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PubMed1984

The role of steroid hormones, prolactin and placental lactogen on mammary gland development in ewes and heifers.

In the first part of the investigations the interaction between oestradiol-17 beta, progesterone and prolactin on the formation of the lobuloalveolar structure of the mammary gland was studied in 21 nulliparous intact postpubertal ewes. Tissue specimens of the mammary gland were evaluated by light microscopical examination and prolactin was measured in blood samples. Combined treatment with oestradiol and progesterone induced physiological development of the lobuloalveolar structure of the mammary gland in the presence of prolactin. Suppression of prolactin by bromocriptine prevented this effect. Treatment with progesterone alone was not effective and revealed histological structures comparable to the controls. The interaction of oestradiol-17 beta with prolactin appears to be a main trigger for mammary gland development. In the second part of the investigations the effect of bromocriptine treatment during pregnancy on mammary gland development was studied in primigravid ewes and heifers. Mammary gland specimens were obtained for light and electron microscopical evaluation in ewes and heifers 5 and 10 days respectively before the expected date of parturition. Concentrations of prolactin and ovine placental lactogen were determined by radioimmunoassay. Bromocriptine treatment suppressed prolactin concentrations in ewes to minimal values but did not affect ovine placental lactogen concentrations. The histological evaluation revealed almost comparable stages of mammogenesis in both ewes and heifers. This effect can be attributed, at least in ewes, to the action of placental lactogen on mammogenesis. Placental lactogen might therefore be of physiological relevance during mammogenesis.

Animals↗
PubMed1984

Effect of dehydration, haemorrhage and oviposition on serum concentrations of vasotocin, mesotocin and prolactin in the chicken.

Serum concentrations of arginine vasotocin (AVT), mesotocin and prolactin were determined by radioimmunoassay in Rhode Island Red chickens during and after dehydration, haemorrhage and oviposition. During dehydration increased circulating levels of AVT, mesotocin and prolactin were found. As water deprivation proceeded, marked differences were observed. After an initial rise in serum AVT, mesotocin and prolactin levels during mild and moderate dehydration, concentrations of both AVT and prolactin tended to normalize during continued water deprivation, while those of mesotocin remained high throughout the whole dehydration experiment with the highest at the end of the water-deprivation period. Removal of 5 ml blood at intervals of 10 min during six consecutive time-periods did not affect serum osmolality and circulating levels of AVT and prolactin, but slightly increased mesotocin. These results suggest an osmoregulatory role for AVT and prolactin, whereas mesotocin may be involved in volume control. Finally, 1 min after oviposition, control values of 19.5 +/- 3.4 pmol AVT/1 (n = 9) were raised more than sevenfold to 142.9 +/- 12.5 pmol/l (n = 11). Thereafter, a decline occurred with a half-life for AVT of 13 min with raised serum levels up to 31 min after oviposition. In contrast, the serum concentrations of mesotocin and prolactin remained unaffected by oviposition.

Animals↗
PubMed1984

Inverse changes in plasma prolactin and LH concentrations in female canaries after disruption and reinitiation of incubation.

Prolactin and LH concentrations were measured in the plasma of female canaries sampled during the breeding cycle and after disruption and reinitiation of incubation behaviour. The late incubation period was characterized by low LH and high prolactin concentrations, and canaries separated from their nests at this stage showed an increased in LH and a decline in prolactin within 3 h. In one experiment mean (+/- S.E.M.) concentrations before and 24 h after nest deprivation were: prolactin 397 +/- 86 and 18 +/- 5 micrograms/l; LH 1.04 +/- 0.21 and 2.03 +/- 0.17 micrograms/l. Female canaries which abandoned their nests after the eggs had been removed also showed an increase in LH together with a fall in prolactin 24 h after egg removal. When nest-deprived canaries were allowed to resume incubation, plasma prolactin increased again within 5 h and after 2 days had reached levels normal for incubating birds (398 +/- 46 micrograms/l). Concentrations of LH changes more gradually but had decreased 2 days after the resumption of incubation. Thus prolactin and LH show inverse changes after the disruption and reinitiation of incubation behaviour; it is not clear, however, if the change in one is dependent on the other or if both hormones are responding to the same external stimulus.

