal and schizophrenic subjects. Antischizophrenic drugs of all chemical classes stimulated prolactin release,while chemically related drugs and other psychotropic agents ineffective in schizophrenia did not. The prolactin response to neuroleptic therapy occurred in all patients, and tolerance did not develop. Within subjects, prolactin responses were graded according to neuroleptic dose, but the upper limit of sensitivity of the response curve was achieved at doses below the therapeutic range. Relative prolactin-stimulating potency in humans of chlorpromazine, thioridazine, trifluoperazine, butaperazine, and haloperidol correlated well with their relative clinical potencies.

Chlorpromazine↗
PubMed1978

Neuroleptic-induced prolactin level elevation and breast cancer: an emerging clinical issue.

This article reviews the evidence that neuroleptics may increase the risk of breast cancer via their effects on prolactin secretion. All available neuroleptics, including reserpine, raise serum prolactin levels. Elevated serum prolactin level increases the incidence of spontaneously occurring mammary tumors in mice, and increases the growth of established carcinogen-induced mammary tumors in rats. Caution is necessary in extrapolating this relationship to human mammary tumors because human and rodent tumors differ in some important characteristics, including hormone responsiveness. Serum prolactin levels in women with, or at risk for, breast cancer have generally been normal, and only a minority of human mammary tumors respond to changes in serum prolactin levels. Epidemiologic studies have failed to demonstrate an increased risk of breast cancer associated with the use of neuroleptics or reserpine. Thus, although some human mammary tumors are prolactin dependent, the available evidence does not demonstrate an increased risk of breast cancer in women receiving neuroleptics. We conclude that (1) additional epidemiologic studies of the incidence of mammary tumors in women treated with neuroleptics are desirable; (2) it is premature to mandate warning patients of an unknown and undemonstrated increase in the risk of developing breast cancer associated with neuroleptic treatment; (3) detection of existing mammary tumors by breast examination prior to administration of neuroleptics is desirable; and (4) development of antipsychotic drugs that do not increase serum prolactin level may be indicated.

Animals↗
PubMed2001

Characterization of a prolactin gene polymorphism and its associations with systemic lupus erythematosus.

OBJECTIVE: Hyperprolactinemia is associated with systemic lupus erythematosus (SLE), but the mechanism is unknown. Prolactin is expressed in T lymphocytes and is under the control of an alternative promoter region. We characterized a G/T single-nucleotide polymorphism (SNP) at position -1149 of this promoter and assessed its prevalence in patients with SLE. METHODS: Electrophoretic mobility shift assays (EMSAs) were performed to determine DNA protein complex formation in the prolactin promoter. Transient transfection of reporter gene constructs containing the G/T promoter alleles into the Jurkat T cell line were used to determine transcription activity. Peripheral blood lymphocytes (PBLs) were treated in vitro with phytohemagglutinin (PHA) to determine levels of prolactin messenger RNA (mRNA). RESULTS: EMSAs indicated that binding of a GATA-related transcription factor was altered by the G/T SNP at position -1149. Transient transfection studies in Jurkat cells showed that the G allele consistently produced higher promoter activity. PHA treatment of PBLs in vitro induced a greater increment of prolactin mRNA from patients with the GG(-1149) genotype than from those with the TT(-1149) genotype. Disease association studies in a cohort of SLE patients demonstrated an increased frequency of the prolactin -1149 G allele compared with control subjects. CONCLUSION: We found a functionally significant polymorphism that alters prolactin promoter activity and mRNA levels in the lymphocytes. Altered local prolactin production by immune cells may contribute to disease progression by affecting T cell function.

Alleles↗
PubMed1991

Capillary prolactin measurement for diagnosis of seizures.

Measurement of serum prolactin levels can be useful in the diagnosis of epilepsy, since prolactin levels often rise after seizures, but not after most imitators of epilepsy. Utility of the test is limited by the need to obtain blood 10 to 20 minutes after the episode. The present study documents the validity of prolactin measurements using capillary blood, which was obtained by the finger-stick method after a possible seizure and then applied to filter paper. Venous and capillary prolactin levels were determined 10 to 20 minutes after seizure-like episodes in 20 patients who were studied in an epilepsy monitoring unit. Venous and capillary prolactin values correlated, with a Pearson coefficient of 0.90. Using a criteria of any elevation above the laboratory upper limit of normal, capillary prolactin values correctly identified seizure versus pseudoseizure in 9 (100%) of 9 patients with generalized tonic-clonic seizures, in 5 (71%) of 7 patients with complex partial seizures, and 4 (100%) of 4 patients with pseudoseizures. Prolactin values were unaffected by leaving filter paper samples at room temperature for up to 1 week. This study suggests the utility of diagnostic capillary blood collection kits to assist in the diagnosis of epilepsy in outpatients.

