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PubMed1982

Prolactin and luteinizing hormone receptors in marsupial corpora lutea: relationship to control of luteal function.

Prolactin and LH receptor concentrations in tammar wallaby corpora lutea (CL) have been examined and related to the control of luteal function in this and other marsupial species. During embryonic diapause, quiescent CL contained high concentrations of prolactin receptors. This was consistent with an earlier suggestion that prolactin may act directly on the CL to maintain its quiescent state. However, despite an apparent seasonal change in the mechanism by which the CL is maintained in quiescence, the number of luteal prolactin receptors remained constant throughout the year. Reactivation of quiescent CL led to an approximate halving of prolactin receptors on a per cell basis, but pregnancy had no effect. None of the wallaby CL showed any significant degree of LH binding, although wallaby follicles and testicular tissue did show binding. This lack of LH binding was consistent with previous findings that quiescent wallaby CL reactivate in response to hypophysectomy and are refractory to LH when cultured in vitro. Parturition, which occurs approximately 2 days before ovulation in this species, had no effect on numbers of either prolactin or LH receptors despite the occurrence of a peak of plasma prolactin at this time. The red kangaroo, which also exhibits embryonic diapause, showed a similar pattern of luteal receptor numbers with high prolactin and negligible LH binding, whereas the brush-tailed possum, which does not exhibit embryonic diapause, gave a pattern more like that seen in Eutheria with many more LH than prolactin receptors.

Animals↗
PubMed1983

Antagonism of serum tri-iodothyronine changes after injections of prolactin in the domestic fowl before and after hatching.

The influence of an intravenous injection of ovine prolactin on circulating levels of thyroid hormones was studied in Rhode Island Red embryos and chicks after hatching. In the chick embryo, 2 h after injection of 0.1 microgram prolactin (on incubation day 19), serum triiodothyronine (T3) increased threefold; after 10 or 100 micrograms prolactin (on incubation day 18) serum T3 increased 15- to 25-fold. These profound increases were not observed in chicks after hatching. Serum concentrations and thyroid content of thyroxine (T4) in embryos and chicks of all ages studied were not influenced by the prolactin injections. Maximal serum concentrations of reverse T3 (rT3) were found on incubation day 18 (110.25 +/- 23.36 pmol/l; 71.66 +/- 15.18 pg/ml; n = 8), whereas after hatching no rT3 could be detected. An injection of 10 micrograms prolactin on day 18 depressed serum rT3 after 2 h to 5.68 +/- 3.20 pmol/l (3.69 +/- 2.08 pg/ml; n = 8; P less than 0.001); the effect of 100 micrograms prolactin was less pronounced. After hatching, chronic administration of prolactin resulted in decreased serum levels of T3, but not of T4, and hypertrophy of the follicles in the thyroid gland. It is concluded that prolactin plays a major role in the maturation of embryonic thyroid metabolism by changing the T4-5-monodeiodination into a T4-5'-monodeiodination. The hypertrophy of the thyroid gland observed after hatching following prolonged prolactin administration may be due to decreased negative feedback of T3 on the hypophysis.

Animals↗
PubMed1984

Suckling and serum prolactin and LH concentrations in lactating rats.

The frequency of pup sucking behaviour was related to serum concentrations of prolactin and LH in rats during various phases of lactation. Sucking frequency and prolactin levels decreased and LH levels increased as lactation progressed. There was no clear relationship between sucking frequency and either prolactin or LH levels. Serum prolactin concentrations were highest when the rats spent most of their time away from their pups and lowest when the rats spent most of their time with the pups attached to their nipples. Prolactin was secreted episodically during prolonged continuous nipple stimulation. Removal of the pups in late lactation and replacement with a newborn litter increased sucking frequency but did not affect serum LH levels and only marginally increased serum prolactin levels. Injection of the dopamine receptor antagonist domperidone produced a far more pronounced release of prolactin from the pituitary gland in early than in late lactation. A circadian control mechanism and an episodic pattern of release may contribute to the great variation in serum prolactin concentrations seen in early lactation; decreased pituitary sensitivity to dopamine receptor blockade may be related to the low concentration of serum prolactin found in late lactation.