Animals↗
PubMed1984

Stimulation of prolactin secretion by oestradiol in the rat is associated with increased hypothalamic release of thyrotrophin-releasing hormone.

We have studied the effect of oestradiol (OE2) on secretion of prolactin and TSH by rat pituitary glands and correlated this with changes in hypothalamic content and release of thyrotrophin-releasing hormone (TRH). Ovariectomized Wistar rats received s.c. silicone elastomer implants of OE2 at a dose known to give pro-oestrous OE2 levels. After 1 week rats were decapitated, blood was collected for assay of prolactin and TSH, blocks of hypothalamus were dissected out and pituitary glands were removed and bisected. Medium bathing hemipituitary glands was collected for measurement of prolactin and TSH after a 30-min incubation. Immunoreactive TRH was measured in medium removed from hypothalami and in extracts of homogenized hypothalami. Serum prolactin was higher in OE2-treated than in control animals (59.3 +/- 19.5 (S.E.M.) vs 9.4 +/- 1.5 micrograms/l; P less than 0.05) and this was associated with a threefold increase in pituitary prolactin in the medium. By contrast, TSH concentrations in serum and pituitary incubation medium were not significantly different in the two groups. There was no difference between the groups in hypothalamic content of TRH but TRH release in the incubation medium was increased by OE2 (30.2 +/- 6.5 vs 10.0 +/- 1.3 pg/mg protein per 30 min; P less than 0.01). In summary, physiological levels of OE2 stimulated prolactin secretion without change in TSH and this was associated with a threefold increase in hypothalamic release of TRH. These findings suggest that the stimulating effect of OE2 on prolactin secretion may, in part, be mediated by hypothalamic TRH.

Animals↗
PubMed1985

Effect of immunoneutralization of thyrotrophin-releasing hormone on the release of thyrotrophin and prolactin during suckling or in response to electrical stimulation of the hypothalamus in the anaesthetized rat.

The aim of the present study was to use the technique of immunoneutralization with anti-thyrotrophin-releasing hormone (anti-TRH) serum to investigate the role of TRH in mediating the TSH and prolactin responses to electrical stimulation of the hypothalamus and the prolactin response to suckling in lactating rats. Electrical stimulation of either the median eminence or paraventricular nuclei of male or female rats anaesthetized with urethane resulted in significant increases in the plasma concentrations of both TSH and prolactin. Injection of sheep anti-TRH serum blocked the rise in plasma TSH concentration in response to stimulation of either brain area, but did not block the increase in plasma prolactin concentration. In anaesthetized, lactating female rats, the suckling stimulus produced a significant increase in the plasma prolactin concentration, but did not alter the plasma TSH concentration. Injection of anti-TRH serum, but not control non-immune or anti-bovine serum albumin, significantly decreased the basal release of TSH but did not abolish the prolactin response to suckling. These results show that TRH is the principal mediator of the neural control of TSH release in the rat, but is not crucial for the release of prolactin in response to either hypothalamic stimulation or suckling.

Animal Population Groups↗
PubMed1985

Prolactin in cerebrospinal fluid increases the synthesis and release of hypothalamic gamma-aminobutyric acid.

The effect of intracerebroventricularly (i.v.t.)-injected rat prolactin (2 micrograms/rat) on the function of tuberoinfundibular gamma-aminobutyric acid (GABA)ergic neurones was assessed in adult male rats by measuring the activity of glutamic acid decarboxylase (GAD) in the mediobasal hypothalamus (MBH) and the concentrations of GABA in hypophysial portal plasma and in the anterior pituitary gland. Fourteen hours after i.v.t. injection of rat prolactin the activity of GAD in the MBH was significantly (P less than 0.05) increased and it remained elevated for at least 16 h after injection. The mean concentrations of GABA in hypophysial portal plasma and in the anterior pituitary were twice those found in vehicle-treated controls 16 h after administration of rat prolactin; no significant effects were observed at earlier time-periods. A significant (P less than 0.01) and long-lasting decrease in endogenous plasma prolactin concentrations was detected 2 h after the i.v.t. injection of rat prolactin and the concentrations remained suppressed for up to 16 h. The present results are consistent with the concept that the activity of tuberoinfundibular GABAergic neurones is regulated, at least in part, by circulating prolactin. The ability of prolactin to accelerate the synthesis and release of GABA in the MBH might constitute a short loop feedback system by which the hormone regulates its own secretion.