Adult↗
PubMed1979

Serum, pituitary and urine concentrations of prolactin and growth hormone in eight strains of mice with varying incidence of mammary tumors.

Eight inbred strains of mice with varying incidences of spontaneous mammary tumor were compared in regard to prolactin and growth hormone concentrations in sera, pituitary glands and urine. Serum prolactin was compared under basal conditions as well as after stimulation with perphenazine. Both hormones were measured with specific, homologous radioimmunoassays. Although some strains having a high incidence of mammary tumors had high levels of prolactin in sera, urine and pituitary glands, neither basal nor perphenazine-induced serum concentrations showed a consistent pattern across mouse strains that correlated with the incidence of mammary tumors. Growth hormone levels in sera, pituitary glands and urine also had no characteristic pattern that applied to all strains studied. The ratio of prolactin depleted from the pituitary gland to prolactin detected in serum after perphenazine injection, which reflected the metabolic clearance rate of prolactin, was highest in two strains with a high incidence of mammary tumors and relatively lower in low-tumor strains. These results suggest that if prolactin plays a part in mammary tumor development in mice, its mechanism varies with strains: while hyperprolactinemia may be the means in some strains, a peculiarity in the metabolism of the hormone may be more important in others.

Animals↗
PubMed1984

Hormonal regulation of the annual pelage color cycle in the Djungarian hamster, Phodopus sungorus. II. Role of prolactin.

This study investigated whether photoperiod-induced changes in circulating prolactin levels, which have been observed in the Djungarian hamster ( Yellon and Goldman, '83; Duncan and Goldman, ' 83a ), might be involved in seasonal pelage color changes in this species. Injection of ovine prolactin (100 micrograms/day) inhibited the short photoperiod-induced winter molt. This finding indicated that the suppression of endogenous prolactin levels normally occurring in short photoperiod-housed hamsters (Duncan and Goldman, ' 83a ) may induce the winter molt. Suppression of prolactin secretion with bromoergocryptine (200 micrograms/day) strongly inhibited the spring molt, while concomitant treatment with ovine prolactin (100 micrograms/day) overcame this effect of bromoergocryptine. Injection of bromoergocryptine (200 micrograms/day) stimulated the winter molt in castrated hamsters housed in long photoperiod; concomitant injection of prolactin (100 micrograms/day) reversed this effect as well. These findings strongly suggested that an increase in endogenous prolactin levels may be necessary for the development and maintenance of the summer pelage.

Animals↗
PubMed1979

Effects of pyridoxine hydrochloride (vitamin B6) on chlorpromazine-induced serum prolactin rise in male rats.

To investigate if vitamin B6 inhibits prolactin release and to compare this effect to that of bromocriptine, a known suppressor of prolactin release, a study was conducted in male rats. Animals were pretreated with pyridoxine hydrochloride, pyridoxal hydrochloride, saline, or bromocriptine 30 min prior to receiving varying doses of chlorpromazine hydrochloride. Blood samples were obtained 90 min later and analyzed for serum prolactin by a double-antibody radioimmunoassay. Another study involved pyridoxal hydrochloride and saline pretreatments 30 min prior to doses of chlorpromazine hydrochloride. Blood samples collected 60 min later were also analyzed for serum prolactin. Pyridoxine hydrochloride significantly suppressed the chlorpromazine-induced prolactin rise (p less than 0.01). However, the suppression was significantly less than that produced by bromocriptine (p less than 0.01). Pyridoxal hydrochloride, another natural form of vitamin B6, failed to suppress prolactin under the conditions of both studies. This investigation may lend support to the concept that pyridoxine hydrochloride partially inhibits prolactin by a mechanism not involving dopamine.

Animals↗
PubMed1984

Action of prolactin in regressing prostate: independent of action mediated by androgen receptors.