Animals↗
PubMed1985

Mechanisms of release of prolactin from fowl anterior pituitary glands incubated in vitro: effects of calcium and cyclic adenosine monophosphate.

Fowl anterior pituitary glands were bisected and each half was pretreated in either Medium 199 or medium containing EGTA to deplete endogenous calcium (Ca2+) stores, after which they were incubated in Medium 199, or Ca2+-free medium, containing prolactin release-stimulating agents and verapamil, a Ca2+ channel blocker. High K+ concentrations, hypothalamic extract, synthetic thyrotrophin-releasing hormone (TRH) and dibutyryl cyclic AMP (dbcAMP) all stimulated release of prolactin from control (non EGTA-treated) hemianterior pituitary glands. The effects of TRH and dbcAMP were not additive, but the response to submaximal concentrations of TRH was augmented by theophylline, a phosphodiesterase inhibitor. Reduction of Ca2+ availability with EGTA or verapamil reduced basal release of prolactin, prevented the prolactin-stimulating effects of high K+ concentrations and TRH, and markedly attenuated responses to hypothalamic extract and dbcAMP, EGTA being more effective than verapamil. Increasing the Ca2+ concentration of the medium did not augment basal or stimulated release of prolactin. These results suggest that both Ca2+ and cyclic AMP may act as intracellular mediators in the release of prolactin. Both basal and stimulated release of prolactin depend upon the presence of Ca2+. Although influx from the medium may be the major source of Ca2+, endogenous stores of Ca2+, perhaps mobilized by dbcAMP, may be able to maintain some release of prolactin. The prolactin-stimulating effects of TRH may be mediated by cyclic AMP.

Animals↗
PubMed1988

Identification of multiple low molecular weight placental prolactin-like proteins produced by rat trophoblast cells.

Rat trophoblast tissue was found to synthesize a number of low molecular weight proteins possessing prolactin-like characteristics. There appear to be at least three proteins that cross-react with antisera to pituitary prolactin. Two of the proteins had a molecular weight of 25,000, similar to ovine pituitary prolactin, and isoelectric points of 6.8 and 7.0. The third immunoreactive protein had a lower molecular weight (23,500), similar in size to human placental lactogen, and a slightly more acidic isoelectric point of 6.75. The molecular weight variants cross-reacted with an antipeptide serum that was generated to a synthetic peptide representing amino acids 150 to 164 of rat placental lactogen-2 (PL-2). Based on this analysis, we consider these proteins to be related to PL-2. Analysis of trophoblast proteins by gel-filtration chromatography resulted in the identification of another trophoblast prolactin. This material eluted earlier than PL-2-related proteins on a gel-filtration column, possessed prolactin-like activity (determined by competition with ovine pituitary prolactin for rabbit mammary gland or rat liver prolactin receptors) but showed limited cross-reactivity with either the antiserum to pituitary prolactin or the antiserum to the PL-2 peptide. We have thus identified multiple low molecular weight trophoblast prolactins, possessing different biochemical and immunological characteristics.

Animals↗
PubMed1989

Effects of altered photoperiod or maternal melatonin administration on plasma prolactin concentrations in fetal lambs.

During winter (December to March), when late-pregnant ewes were maintained under an artificial long-day photoperiod (16 h light) for 3 weeks or more before insertion of fetal vascular cannulae between 118 and 120 days of gestation (full term, 147 days), plasma prolactin concentrations in their fetal lambs were significantly increased throughout the last 3 weeks of gestation in comparison with values in similar aged fetuses from ewes experiencing only the natural short-day (less than 9 h light) winter photoperiod. When additional lighting was given only after vascular cannulation, fetal plasma prolactin increased steadily from low values, characteristic of winter pregnancies, to high values, characteristic of long-day (16 h light:8 h darkness) pregnancies. Maternal plasma prolactin concentrations changed in a similar way. During summer pregnancies (greater than 16 h light), plasma prolactin in fetal lambs was significantly reduced within 48 h when ewes were given melatonin by i.v. infusion for 14 h each night to simulate the winter duration of the nocturnal increase in plasma melatonin. Maternal plasma prolactin concentrations also decreased significantly when melatonin was given for 3 weeks, but not in a shorter experiment. Increases in fetal plasma prolactin were proportional to the basal prolactin concentration in fetuses injected i.v. with TRH or a dopaminergic antagonist, metoclopramide, to assess how photoperiod influenced the responsiveness of prolactin secretion to acute stimulation. The results confirm that photoperiod, rather than developmental maturity, is the principal determinant of plasma prolactin in the fetal lamb during the last third of gestation, and provide evidence that photoperiodic information is transmitted to the fetus through the diurnal rhythm of melatonin in the ewe.