Animals↗
PubMed1985

Increased dopaminergic inhibition of prolactin in the hypoprolactinaemic IPL nude rat.

In this study, aimed at investigating whether dopaminergic regulation of prolactin could be implicated in the hypoprolactinaemia observed in the IPL nude rat, dopaminergic inhibition of prolactin was suppressed using a catecholamine synthesis inhibitor alpha-methyltyrosine (MT) and a dopaminergic antagonist sulpiride. Adult male rats (IPL nude and normal) were injected through implanted atrial cannulae with either MT (250 mg/kg) or physiological saline (control). Rats were decapitated 2 h after the injection. Plasma prolactin levels, compared with basal values, increased by 15.6 +/- 1.9 (S.E.M.)- and 5.89 +/- 0.6-fold in IPL nude and normal rats respectively. This difference was highly significant. The pituitary prolactin content was decreased in both groups. In a second experiment, adult male IPL nude or normal rats were injected with either sulpiride (1 mg/kg) or saline and decapitated 2, 4, 8, 12, 14 and 24 h later. Plasma prolactin levels, compared with basal values, were increased in rats injected with sulpiride by 9.2 +/- 1.8 and 3.4 +/- 0.7-fold in IPL nude and normal rats respectively. The pituitary prolactin content was reduced more in IPL nude than in normal sulpiride-injected rats. These data suggest that prolactin secretion, as well as synthesis, is under an increased dopaminergic inhibition in the male IPL nude rat.

Animals↗
PubMed1986

Superior cervical ganglionectomy prevents gonadal regression and increased plasma prolactin concentrations induced by long days in goats.

The effects of the abolition of the diurnal change in melatonin secretion on the photoperiodic response of the gonadal axis and prolactin secretion to long days were examined in female goats. Female Saanen goats, reared under short-day conditions (8 h light: 16 h darkness; lights on at 05.00 h) at 22 +/- 2 degrees C for 5 months, were bilaterally superior cervical ganglionectomized (SCGX). One month after surgery, both SCGX and intact control goats were divided into two groups. Animals in group 1 were maintained under short days and those in group 2 moved to long days (16 h light: 8 h darkness; lights on at 05.00 h). In group 1, both SCGX and intact goats ovulated periodically and basal plasma prolactin levels were maintained throughout the day. In intact controls, exposure to long days suppressed ovulation and increased prolactin secretion for the first 150-200 days of exposure. The animals became photorefractory after this time; ovulation recurred and prolactin secretion returned to basal levels. Superior cervical ganglionectomy abolished or weakened the suppression of gonadal function and eliminated the increase in prolactin secretion induced by exposure to long days in the intact controls. These results suggest that the pattern of melatonin secretion under long days is necessary to induce the photoperiodic response of gonadal function and prolactin secretion to long days and that, under natural conditions, melatonin regulates the seasonal changes in gonadal function and prolactin secretion by mediating the effect of long days.

Animals↗
PubMed1987

Release of big and small molecular forms of prolactin: dependence upon dynamic state of the lactotroph.

Secretion of different molecular forms of prolactin was studied from a multidisciplinary standpoint in three different experimental rat models which covered the broadest range of lactotrophic activity. The results obtained allowed the recognition of common secretory patterns in stimulated, inhibited and hyperstimulated lactotrophic activity. Polymeric (big) prolactin is stored exclusively in membrane-bound secretory granules and appears to be a convenient biochemical marker with which to quantify the pool of hormone stored in the cell cytoplasm, while monomeric (small) prolactin represents a pool of newly synthesized hormone which is loosely coupled to organelles involved in its intracellular processing. Most of the prolactin in stimulated lactotrophs is processed through a regulated pathway and the hormone released by exocytosis of secretory granules. Interruption of stimulation resulted in accumulation of secretory granules and polymeric prolactin. In hyperstimulated lactotrophs the polymerization and aggregation of prolactin into secretory granules was bypassed and most of the hormone released directly after its synthesis. The pattern of prolactin secretion could be closely correlated with the dynamic state of the lactotroph.

Animals↗
PubMed1988

Calcitonin inhibition of prolactin secretion in isolated rat pituitary cells.