Hyperprolactinemia, achieved by grafting pituitaries under the renal capsule, has been shown to cause a delay in the rate of castration-induced prostatic regression in rats. The mechanism of this prolactin action is not established, although it has been suggested that the action of prolactin in the rat prostate is mediated through the action of androgen. To explore the possibility that a small amount of residual endogenous androgen present in the prostate at the time of castration acts synergistically with prolactin to cause this delay in prostatic regression, Flutamide has been used in the present study in an attempt to inhibit this residual androgen effect by blocking its interaction with androgen receptors. Two experiments were conducted. In experiment 1, daily sc injections of Flutamide (25 mg/kg) for 7 days to castrated rats supplemented with dihydrotestosterone-filled silastic tubing either 1 or 4 cm long completely suppressed both prostatic weight and protein content to the level that was normally observed in castrated rats receiving empty tubings. Furthermore, treatment of Flutamide to castrated rats did not cause an increase in prostatic weight and protein content over those of castrated rats treated with the vehicle only. These results indicate that Flutamide, at this dosage, is a potent antiandrogen and that the compound itself does not have any androgenic activity in the rat prostate. In experiment 2, adult male rats were castrated and received two female pituitaries grafted under the renal capsule. One week later, their serum prolactin levels increased from 20 +/- 3 ng/ml to 102 +/- 8 ng ml. This elevated level of serum prolactin was associated with a delay in the rate of prostatic regression. Administration of Flutamide, at a dose (25 mg/kg) which completely suppressed prostatic growth, failed to inhibit the delay in prostatic regression in castrated rats bearing the pituitary grafts. Since Flutamide inhibits the androgen action in the prostate by blocking the binding of intracellular dihydrotestosterone to androgen receptors, the failure of Flutamide to block the effect of prolactin suggests that the prolactin action in regressing prostates is not mediated by androgen receptors.

Animals↗
PubMed1993

Plasma prolactin during the breeding season in adult and immature macaroni (Eudyptes chrysolophus) and gentoo (Pygoscelis papua) penguins.

Plasma prolactin levels were measured in free-living breeding adult and immature (pre-breeding) macaroni (Eudyptes chrysolophus) and gentoo (Pygoscelis papua) penguins at Bird Island, South Georgia (54 degrees S, 38 degrees W). Macaroni and gentoo penguins first breed at 5-6 and 2 years of age, respectively. In adult birds, of both species, prolactin was low (< 1.0 microgram. liter-1) during the courtship period and then increased during early (gentoo) to mid (macaroni) incubation (to 3.9-4.7 and 2.4-3.5 micrograms.liter-1, respectively), remaining elevated until the creche period, by which time continuous nest attendance by the adults had ceased. This pattern is similar to that seen in other altricial species and is consistent with delayed onset of brood patch development and full incubation efficiency, which has been previously reported in penguins. Adult female macaroni penguins showed a marked, but transient, increase in prolactin concentrations within 24 hr of the first egg being laid (from 1.7 to 7.0 micrograms.liter-1), plasma levels decreasing following clutch completion (to prelaying levels) before increasing again during incubation. Elevated plasma prolactin levels occurred in all age classes of immature (nonbreeding) birds in both macaroni (1- to 5 year-olds) and gentoo (1-year-olds) penguins. However, compared to that in adult birds, the increase in prolactin was more transient in immatures, a smaller proportion of immatures had detectable prolactin levels at each stage of the breeding cycle, and, at least in 1- and 2-year-olds, absolute levels of prolactin were lower.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Factors affecting plasma concentrations of prolactin in the common eider Somateria mollissima.

In the common eider only the females incubate while they fast for 25 days. Thus, since they rely entirely on their body reserves for successful incubation, they can be defined as capital incubators. To assess the potential effects of their initial body mass, the incubation duration, and depletion in body reserves on prolactinemia, blood samples of eiders were analyzed during the breeding cycle and an experimental manipulation of the duration of incubation. Levels of circulating prolactin increased at the onset of incubation and then reached a high and stable level during incubation before increasing sharply before hatching. The prolactin level decreased significantly upon hatching. Captive females deprived from their eggs exhibited a rapid decrease in prolactinemia, suggesting that egg stimuli are necessary to prolactin secretion. Aunts, i.e., helper females caring for conspecific young, presented prolactin levels higher than nonbreeding captive females but not significantly different from those of females at hatching. Plasma prolactin at hatch was directly related to body mass loss. Birds with shortened incubation have higher body masses and showed higher levels of prolactinemia at hatching than the control group, in accordance with the idea that circulant prolactin at hatching is linked to body condition. Females which underwent an extended incubation (and started to eat again) displayed a low body mass and a high prolactinemia. These data therefore suggest that refeeding, albeit increasing the risk of predation, enhances prolactin secretion and allows the bird to continue incubation despite that it has reached a poor body condition.

