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PubMed1975

Prolactin and growth hormone cells in the human hypophysis: a study with immunoenzyme histochemistry and differential staining.

Growth hormone and prolactin cells were immunostained in human hypophyses with antibody against rat growth hormone or prolactin and the peroxidase-antiperoxidase complex. Growth hormone cells were round and, in normal pituitaries, arranged in sizable groups. Prolactin cells occurred singly and were less numerous; they were often extensively branched. Only a few prolactin cells stained with carmoisine. Incubation of the antibody with an excess of the appropriate antigen greatly diminished or abolished immunostaining; absorption of anti-prolactin with growth hormone often enhanced it. Prolactin cells were somewhat hypertrophied and hyperplastic in a neonate. Many of them stained with carmoisine. An even greater hypertrophy and hyperplasia of these cells (which pushed apart the growth hormone cells) was found in a lactating woman. Immunostained giant prolactin cells were also observed. Staining of the prolactin cells with carmoisine was extensive. Upon prolonged exposure to anti-growth hormone antibody, ACTH/MSH cells also showed immunostaining which was abolished by absorption of the antiserum with growth hormone but not with synthetic 1-24ACTH. Growth hormone cells evidently correspond to the alpha acidophils of Romeis, prolactin cells in lactation to his eta cells; the relation of his epsilon cells to the pleomorphic "resting" prolactin cells is not clear.

Adult↗
PubMed2001

Effects of diethylstilbestrol on the cytogenesis of prolactin cells in the pars distalis of the pituitary gland of the mouse.

This study was carried out to examine the developmental stage when prolactin cells differentiate in mice and to examine the effects of diethylstilbestrol on the development of prolactin cells in the fetal and neonatal pituitary glands. A small number of immunoreactive prolactin cells appeared first on embryonic day 15 in control (injected with oil) pituitary glands, whereas they did not increase in number until postnatal day 2. In diethylstilbestrol-treated mice (5 mg/kg body weight, 24 h before killing), a small number of immunoreactive prolactin cells were detectable as early as embryonic day 14, but not on day 13. They increased in number on embryonic days 15 and 16, and decreased markedly on days 17 and 18, followed by a rapid increase after birth. This transient reduction in the response to diethylstilbestrol was partially restored by treatment with metyrapone, a specific inhibitor of corticosteroid production. These results suggest that in the mouse: (1) differentiation of prolactin cells occurs between embryonic days 13 and 14, (2) prolactin gene expression is suppressed in the nascent prolactin cells presumably due to the presence of high levels of estrogen-binding protein, alpha-fetoprotein, and (3) prolactin gene expression is also suppressed by elevation of circulating glucocorticoids during the perinatal period. The present results suggest that, in the mouse, at least a proportion of prolactin cells are not derived from growth hormone cells, because the diethylstilbestrol-induced prolactin cells appear earlier than growth hormone gene expression.

Animals↗
PubMed1981

Is prolactin secreted ectopically?

The ectopic secretion of prolactin by neoplasms has been reported only rarely although in one preliminary report it has been found to be present commonly in tumor extracts. To ascertain whether this is due to a true rarity of prolactin-secreting tumors or to the fact that prolactin hypersecretion causes few notable clinical symptoms in patients with cancer, we measured prolactin levels by radioimmunoassay in the serums of 215 patients who had a variety of malignancies. Prolactin levels were elevated (greater than 25 ng/ml) in 15 patients. In 12 of these 15 patients, the elevations could be explained by the use of phenothiazine or opiates, or prior irradiation to the chest wall or head. Additional serum samples showed clearly normal prolactin levels in one of the patients. Of the entire series of 215 patients, therefore, only two patients (1 percent) had modestly elevated prolactin levels without having known causes for hyperprolactinemia: one patient with squamous cell carcinoma of the lung (prolactin 34.1 ng/ml) and one patient with breast cancer (prolactin 45.4 ng/ml). Even in these two patients the hyperprolactinemia could as likely be due to stimulation of afferent nerves in the chest wall as to ectopic secretion by the tumors. There is no clear evidence in our study or in the literature that prolactin is secreted ectopically; this is in sharp contrast to many studies showing the high frequencies of the ectopic secretion of a number of other hormones. Why this is so is unknown.

Humans↗
PubMed1985

Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy.