Animals↗
PubMed1993

Ruminants express a prolactin receptor of M(r) 33,000-36,000 in the mammary gland throughout pregnancy and lactation.

Developmental variation in the expression of the prolactin receptor in the ruminant mammary gland was investigated. Affinity chromatography revealed that bovine prolactin and human GH each bound to the same mammary gland proteins, yielding fractions enriched in binding activity and a protein of M(r) 36,000, assumed to be a bovine prolactin receptor. Affinity cross-linking of 125I-labelled human GH to mammary microsomes confirmed that the M(r) 36,000 protein was a bovine prolactin receptor. Binding assays of receptors in microsomes from the mammary tissue of cows and ewes at various stages of the lactational/reproductive cycle indicated developmental regulation of receptor concentration, but not receptor type, as no other bovine prolactin receptor type was detected by affinity cross-linking. These results suggest that differences in the response to prolactin in the mammary gland at various developmental stages in ruminants are not due to the expression of different forms of the prolactin receptor, and the lack of a prolactin effect on established lactation in ruminants is not due to the absence of the M(r) 36,000 form of the prolactin receptor.

Animals↗
PubMed1994

Physiological roles of thyrotrophin-releasing hormone and vasoactive intestinal peptide on the pulsatile secretory patterns of prolactin in pituitary-grafted female rats.

Much is known about the fact that thyrotrophin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulate prolactin secretion but areas of uncertainty remain. This work was undertaken to describe the effects of TRH and VIP on the pulsatile secretion pattern of prolactin, in adult sham-operated and pituitary-grafted hyperprolactinaemic female rats. Two pulses of TRH (1 microgram/rat) or one pulse of VIP (20 micrograms/rat) were given 60 or 120 min after the period of blood sampling. Pituitary grafting increased the mean values of prolactin, absolute amplitude and duration of the peaks and decreased their frequency, compared with control animals. In sham-operated rats, TRH elevated prolactin levels by increasing the absolute and relative amplitudes and duration of the pulses, along with a decrease in their frequency. No priming effects of TRH were observed in this study. Hyperprolactinaemia blunted TRH effects on the pulsatile secretion pattern of prolactin. In sham-operated rats, VIP administration increased the absolute and relative amplitudes of the prolactin peaks. None of the other parameters studied were changed. In pituitary-grafted animals, VIP administration increased the absolute and relative amplitudes of the prolactin peaks but to a lesser extent compared with controls. These data suggest that TRH and VIP affect prolactin pulsatility differentially. The effects of TRH and VIP were blunted to some extent by exposure to previously elevated circulating prolactin levels.

Animals↗
PubMed2002

Effect of prolactin and dopaminergic drugs on uterine response to chronic estrogen exposure.

The aim of this work was to examine the role of prolactin and dopaminergic drugs, which affect prolactin secretion, on proliferative and morphogenetic reactions in the uterus under continuous estrogen treatment. Ovariectomized mice received injections of estradiol dipropionate (2 microg per 100 g, weekly) or vehicle and daily injections of prolactin (0.25 mg/100 g) or saline (0.05 ml) for 30 days. Other groups of mice received injections of estradiol or vehicle and injections of saline, and were allowed to drink bromocriptine (25 mg/l), metoclopramide (25 mg/l), or only tap water for 30 days. Prolactin administration results in a decrease in the incidence of abnormal glands with abnormal epithelium, the incidence of atypical hyperplasia, uterine weight, proliferation (the number of mitotic and bromodeoxyuridine-labeled cells) and the levels of estrogen receptor-alpha, but causes an increase in the level of beta-catenin in uterine tissues of estrogen-treated mice. The effect of metoclopramide, which increases prolactin secretion, is principally similar to prolactin, but much less expressed. Bromocriptine, which reduces prolactin levels, increases uterine weight, proliferation, the levels of estrogen receptor-alpha, the incidence of abnormal glands with abnormal epithelium, the incidence of complex and atypical hyperplasia, and decreases the level of beta-catenin in uterine structures of estrogen-treated mice. In the absence of estradiol, none of the treatments used had any effect on the parameters tested. Thus, prolactin or metoclopramide produce antiestrogenic effects in the uterus of mice and prevent the formation of atypical hyperplasia which has an unfavorable prognosis, but bromocriptine has the opposite effect. Estrogen receptor-alpha and beta-catenin were associated with the actions of prolactin, metoclopramide and bromocriptine on estrogen-dependent processes in the uterus.