Animals↗
PubMed2000

Prolactin and parental behavior in Adélie penguins: effects of absence from nest, incubation length, and nest failure.

Adélie penguin (Pygoscelis adeliae) males and females, nesting in Antarctica, alternate attendance at the nest with absences of many days to forage at sea. We investigated the importance of tactile input from egg and chicks on prolactin levels by observing nest attendance patterns and obtaining blood samples (1) during the first nest exchange of the incubation stage, (2) from birds whose incubation period was artificially increased or decreased by about 10 days, and (3) from birds whose nests had failed. Prolactin levels in females after 8 to 11 days of absence from the breeding colony did not differ from those in incubating males and did not change after females resumed incubation. Moving eggs between nests resulted in nests in which chicks hatched after about 26, 36 (normal), or 46 days. Duration of incubation did not affect prolactin levels in the parents measured during incubation, at the pip stage, hatch stage, or early brood stage. Adults first left their chicks unguarded on about the same calendar date, regardless of chick age. However, chicks from long incubation nests averaged 8 days younger when they were left unguarded than chicks from control or short-incubation nests. In females, there was no effect of nest failure on prolactin levels. In males, prolactin levels were slightly lower after nest failure than in males tending nests. Testosterone was significantly higher in males after nest failure than in males still tending nests. Prolactin is elevated in Adélie penguins as part of the program of cyclical hormonal changes that accompany the lengthy reproductive season and is relatively independent of tactile input. Sustained prolactin secretion is probably required for the maintenance of parental behavior in offshore feeding species that must be absent from the nest for many days at a time.

Animals↗
PubMed2001

Prolactin receptors in the brain during pregnancy and lactation: implications for behavior.

Numerous studies have documented prolactin regulation of a variety of brain functions, including maternal behavior, regulation of oxytocin neurons, regulation of feeding and appetite, suppression of ACTH secretion in response to stress, and suppression of fertility. We have observed marked changes in expression of prolactin receptors in specific hypothalamic nuclei during pregnancy and lactation. This has important implications for neuronal functions regulated by prolactin. In light of the high circulating levels of prolactin during pregnancy and lactation and the increased expression of prolactin receptors in the hypothalamus, many of these functions may be enhanced or exaggerated in the maternal brain. The adaptations of the maternal brain allow the female to exhibit the appropriate behavior to feed and nurture her offspring, to adjust to the nutritional and metabolic demands of milk production, and to maintain appropriate hormone secretion to allow milk synthesis, secretion, and ejection. This review aims to summarize the evidence that prolactin plays a key role in regulating hypothalamic function during lactation and to discuss the hypothesis that the overall role of prolactin is to organize and coordinate this wide range of behavioral and neuroendocrine adaptations during pregnancy and lactation.

Animals↗
PubMed1996

Prolactin: a novel and safe immunomodulating hormone for the treatment of immunodepression following severe hemorrhage.

Recent studies have shown that the anterior pituitary hormone prolactin, together with various cytokines, plays an important role in maintaining normal immune responses. Although there is evidence that prolactin may be a significant immunotropic hormone that can counteract the immunosuppressive effects of drugs such as cyclosporine, morphine, or glucocorticoids, it remains unknown whether prolactin administration has any salutary effects on the depressed immune responses following severe hemorrhage. To study this, mice were bled to and maintained at a mean arterial pressure of 35 mm Hg for 60 min, then adequately resuscitated and segregated into two groups. One group received saline-vehicle (hem-SS); animals in the other group were treated with prolactin (hem-PRL) (100 micrograms per 25 g BW, subcutaneously) immediately before resuscitation. Two hours following saline or prolactin injection, splenocytes (SPL) were harvested and assessed for proliferative capacity (PC) and their ability to release IL-2 and IL-3. Supernatant lymphokine levels were determined by bioassay. The proliferative capacity of the splenocytes, as well as their ability to release IL-2 and IL-3, was significantly depressed in the vehicle-treated hemorrhaged animals, compared to shams. Treatment with prolactin restored the depressed splenocyte functions seen after severe hemorrhage. These results support the notion that the immunosuppression following hemorrhage and trauma may be mediated by hormones from the hypothalamic-pituitary-adrenal axis. Furthermore, our results suggest that the use of prolactin, which did not produce any adverse hemodynamic effects, represents a novel and safe immunomodulating hormone for the treatment of immunodepression following severe blood loss.