This study was performed to establish the dynamics of human chorionic gonadotropin, prolactin, and growth hormone throughout pregnancy in serum and amniotic fluid. Two hundred fifty healthy women at 8 to 42 weeks' gestation were studied. The highest serum human chorionic gonadotropin level was measured between weeks 8 to 12 (53,715 +/- 3574 mIU/ml, mean +/- SEM), with a decline to a mean plateau of 11,806 +/- 1250 mIU/ml from week 18. Amniotic fluid human chorionic gonadotropin had a similar pattern with a mean of 68,100 +/- 8422 mIU/ml at weeks 8 to 10, declining from week 18 to a plateau of 2005 +/- 260 mIU/ml. Human chorionic gonadotropin showed a significant correlation (r = 0.85, p less than 0.001) between levels of both compartments demonstrating an even distribution. Prolactin levels showed a dichotomy of patterns and levels. Serum prolactin showed a continuous rise from 45.3 +/- 14 ng/ml at week 8 to 224 +/- 20 ng/ml at week 36. In contrast, amniotic fluid prolactin remained low until week 14 (33.1 +/- 0.8 ng/ml), followed by a sharp and significant (p less than 0.001) increase to a plateau of 3750 +/- 200 ng/ml between weeks 18 to 26, declining to a second plateau of 500 +/- 50 ng/ml at week 36. Serum growth hormone increased from a mean of 3.5 +/- 1.4 ng/ml seen at weeks 8 to 10 to a mean of 14 +/- 2.0 ng/ml at weeks 28 to 30, followed by a plateau of similar levels. The pattern of growth hormone secretion in amniotic fluid demonstrated a sharp increase during the 14-16 interval with a maximum mean level of 15.5 +/- 1.5 ng/ml and a slow steady decline thereafter. In conclusion, the similar pattern and concentration of human chorionic gonadotropin throughout pregnancy in both maternal and amniotic fluid are probably the result of direct human chorionic gonadotropin diffusion from the placenta. The dissimilar pattern and concentration of prolactin are the result of two different sources of prolactin secretion during pregnancy. Serum prolactin originates from the pituitary and amniotic fluid prolactin from the decidua. Since the pattern of growth hormone secretion resembles that of prolactin, it is possible that growth hormone, like prolactin, is secreted by the same sources.

Amniotic Fluid↗
PubMed1986

Influence of sequential doses of 5-hydroxytryptophan on prolactin release.

It is known that the administration of serotonin or its precursors induces the release of prolactin. This study was performed (1) to determine the minimal dose of 5-hydroxytryptophan that would produce a consistent and significant prolactin increase and (2) to establish the frequency of 5-hydroxytryptophan administration necessary to induce a persistent prolactin increase. Nine normal male subjects participated in 27 independent studies following pretreatment with 100 mg of carbidopa given every 8 hours for 2 days. Doses of 0.2, 0.4, and 0.8 mg/kg/hr of 5-hydroxytryptophan were initially infused for 30 minutes, and serum prolactin was measured every 15 minutes for 2 1/2 hours. The urinary 5-hydroxyindoleacetic acid/creatinine ratio was determined in aliquots collected during 3 hours before, during, and after the intravenous infusion. 5-Hydroxytryptophan at a dosage of 0.4 mg/kg/hr was the minimal amount to elicit a consistent and significant prolactin increase (p less than 0.01). A positive correlation (r = 0.907, p less than 0.002) was also demonstrated between the maximal prolactin response and the 5-hydroxyindoleacetic acid/creatinine ratio. Thus 0.4 mg/kg/hr of 5-hydroxytryptophan was administered sequentially three times at intervals of 2, 4, 6, 8, and 12 hours. With exception of the 12-hour interval a significantly smaller plasma prolactin increase was seen following the third dose of 5-hydroxytryptophan (p less than 0.05). Furthermore, the nadir for this diminished prolactin response occurred at 4 hours (p less than 0.01). This phenomenon may represent a down regulation of the serotonin receptors induced by the repetitive administration of 5-hydroxytryptophan. In conclusion, this study has demonstrated a dose-related prolactin response to increasing doses of 5-hydroxytryptophan. The maximum down regulation of prolactin release occurred when 5-hydroxytryptophan was administered at 4-hour intervals.

5-Hydroxytryptophan↗
PubMed1990

In vitro induction of prolactin production and aromatase activity by gonadal steroids exclusively in the stroma of separated proliferative human endometrium.