Animals↗
PubMed2003

Effects of acute prolactin manipulation on sexual drive and function in males.

The neuroendocrine response to sexual activity in humans is characterized by a pronounced orgasm-dependent increase of plasma levels of prolactin. In contrast to the well-known inhibitory effects of chronic hyperprolactinemia on sexual drive and function, the impact of acute prolactin alterations on human sexual physiology is unknown. Therefore, this study was designed to investigate the effects of acute manipulation of plasma prolactin on sexual behavior. Ten healthy males participated in a single-blind, placebo-controlled, balanced cross-over design. Prolactin levels were pharmacologically increased to high levels (protirelin, 50 micro g i.v.) or reduced to low physiological concentrations (cabergoline, 0.5 mg p.o.). Sexual arousal and orgasm were then induced by an erotic film and masturbation. In addition to continuous neuroendocrine and cardiovascular recordings, the quality and intensity of the acute sexual drive, arousal, orgasm and refractory period were assessed by extensive psychometric measures. Administration of cabergoline decreased prolactin levels and significantly enhanced all parameters of sexual drive (P<0.05), function (P<0.01) and positive perception of the refractory period (P<0.01). Administration of protirelin increased prolactin concentrations and produced small, but not significant reductions of sexual parameters. The sexual effects observed from cabergoline were completely abrogated by coadministration of protirelin. Although different pharmacological sites of action of prolactin-altering drugs have to be considered, these data demonstrate that acute changes in prolactin plasma levels may be one factor modulating sexual drive and function. Therefore, besides a neuroendocrine reproductive reflex, a post-orgasmic prolactin increase may represent one factor modulating central nervous system centers controlling sexual drive and behavior. These findings may offer a new pharmacological approach for the treatment of sexual disorders.

Adult↗
PubMed1997

Effect of feeding and feed deprivation on plasma concentrations of prolactin, insulin, growth hormone, and metabolites in horses.

Two experiments were conducted to determine 1) the prolactin response to different kinds of feedstuffs in stallions and 2) the effects of total feed deprivation on prolactin secretion in mares and its interaction with the prolactin response to feeding. Experiment 1 was performed with stallions as a 6 x 6 Latin square: A) no feed; B) pelleted feed fed to meet 82.5% of the horses' CP requirements; C) pelleted feed at 25% of the amount in B; D) pelleted feed as in B plus water ad libitum; E) cracked corn at the weight in B; and F) chopped alfalfa at the weight in B. The positive prolactin responses (P < .05) to feeding were similar for treatments B through F. The insulin response to feeding was highest (P < .05) in stallions fed water with the pelleted feed. In Exp. 2, 72 h of feed deprivation did not affect (P > .1) daily prolactin secretion. Feeding of a meal on the 3rd d of deprivation increased (P < .05) plasma prolactin, insulin, and glucose concentrations similarly in all mares. There was a positive growth hormone response (P < .1) after feeding in feed-deprived mares but not in fed mares. The prolactin response (P < .001) to thyrotropin-releasing hormone was greater (P = .083) for feed-deprived mares than for controls, whereas the response to sulpiride (P < .001) only tended to differ (P = .16) between groups. We conclude that prolactin secretion may be stimulated by aspects of eating other than the feedstuff itself. Total feed deprivation had little effect on the subsequent prolactin response to a meal or to other known secretagogues.

Analysis of Variance↗
PubMed1993

Heterogeneity of human prolactin levels in serum during the early postpartum period.