Salmon calcitonin inhibited TRH-stimulated release of prolactin in isolated pituitary cells from untreated female rats. These cells were still capable of responding to the fresh addition of TRH after the removal of calcitonin. Calcitonin gene-related peptide had only a weak effect in inhibiting prolactin release in these cells. Pituitary cells isolated from female rats which had been treated with weekly s.c. injections of 1 mg oestradiol dipropionate for 4 weeks, exhibited a marked increase in the magnitude of the inhibition of prolactin release by salmon calcitonin. Both basal and TRH-stimulated release of prolactin were inhibited by concentrations of 0.1 nmol salmon calcitonin/l or higher. Prolactin release from these cells was also inhibited at somewhat higher concentrations by calcitonin gene-related peptide. Our results demonstrate that calcitonin can directly inhibit basal as well as TRH-stimulated prolactin release by acting directly at the pituitary. The results strongly suggest that the peptide may be involved in the regulation of prolactin release in certain physiological conditions.

Animals↗
PubMed1988

Reductions in plasma LH concentration and testicular weight in ring doves following intracranial injection of prolactin or growth hormone.

Testicular weights and concentrations of LH in plasma were measured in individually housed adult male ring doves given five daily intracerebroventricular injections of saline-NaHCO3 vehicle (2 microliter), ovine prolactin (0.1, 0.5, 1.0 or 2.0 micrograms/day), turkey prolactin (1.0 micrograms/day), turkey GH (1.0 micrograms/day) or ovine GH (1.0 micrograms/day). Administration of ovine prolactin resulted in a dose-dependent suppression of plasma LH concentration, with values in the two highest dose groups averaging three- to fivefold less than those of vehicle-injected controls. Reductions of similar magnitude were obtained following intracranial administration of turkey, ovine or human GH. Whilst effective in reducing plasma LH, turkey prolactin was less effective than an equivalent dose of ovine prolactin. Testicular regression was observed in all treatment groups which showed a significant decrease in plasma LH concentrations. Because crop sacs remained undeveloped in all treatment groups, it was concluded that these centrally administered hormones acted primarily at the level of the brain or pituitary to exert their suppressive effects. The possibility that prolactin and GH interact with different binding sites to inhibit LH secretion is discussed, together with evidence for a possible role of prolactin and GH in gonadotrophin regulation under normal physiological conditions.

Animals↗
PubMed1989

International Standards for human prolactin: calibration by international collaborative study.

Three ampouled preparations of purified human prolactin were assessed by 20 laboratories in eight countries for their suitability to serve as International Standards for the estimation of human prolactin in serum. Bioassays (pigeon crop sac assays and NB2 cell assays) were carried out in two laboratories, radioreceptor assays by one laboratory and radioimmunoassays by 17 laboratories. By physicochemical analysis the preparations appeared similar. Each preparation contained small amounts of contaminants and/or prolactin variants. No major differences among the three preparations were detected by immunoassay although, in one radioreceptor assay system, one of the preparations was found to differ from the other two. On the basis of all the available information, the Expert Committee on Biological Standardization of the World Health Organization (ECBS) in 1986 established the preparation in ampoules coded 83/562 as the Second International Standard for Prolactin and in October 1988 established the preparation in ampoules coded 84/500 as the Third International Standard for Prolactin. A value of 0.053 IU (53 mIU) prolactin activity/ampoule was assigned to both the Second and Third IS on the basis that this unitage would, insofar as possible, maintain continuity of the IU defined by the First International Reference Preparation of Prolactin, human, for Immunoassay (coded 75/504).

Amniotic Fluid↗
PubMed1990

The depletion of plasma prolactin by pantethine in oestrogen-primed hyperprolactinaemic rats.