Prolactin production by decidualized human endometrium has been demonstrated in organ explant cultures and presumed to be of stromal origin by immunocytochemistry and the presence of simultaneous stromal histologic changes. To test the hypothesis that endometrial prolactin production is exclusively of stromal origin, late proliferative human endometrium was separated into glands and stroma and cultured for 3 days. Confluent cultures were incubated with progesterone, 50 ng/ml; estradiol, 5 ng/ml; or both progesterone and estradiol for 4, 8, and 15 days. Prolactin concentration was measured at 2-day intervals by specific radioimmunoassay throughout a 15-day culture in all samples. Aromatase activity at 15 days was assayed by the production of tritiated water from 1 beta 3H-androstenedione. Possible contamination of gland cultures by stromal cells was controlled by the substitution of D-valine in the culture media. No prolactin was detected in the D-valine-treated gland cultures. Stromal cell cultures demonstrated increasing prolactin with continuous incubation with progesterone (15-day control: 11.28 +/- 0.91 ng/100 micrograms deoxyribonucleic acid versus 15-day progesterone: 245.8 +/- 4.24 ng/100 micrograms). Prolactin levels increased after progesterone was removed at day 4 and 8, reaching peak production 4 days later, followed by a steady decline. Estradiol induced a sustained increase in prolactin production even after withdrawal of steroids. Aromatase activity in gland cells exposed to steroids exhibited no change with time. Steroid-treated stromal cell cultures showed an increase in aromatase activity in all 15-day (controls: 21.6 +/- 0.7 pmol substrate converted per mg of deoxyribonucleic acid per 24 hours versus progesterone: 43.4 +/- 4.2 versus estradiol: 34.2 +/- 3.5 versus progesterone and estradiol: 47.5 +/- 2.4) but not in 4- or 8-day incubations. These studies support these conclusions: (1) nongestational endometrial prolactin is of stromal, not glandular origin; (2) stromal prolactin production is induced and maintained by progesterone: (3) stromal prolactin production is induced by estradiol but does not require continued exposure for maintenance; (4) aromatase activity is increased by long-term exposure to progesterone and estradiol in stroma but not in glands.

Adult↗
PubMed1983

The effects of intraventricular prolactin infusions on pituitary responsiveness to thyrotropin-releasing hormone, 5-hydroxytryptophan or morphine in rhesus monkeys.

The effects of intraventricular infusions of ovine prolactin (oPrl) on both endogenous prolactin levels in serum, and upon the release of prolactin and cortisol in response to treatment with either TRH, 5-HTP or morphine were studied in rhesus monkeys. A single injection of oPrl (10.8 micrograms) into the lateral ventricles of castrated males resulted in CSF levels of around 350 ng/ml 60 min later, but no oPrl could be detected in the blood. Endogenous (rhesus) prolactin levels in serum fell during this time to about half their initial values in oPrl-treated animals but not in the bovine serum albumin (BSA)-injected controls. Ovine prolactin was infused continuously into either the lateral or third ventricles of ovariectomized, estrogen-treated females for 6 days from an osmotic minipump (2.7 micrograms/h). CSF levels of oPrl were about 250 ng/ml though none was found in the serum. The release of endogenous prolactin by TRH (1 microgram) was greatly reduced compared with BSA-treated controls. 5-HTP (2.5 mg/kg together with carbidopa pretreatment) also stimulated much less prolactin release in females chronically infused with oPrl and there was some evidence for a similar effect in males following a single intraventricular injection. CSF levels of 5-HTP itself, and of 5-HIAA and HVA were similar throughout this experiment in both oPrl and BSA-infused animals. Finally, prolactin released by morphine (5 mg) was highly attenuated in females receiving oPrl intraventricularly. In contrast to those on serum prolactin, the effects of these various treatments on serum cortisol were unaltered by intraventricular oPrl. These results suggest that the primate brain contains a neural system which is directly responsive to prolactin, and which can modulate this hormone's release under either basal conditions or following treatment with substances that stimulate its release by acting either directly on the pituitary or upon the neural systems regulating pituitary function. These results are compatible with the presence of increased dopamine in the portal blood, though this was not measured in these experiments.

5-Hydroxytryptophan↗
PubMed1985

Strain differences in pituitary prolactin content: relationship to number of hypothalamic dopamine neurons.