Animals↗
PubMed1988

Human corpus luteum: immunocytochemical evidence for presence of prolactin.

Six human corpora lutea (day 17-25) of the menstrual cycle and 4 ovarian stromal tissues from 7 cycling women were examined for the presence of the hormone, prolactin, by immunohistochemistry using the indirect peroxidase-antiperoxidase method. After mounting tissue sections of 4 micron, endogenous peroxidases were removed with hydrogen peroxide and the sections were incubated for 1 h at room temperature followed by 16 h at 4 degrees C with a highly specific antisera for human prolactin, nonimmunized normal rabbit serum for a control reaction, or antiserum preadsorbed with excess human prolactin for specificity determination. Following the reaction with the second antibody (goat antirabbit IgG) for 1 h at room temperature, prolactin was localized using peroxidase anti-peroxidase and 3.3'-diaminobenzidine as the chromogen. Prolactin was present and could be localized in the luteal cells of all 6 corpora lutea, but not in any of the ovarian stroma studied. Human adenohypophysis served as a positive tissue control for prolactin immunopositive staining. The localization of immunoreactive prolactin in the corpus luteum demonstrates directly the presence of this hormone in the human ovary, adding further evidence for its role in luteal function.

Corpus Luteum↗
PubMed1989

Morphometric evaluation of subcellular changes induced by in vivo TRH treatment in the pituitary gland of Rana perezi: effects on prolactin and thyrotropic cells.

The effects of synthetic thyrotropin-releasing hormone on pituitary prolactin and thyrotropic cells were investigated in adult male Rana perezi (formerly Rana ridibunda) frogs. Animals were given daily injections of synthetic thyrotropin-releasing hormone into the dorsal lymph sac. Prolactin and thyrotropic cells were identified by the colloidal-gold method, using anti-human prolactin and anti-human-beta-thyrotropin hormone as primary antisera. The stereological parameters of the rough endoplasmic reticulum, Golgi complex, and secretory granules of prolactin and thyrotropic cells were evaluated by ultrastructural morphometry (point-counting method). Thyrotropin-releasing hormone caused cytological changes in both cell-types which were consistent with increased synthesis and release of both prolactin and thyrotropin. These changes were still significant after 48 h treatment in the case of thyrotropic cells, while in prolactin cells the thyrotropin-releasing hormone increased the number of secretory granules. After 6 days, the cells resembled essentially those used as controls. These results indicate that thyrotropin-releasing hormone stimulates the synthesis and release of prolactin and thyrotropin, and that the response of each cell type to this hypothalamic stimulus follows a different time-course.

Animals↗
PubMed1984

Mitotic activity of prolactin cells in the pituitary glands of male and female rats of different ages.

The anterior pituitary of colchicine-pretreated male and female rats from 20 days to 12 months of age was stained immunohistochemically with anti-rat prolactin serum. Immunoreactive mitotic cells were identified in all groups of rats. In adult female rats the mitotic index of prolactin cells was higher at oestrus than at other stages of the oestrus cycle and than that in male rats of comparable ages. If adult female rats were ovariectomized on the second day of dioestrus or on the day of proestrus, the mitotic indices at presumptive oestrus were less than those in sham-operated controls at oestrus. Estrogen administration to ovariectomized rats significantly elevated the mitotic index of prolactin cells at 48 h after the treatment. The mitotic indices of prolactin cells in female rats reached a peak at 60 days of age, and then decreased with age. In male rats the mitotic indices showed a steady decrease from the value at 20 days of age. A sex difference in the mitotic indices of prolactin cells was noted from 60 days to 12 months of age. The present results clearly demonstrate that differentiated prolactin cells can undergo mitosis and that a sex difference in the mitotic activity of prolactin cells is present during adult life.

Aging↗