Pantethine was investigated for its potential to deplete prolactin in the plasma and pituitary cells of oestrogen-primed hyperprolactinaemic rats. This compound has been used in the past to deliver cysteamine systemically, through its congener pantetheine, a metabolic precursor for cysteamine. Cysteamine itself, specifically reduces plasma and pituitary prolactin. The addition of pantethine (2-10 mmol/l) to the media of isolated pituitary cells over 4 h did not appreciably alter the intracellular content of immunoreactive prolactin. Moreover, oral administration of pantethine at 0.5 and 1.0 g/kg body weight did not influence the concentration of immunoreactive plasma prolactin. However, the concentration of plasma prolactin fell by 48 and 67%, when pantethine was injected i.p. at 0.5 and 1.0 g/kg body weight, after 4 h. Intravenous administration of pantethine resulted in even greater losses of prolactin, in the order of 50 and 81% depletion for 0.5 and 1.0 g/kg body weight respectively and within 2 h of administration. However, cysteamine was found to be more efficacious than pantethine on a molar basis with regard to depleting the plasma concentration of prolactin in hyperprolactinaemic rats.

Administration, Oral↗
PubMed1992

The ontogenic and functional relationships between growth hormone- and prolactin-releasing cells during the development of the bovine pituitary.

The ontogeny of GH- and prolactin-releasing cells in the developing bovine pituitary was evaluated by reverse haemolytic plaque assays which allows for the detection of hormone release from individual pituitary cells in culture. With this approach, we observed that GH-releasing cells ontogenically preceded prolactin-releasing cells. In fact, GH secretors were observed as early as 59 days of gestational age while cells that released prolactin were not identified until 98 days. The amounts of both GH- and prolactin-releasing cells increased with time to reach more than 50% and 20% of all pituitary cells near term (term approximately 280 days) respectively. Interestingly, the first cells shown to release prolactin also released GH (i.e. were mammosomatotropes). This temporal and functional relationship between GH and prolactin secretors provides suggestive evidence that GH-secreting cells act as the progenitor cells for prolactin secretors via a functional intermediate, the mammosomatotrope.

Animals↗
PubMed1992

Tissue kallikrein is associated with prolactin-secreting cells within human growth hormone-secreting adenomas.

Tissue kallikrein is a serine protease which may be involved in the intracellular processing of prolactin in the anterior pituitary gland. The expression of tissue kallikrein, in the rat, is promoted by oestrogen and inhibited by dopamine. Human and rat prolactinomas contain markedly increased amounts of tissue kallikrein; this is comparatively reduced if patients are pretreated with the dopamine agonist, bromocriptine, before surgery. Some GH-secreting adenomas are mixed and also contain prolactin-secreting cells. We therefore investigated 27 GH-immunostaining human pituitary adenomas for the presence of immunoreactive tissue kallikrein. Sixteen of the adenomas had positive immunostaining for prolactin; eight of these patients had associated clinical hyperprolactinaemia before the tumour was removed. Tissue kallikrein immunoreactivity was found in ten adenomas, all of which also had prolactin immunopositivity. There was a close relationship between the percentage of cells staining for prolactin and tissue kallikrein but not for GH. A further eight adenomas had patchy positivity, i.e. less than 1% of cells immunostained for tissue kallikrein and six of these also had some prolactin-staining cells. Nine out of eleven purely GH-staining adenomas had no tissue kallikrein immunopositivity, the remaining two showing patchy staining. A review of bromocriptine responsiveness, as assessed by mean GH hormone levels during oral glucose tolerance tests before and after therapy was commenced, indicated that patients with adenomas which stained for prolactin and tissue kallikrein were more likely to respond to bromocriptine than those which failed to do so.

Adenoma↗
PubMed1992

Influence of lactotroph cell density on prolactin secretion in rats.

The relationships between the stimulation of prolactin secretion and proliferation of lactotrophs was studied from a multidisciplinary standpoint in three experimental models. Administration of both oestrogen and sulpiride resulted in a significant increase in prolactin secretion and in the lactotroph population. A single injection of 10 micrograms oestradiol benzoate (OB) induced a twofold increase in the proliferation of lactotrophs (morphometrically as volume density), which increased further (2.5-fold) after three OB injections. Parallel changes were observed in the net counts made on lactotrophs sectioned through the nucleus to avoid possible distortions in volume density caused by hypertrophic cytoplasms. Comparable results were obtained with the mitotic index in the same groups of rats exposed to treatment with colchicine. The effect of sulpiride on proliferation of lactotrophs was also significant (1.7-fold) but less pronounced than in rats treated with oestrogens. The treatments with oestrogen and sulpiride did not stimulate lactotrophic activity in a similar way, as judged by the levels of serum prolactin and the storage patterns of small and big prolactin in pituitary glands. Serum prolactin (mean +/- S.E.M.) in control ovariectomized rats was 4.0 +/- 0.9 micrograms/l and one and three injections of OB raised these levels to 14.4 +/- 5.0 and 28.8 +/- 4.6 micrograms/l respectively. The highest levels of serum prolactin were seen in sulpiride-treated rats (467.2 +/- 28.7 micrograms/l). Striking differences occurred in the pituitary contents of big prolactin, the control values increasing from 5.3 +/- 0.5 to 10.2 +/- 1.3 micrograms/mg after one OB injection and to 14.7 +/- 0.7 micrograms/mg after three OB injections.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of placing micro-implants of melatonin in the mediobasal hypothalamus and preoptic area on the secretion of prolactin and beta-endorphin in rams.