BALB/cJ mice have more tuberoinfundibular dopamine neurons, and thus greater tyrosine hydroxylase activity, than CBA/J mice. Strain differences in the synthesis and release of prolactin would also be predicted since dopamine released from the tuberoinfundibular neurons is the prolactin inhibitory factor which plays a role in the regulation of both prolactin synthesis and release. As expected, CBA/J mice, with fewer dopamine neurons, synthesized and released significantly more prolactin than BALB/cJ mice; that is, both pituitary and serum prolactin concentrations were greater in CBA/J mice. To determine if there were more cells containing prolactin or more prolactin per cell, pituitaries were stained with antibodies to prolactin and densitometric analysis made of both the average staining per unit area and total staining per pituitary. For both indices CBA/J mice had more staining than BALB/cJ mice. Using these criteria the difference in staining was attributed to more prolactin-stained lactotrophs in the CBA/J strain. Although no differences in the number of acidophils demonstrated by Pearse Trichrome method were observed, acidophils from BALB/cJ mice appeared smaller and contained less cytoplasm than those from CBA/J mice. We conclude that strain differences in the number of tuberoinfundibular dopamine neurons are inversely related to the number of immunocytochemically demonstrable prolactin-containing cells in the anterior pituitary.

Animals↗
PubMed1984

Stimulatory and inhibitory effects of prostaglandin E2 on prolactin release in the domestic fowl.

In vivo prolactin secretion was increased in immature cockerels 20-30 min after the intravenous administration of prostaglandin (PG) E2 at a dose of 200 micrograms/kg. The addition of PGE2 to incubation medium had no direct effect on the release of pituitary prolactin during short-term (3-hr) culture, but augmented the stimulatory effect of hypothalamic tissue on prolactin secretion. The stimulatory effect of serotonin, noradrenaline, acetylcholine, and histamine on hypothalamus-induced prolactin release was also increased when pituitaries were coincubated with 10(-7)M PGE2, as was the stimulatory effect of thyrotrophin-releasing hormone (TRH) and hypothalamic extract (HE). The long-term (24-hr) preincubation of pituitaries with 10(-7)M PGE2 reduced the responsiveness of the prolactin-secreting cells to TRH or HE stimulation. PGE2 treatment also reduced the stimulatory effect of hypothalamic tissue on prolactin release and diminished the stimulatory effect of serotonin on hypothalamus-induced prolactin secretion. A 24-hr preincubation of hypothalamic tissue with 10(-7)M PGE2 also reduced its stimulatory effect on prolactin release when subsequently incubated with control pituitary glands. These results demonstrate that PGE2 initially stimulates in vivo and in vitro prolactin secretion in the fowl, possibly by increasing the release of hypothalamic prolactin-releasing activity and/or by increasing pituitary sensitivity to provocative stimuli. Chronic PGE2 stimulation appears to result in a reduction in pituitary responsiveness to stimulatory influences and in the release of hypothalamic-releasing activity.

Acetylcholine↗
PubMed1985

Environmental control of prolactin synthesis in the teleost fish Oreochromis (formerly Sarotherodon) mossambicus.

In the cichlid fish Oreochromis mossambicus prolactin cell activity is inversely related to the osmolarity and the Ca2+ concentration of the ambient water. Prolactin cell activity was estimated, at the end of a 3-week experimental period, by determination of the rate of prolactin synthesis during incubation of the rostral parts of the pituitary gland, in the presence of [3H]lysine. Since the secretory activity of isolated prolactin cells is known to be inversely related to the osmolarity of the incubation medium, the possibility was investigated that the effects of changes in ionic composition of the ambient water on prolactin secretion in vivo are mediated by changes in osmolarity of the blood plasma. No support was found for this hypothesis. In fish exposed to high water osmolarities prolactin cell activity was reduced, while plasma osmolarity increased. In contrast, at high Ca2+ concentrations of the water, when prolactin secretion was inhibited to a similar extent, plasma osmolarity was significantly reduced. Although direct effects of plasma osmolarity on prolactin cells cannot be excluded completely, it is unlikely that plasma osmolarity is the predominant factor in the control of prolactin cell activity in situ. The physiological significance of the capacity of isolated prolactin cells to respond to changes in osmolarity of the ambient medium--a capacity shared with some other endocrine cell types--is therefore unclear.

Animals↗
PubMed1986

Antagonistic effects of prolactin and oxytocin on tail fin regression and acid phosphatase activity in metamorphosing Ambystoma tigrinum.