The distribution of molecular forms of prolactin in serum of women during the 1st postpartum week was studied using column chromatography. Serum was analyzed 1, 4 and 7 days postpartum. Using this technique, three molecular forms of prolactin were detected with approximate molecular weights of < or = 100, 48 and 22 kDa; these were termed 'big-big', 'big' and 'little' prolactin, respectively. The relative amount of each form was measured in relation to the total amount of immunoreactive prolactin eluted from the column. Throughout the first postpartum week big-big prolactin represented a minor fraction of the total immunoreactive prolactin in the serum of lactating women: 4.9%, 5.2% and 4.6% on days 1, 4 and 7, respectively. There was a gradual decrease in the higher molecular weight forms of prolactin (big-big plus big prolactin) from the 1st to the 7th postpartum day. This was associated with a significant increase of the little prolactin from 62.8 +/- 7.2% at the 1st postpartum day to 72.6 +/- 6.5% at the 7th day (p < 0.05).

Adult↗
PubMed1996

Prolactin response to metoclopramide and thyrotropin-releasing hormone in normoprolactinemic and hyperprolactinemic women: a comparison of diagnostic validity.

The objective was to define the diagnostic validity of prolactin response tests by comparing the stimulating effect of thyrotropin-releasing hormone (TRH) and metoclopramide on prolactin secretion in patients with and without functional hyperprolactinemia. Prolactin response studies were performed in 18 patients with functional hyperprolactinemia (defined as prolactin serum levels > or = 16 and < 50 ng/ml during the follicular phase without evidence of prolactinoma) and 18 controls with similar age who had normal serum prolactin levels. Tests were done on the 7th, 8th or 9th day of the follicular phase under standardized conditions (at 08.00-09.00, after a 1-h rest and overnight fasting) with 200 micrograms TRH or 10 mg metoclopramide i.v. After metoclopramide, higher maximal prolactin levels were observed in the study group as well as in the control group than after TRH (metoclopramide mean: 243 +/- 62 ng/ml vs. 181 +/- 100 ng/ml, U-test: p = 0.0019; TRH mean: 101 +/- 23 ng/ml vs. 41 +/- 20 ng/ml, U-test: p = 0.0001). There was no significant difference in the relative increment of prolactin serum levels between both groups, neither after metoclopramide nor after TRH (after metoclopramide, mean: 13.5 +/- 5.8 vs. 17.2 +/- 9.2, U-test: p = 0.137; after TRH, mean 3.6 +/- 1.1 vs. 3.8 +/- 1.9, U-test: p = 0.899). No correlation between prolactin basal and peak levels, either after TRH or after metoclopramide, could be found, neither in the study (metoclopramide test: p = 0.738; TRH test: p = 0.076) nor in the control group (metoclopramide test: p = 0.331; TRH test: p = 0.360). While significantly higher prolactin peaks were recorded after metoclopramide than after TRH in both groups, no difference in the response to TRH and metoclopramide, regarding absolute and relative increment, could be found.

Adult↗
PubMed1975

Environmental and lactational variables affecting prolactin concentrations in bovine milk.

Relationships were examined between prolactin concentrations in bovine milk and various environmental and lactational variables. Prolactin was quantified by radioimmunoassay in 1.316 milk samples from two experiments. Environmental temperatures preceding milking, stage of lactation, daily miik yield, and dominance rank of the cow were correlated significantly with milk prolactin concentration. Stepwise multiple regression analysis was used to determine, in order of importance, the variables having significant independent effects on milk prolactin. Ambient temperature extremes, high and low, exerted the greatest effects and were each associated with elevated concentrations of prolactin. In Experiment I,conducted throughout the year, the variable representing maximum temperature preceding milking accounted for 14.3% of the variation in milk prolactin. In Experiment II, conducted during late fall and early winter, the minimum temperature preceding milking accounted for 21.1% of the variation. Although earlier stages of lactation and larger daily milk yields were associated with higher prolactin concentrations, inclusion of lactation stage in the stepwise regression model tended to eliminate almost all the variance of prolactinpreviously associated with daily yield. Dominance measurements indicated that more submissive cows had higher milk prolactin. Individual cows tended to have characteristic prolactin, but this tendency was eliminated by statistical adjustment of the data for environmental and lactational variables.