In a previous study, we showed that the local administration of melatonin in the mediobasal hypothalamus (MBH), but not the preoptic area (POA), caused a premature increase in the secretion of FSH and growth of the testes in sexually inactive Soay rams exposed to long days. To extend these observations, we have now measured blood concentrations of prolactin and beta-endorphin and the associated peripheral responses in the same animals, to establish whether the treatments produced multiple endocrine changes such as those which occur following exposure to short days. Groups of rams were initially exposed to alternating 16 weekly periods of long days (16 h light: 8 h darkness; 16L:8D) and short days (8L:16D) for at least 9 months to entrain the seasonal cycles in the secretion of the pituitary hormones. The treatments were started at 10 weeks under long days, when the animals had a physiology characteristic of the early summer with high blood plasma concentrations of prolactin (associated with growth of the summer pelage), and low concentrations of beta-endorphin (associated with low body weight). The animals were assigned at random to the following treatments: (i) micro-implants of melatonin in the MBH, (ii) microimplants of melatonin in the POA, (iii) empty implants in the MBH or POA to act as operated controls, and (iv) no surgery to act as unoperated controls (n = 12 rams/treatment). The micro-implants consisted of 22-gauge stainless-steel needles with melatonin fused inside the tip. The implants were inserted bilaterally in the brain, and left in place for 12-14 weeks. The observations continued for a total of 28 weeks while the animals remained under long days. The administration of melatonin in the MBH induced a rapid decreased in plasma concentrations of prolactin while in the POA it induced a less marked but significant effect. The mean times to minimum concentrations of prolactin were 7.4 +/- 0.4, 17.3 +/- 2.8 and 26.0 +/- 0.3 weeks for the MBH, POA and combined control groups respectively (MBH vs control, P < 0.001, POA vs control P < 0.01). In the MBH group, the concentrations of prolactin subsequently increased to a maximum 6 weeks after the end of melatonin treatment. The changes in prolactin were accompanied by changes in growth and moulting of the pelage; only animals in the MBH group showed a conspicuous moult associated with the change from low to high prolactin secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Transcription of prolactin gene in milk secretory cells of the rat mammary gland.

In-situ hybridization and Northern blot hybridization were used to identify mRNA for pituitary prolactin in mammary tissue obtained from female rats 1 day before expected parturition, 1 day after parturition and on day 7 of lactation. Prolactin cDNA was labelled with 32P for Northern analysis and with digoxigenin for in-situ hybridization. Total and poly(A)+ RNA from pituitary, mammary and control (fat and kidney) tissues were analysed by agarose gel electrophoresis with transfer to nitrocellulose and hybridization to a cDNA for rat prolactin. Although present in much smaller amounts than the 1.0 kb transcript in pituitary RNA homogenates, mammary RNA homogenates from all three stages contained mRNA of approximately 1.0 kb which hybridized with the prolactin probe. Similar analyses of fat and kidney failed to reveal any hybridization at the 1.0 kb size. When tissue sections were hybridized to the cDNA probe, specific hybridization was observed in the milk secretory cells of the mammary alveoli and the lactotroph cells of the anterior pituitary, but not in liver cells or in RNAase-treated sections of mammary tissue. In summary, these results demonstrate that milk secretory cells of the rat mammary gland transcribe the gene for prolactin, and they raise the possibility that a primary target tissue for blood-borne prolactin may also synthesize prolactin.

Animals↗

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