We have found that the inhibition of thyroxine-induced tail fin regression by prolactin in larval tiger salamanders is antagonized by oxytocin. Other workers have shown that prolactin blocks the rise in activity of several hydrolytic enzymes that occurs in regressing tissue during metamorphosis. Here, we examine the effects of prolactin and oxytocin--given alone and in combination--on tail fin regression and acid phosphatase specific activity in this tissue. Both long-term (12-day) and short-term (48-hr) treatment paradigms using prolactin and oxytocin are investigated. The results show that long-term prolactin treatment of metamorphosing larvae blocks fin regression and the rise in acid phosphatase specific activity seen in metamorphosing controls; short-term prolactin treatment of metamorphosing larvae inhibits fin regression within 48 hr, but does not block the rise in acid phosphatase activity seen in controls; oxytocin antagonizes the effects of prolactin on tail fin regression; and oxytocin treatment (long-term or short-term) of metamorphosing larvae causes an elevation of acid phosphatase activity above that seen in metamorphosing controls. With long-term treatment, this effect of oxytocin is slightly antagonized by prolactin; with short-term treatment, no antagonism is observed even though an effect of prolactin on fin height is still evident. We have interpreted these results as suggesting that the effect of prolactin on hydrolase activity is not a prerequisite for its inhibitory effect on fin regression to occur.

Acid Phosphatase↗
PubMed1992

Seasonal and lactational effects on the prolactin response to a dopamine antagonist and TRH in the Bennett's wallaby (Macropus rufogriseus rufogriseus).

In the Bennett's wallaby prolactin is thought to maintain lactational and seasonal quiescence and is essential for early lactation. However, plasma prolactin concentrations determined in daily or weekly samples at these times are unchanged. In the present study, female Bennett's wallabies were blood sampled at 2-hr intervals over a 24-hr period during seasonal quiescence on either natural or artificial photoperiods to determine whether a diurnal rise of prolactin occurs at this time. Prolactin concentrations did not exhibit a diurnal change. Further experiments were aimed at determining whether there was an increase in the prolactin response to a dopamine antagonist or TRH during the transition to seasonal quiescence. Nonlactating and lactating female Bennett's wallabies were treated with saline, 0.5, 1, and 2 mg of the dopamine antagonist domperidone and 100 micrograms TRH in October, December, February, and April. In both groups there was a significant elevation in plasma prolactin concentration in response to domperidone with an increasing response at each successive month. In early (October and December) and peak (April) lactation the prolactin response was greater in lactating animals. There was no significant prolactin response to TRH in lactating animals. In nonlactating wallabies, the prolactin response to TRH was increased in February. At peak lactation (April), the response to 1 mg domperidone was blocked when the dose was administered 2 hr after temporary removal of pouch young (RPY). With either larger doses (20 mg) or a 1-mg dose injected 8 hr after RPY, a significant prolactin response was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Plasma levels of prolactin and gonadal steroids in relation to multiple-brooding and renesting in free-living populations of the song sparrow, Melospiza melodia.

Plasma levels of testosterone (T), estradiol (E2), and prolactin were measured in samples collected from free-living song sparrows, Melospiza melodia. In males, plasma levels of T were elevated early in the season when territories were established and when females laid the first clutch of eggs. Thereafter, T levels declined and remained low throughout the remainder of the breeding cycle. However, if the first brood was lost to a predator, or by experimental removal of the nest, plasma levels of T increased as renesting, to replace the clutch, occurred. Circulating levels of prolactin in males began to rise during the egg-laying stage of the first brood, reached a maximum toward the end of the incubation stage, remained elevated until breeding was terminated, and then declined throughout the moulting stage to basal values in October. Prolactin levels remained high throughout the breeding season irrespective of whether a brood was raised successfully or whether the nest was lost and renesting occurred. In females, plasma levels of E2 were elevated prior to the egg-laying stage for each brood as is typical of multiple-brooded species. However, prolactin titers rose dramatically during egg-laying for the first clutch (slightly higher than in males) and were maximal by onset of incubation. Only females of this species incubate, although males do feed young. As in males, plasma prolactin in females remained high between broods and during experimentally induced renesting, and then declined to basal by the end of the moult stage in October. These data suggest that there are no differences in the temporal patterns of prolactin concentrations in blood between multiple-brooding and renesting. In a separate experiment, captive male song sparrows were transferred from a short day to artificial long days (18L 6D) and a control group was maintained on 9L 15D. In the long-day group, prolactin levels rose abruptly over the first 20 days, as the testes developed, and remained high well into postnuptial moult after the gonads had regressed. Prolactin remained basal in the control group. These data suggest that the temporal pattern of circulating prolactin levels throughout the breeding season is regulated at least partly by changing photoperiod. However, nonphotoperiodic factors are also important since photoperiodically induced increases in prolactin are significantly less than those seen in free-living individuals. These differences may be related to parental behavior.