Animals↗
PubMed1982

Chronological profiles of prolactin and growth hormone in lactating cows.

Prolactin and growth hormone were measured in blood plasma at 30-min intervals for three consecutive 24-h periods in 6 cows during midlactation. Concentrations of prolactin in milk and yields of milk also were quantified. Prolactin in blood plasma appeared to have a 24-h rhythm as well asd a 6-h rhythm by time series spectral analysis. Lowest prolactin occurred between 0600 and 0900 h each day, whereas maximums occurred between 1030 and 1600 h. Neither milk prolactin concentration nor yield of milk differed between milkings at 0530 and 1730 h. Concentration of prolactin in milk was not significantly correlated with prolactin concentration of plasma. However, prolactin of plasma averaged over the 12-h prior to milking was associated significantly with yield of milk and with total quantity of milk prolactin removed at that milking.

Animals↗
PubMed1975

Thyrotropin-releasing hormone blockade of the ergocryptine and apomorphine inhibition of prolactin release in vitro.

The interaction of thyrotropin-releasing hormone (TRH) and ergocryptine or apomorphine in affecting prolactin secretion was examined. Ergocryptine and apomorphine inhibited the release of 3H-prolactin labeled in an in vitro incubation of the rat anterior pituitary and led to a retention within the gland of 3H-prolactin. TRH (1.4 X 10(-8) M) partially blocked the inhibitory effect of 4 x 10(10) M ergocryptine on 3H-prolactin release and totally blocked the effect on radioimmunoassayable prolactin release. TRH also completely blocked the inhibitory effects of 5 x 10(-8) M apomorphine on both 3H-prolactin and radioimmunoassayable prolactin release. Since TRH can also completely block the inhibitory effects of dopamine upon prolactin secretion, these results are consistent with apomorphine and ergocryptine stimulating "dopaminergic" sites and also further support the role of TRH as a prolactin-releasing factor.

Animals↗
PubMed1976

Plasma prolactin levels in maturing intact and cryptorchid male rats: development of stress response.

In order to determine the possible role of the seminiferous tubules in the regulation of prolactin secretion during sexual development, male rats were rendered cryptorchid at 22 days of age, and thereafter different groups of animals were decapitated at 8-10 day intervals between Day 32 and Day 70. Cryptorchid rats showed destruction of the germinal epithelium accompanied by increased plasma FSH and, to a much lesser extent, increased plasma LH titers. Nevertheless, plasma prolactin levels were similar to those of intact controls throughout the entire period studied. Plasma prolactin titers in intact controls remained uniformly low from Day 20 to Day 70, contrasting with previous reports in which increasing prolactin levels have been observed during sexual development. To determine the reason for this apparent discrepancy, a longitudinal experiment was conducted in which intact and cryptorchid male rats were bled every 10 days from Day 30 to Day 70, following a 3-min period of exposure to ether fumes. The prolactin response to this stress increased markedly with age. A similar pattern of prolactin was observed in a cross-sectional study in which different groups of intact animals were bled following a 3-min period of ether exposure, at ages ranging from 20 to 70 daysmthe results indicate that unlike FSH secretion, prolactin secretion is not controlled by the seminiferous tubules. In addition, they suggest that the pattern of increasing plasma prolactin previously described in the developing male rat is at least in part caused by an age-dependent increase in responsiveness of prolactin to stress.

Age Factors↗
PubMed1983

Evidence of prolactin short loop feedback in the postpartum lactating rat.

Serum prolactin was studied in lactating and nonlactating rats after restraint stress, chronic estradiol benzoate treatment, and acute L-tryptophan treatment. As expected, these treatments evoked increases in serum prolactin in nonlactating rats. In lactating rats these treatments did not increase basal serum prolactin when litters were removed for 4 hr. Daily estradiol benzoate treatment increased pituitary gland prolactin content after 14 days, but there was no effect on basal serum prolactin. Daily estradiol treatment did not augment prolactin release in response to 30 min of suckling. It is suggested that the short loop feedback by prolactin (i.e., prolactin inhibiting its own secretion) makes the lactating rat refractory to these stimuli of prolactin secretion.

Animals↗