Animals↗
PubMed1988

Oestrogen and progesterone interactions in the control of gonadotrophin and prolactin secretion.

Oestrogen and progesterone have marked effects on the secretion of the gonadotrophins and prolactin. During most of the oestrous or menstrual cycle the secretion of gonadotrophin is maintained at a relatively low level by the negative feedback of oestrogen and progesterone on the hypothalamic-pituitary system. The spontaneous ovulatory surge of gonadotrophin is produced by a positive feedback cascade. The cascade is initiated by an increase in the plasma concentration of oestradiol-17 beta which triggers a surge of luteinizing hormone releasing hormone (LHRH) and an increase in pituitary responsiveness to LHRH. The facilitatory action of oestrogen on pituitary responsiveness is reinforced by progesterone and the priming effect of LHRH. How oestrogen and progesterone exert their effects is not clear but the facilitatory effects of oestrogen take about 24 h, and the stimulation of LHRH release is produced by an indirect effect of oestradiol on neurons which are possibly opioid, dopaminergic or noradrenergic and which modulate the activity of LHRH neurons. In the rat, a spontaneous prolactin surge occurs at the same time as the spontaneous ovulatory gonadotrophin surge. The prolactin surge also appears to involve a positive feedback between the brain-pituitary system and the ovary. However, the mechanism of the prolactin surge is poorly understood mainly because the neural control of prolactin release appears to be mediated by prolactin inhibiting as well as releasing factors, and the precise role of these factors has not been established. The control of prolactin release is further complicated by the fact that oestradiol stimulates prolactin synthesis and release by a direct action on the prolactotrophes. Prolactin and gonadotrophin surges also occur simultaneously in several experimental steroid models. A theoretical model is proposed which could explain how oestrogen and progesterone trigger the simultaneous surge of LH and prolactin.

Animals↗
PubMed1983

Effects of acute and chronic trazodone administration on serum prolactin levels in adult female rats.

Trazodone was tested for its ability to elevate serum prolactin levels in mature female rats. When the drug was administered acutely to female rats at doses up to 80 mg/kg ip, it induced a clear rise in serum prolactin levels, with a minimum effective dose of 20 mg/kg; blood trazodone levels at these doses were between 1.6-2.4 micrograms/ml. However, trazodone could not be considered to be a potent stimulator of prolactin secretion, since the injection of haloperidol at 2 mg/kg elevated serum prolactin to values twice those seen in animals receiving the 80 mg/kg dose of trazodone. When trazodone was administered chronically in the diet for two or four weeks, at an average daily dose of 80 mg/kg, serum trazodone levels were found to be 100-200 ng/ml when measured at each stage of the estrous cycle. Serum prolactin levels in trazodone-treated animals, however, did not differ from those in control rats. Moreover, drug-treated animals showed normal proestrus surges in serum prolactin. The results of these studies thus indicate that acutely, at very high doses, trazodone probably can stimulate prolactin secretion modestly in female rats. However, when consumed chronically at 80 mg/kg/day, the drug has no effects on serum prolactin levels. Therefore, if trazodone stimulates prolactin secretion by altering neurotransmission across dopamine and/or serotonin synapses in brain, it is probably not potent in these actions, at least as concerns those dopamine and serotonin neurons that influence the secretion of prolactin.

Animals↗
PubMed1991

Prolactin, immunoregulation, and autoimmune diseases.

Cells of the immune system synthesize prolactin and express mRNA and receptors for that hormone. Interleukin 1, interleukin 6, gamma interferon, tumor necrosis factor, platelet activator factor, and substance P participate in the release of prolactin. This hormone is involved in the pathogenesis of adjuvant arthritis and restores immunocompetence in experimental models. In vitro studies suggest that lymphocytes are an important target tissue for circulating prolactin. Prolactin antibodies inhibit lymphocyte proliferation. Prolactin is comitogenic with concanavalin A and induces interleukin 2 receptors on the surface of lymphocytes. Prolactin stimulates ornithine decarboxylase and activates protein kinase C, which are pivotal enzymes in the differentiation, proliferation, and function of lymphocytes. Cyclosporine A interferes with prolactin binding to its receptors on lymphocytes. Hyperprolactinemia has been found in patients with systemic lupus erythematosus. Fibromyalgia, rheumatoid arthritis, and low back pain patients present a hyperprolactinemic response to thyrotropin-releasing hormone. Experimental autoimmune uveitis, as well as patients with uveitis whether or not associated with spondyloarthropathies, and patients with psoriatic arthritis may respond to bromocriptine treatment. Suppression of circulating prolactin by bromocriptine appears to improve the immunosuppressive effect of cyclosporine A with significantly less toxicity. Prolactin may also be a new marker of rejection in heart-transplant patients. This body of evidence may have an impact in the study of rheumatic disorders, especially connective tissue diseases. A role for prolactin in autoimmune diseases remains to be demonstrated.

Animals↗
PubMed1996

Serotonergic regulation of renin and prolactin secretion.

Drugs that, directly or indirectly produce activation of serotonin (5-HT) receptors increase plasma concentrations of both prolactin and renin. The serotonergic regulation of prolactin and renin secretion share several common characteristics. Serotonergic neurons originating in the dorsal raphe and terminating in the hypothalamus stimulate the secretion of both prolactin and renin. Destruction of cells in the hypothalamic paraventricular nucleus (PVN) inhibits both the prolactin and renin responses to 5-HT agonists and 5-HT-releasing drugs. Activation of 5-HT2 receptors increases the secretion of both prolactin and renin, while activation of other 5-HT receptor subtypes has differential effects on these hormones. However, there are also differences between the serotonergic mechanisms that regulate the secretion of prolactin and renin. Activation of 5-HT1A receptors increases the secretion of prolactin but not of renin. In addition, activation of peripheral 5-HT2 receptors stimulates the secretion of renin, while activation of peripheral 5-HT3 receptors increases plasma levels of prolactin but not renin. In humans, the effect of 5-HT-releasing drugs and 5-HT agonists on plasma prolactin concentrations has been studied to a greater extent than effects on most other hormones. In contrast, the renin response to 5-HT agonists and 5-HT releasers has not been well characterized in humans. Because of the important role of the renin-angiotensin system in cardiovascular regulation, studies on the serotonergic regulation of renin release in humans could increase our understanding of cardiovascular disorders associated with altered serotonergic function. Examples include anxiety and consequences of cocaine abuse. In conclusion, comparing the serotonergic regulation of prolactin and renin secretion indicates similarities that might shed light on common brain mechanisms that regulate neuroendocrine function.

Animals↗
PubMed1987

The relationship between blood prolactin levels and risk of breast cancer in premenopausal women.

Single specimens of blood have been taken from over 5000 normal volunteer women in each of two sequential (1967-1976, 1977-1984) population-based studied on the Island of Guernsey. Multivariate analysis was used to determine the relationship between prolactin levels and risk factors in breast cancer in 2591 and 1959 premenopausal women in whom blood prolactin had been measured. In both populations the prolactin concentrations appeared to be log-normally distributed and therefore all analyses have been done on log-transformed data. Initially the variables in the statistical model were age at menarche, ages at first and last baby, parity, ponderosity (Quetelet Index), mammographic pattern (as graded by Wolfe), family history of breast cancer, age, menstrual cycle status, time of day of blood sampling, oral contraceptive use, history of breast feeding and methodological changes in the laboratory measurement of prolactin. Of these variables age at menarche, ages at first and last child and family history of breast cancer were found not to be significant and were excluded from the final model. The main finding to emerge was that after standardizing for all the other variables, prolactin levels in the follicular phase were significantly lower than those found at midcycle or during the luteal phase of the menstrual cycle. A peak level of prolactin was found at day 12 of the cycle. Increasing parity was related to a steady decrease in prolactin concentration. Increasing ponderosity was associated with an increased prolactin level as was a DY compared to an N1 mammographic pattern. Women with a history of oral contraceptive use had lowered prolactin concentration. All these effects occurred evenly over the menstrual cycle and were generally found for both data sets. Thus body weight, parity and, indirectly, age at first baby might influence breast cancer risk by being associated with changes in blood prolactin concentration.

Adult↗