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PubMed2005

Control of prolactin secretion by excitatory amino acids.

This article provides an overview of the increasing number of observations indicating that excitatory amino acids are involved in the control of prolactin secretion. The information available suggests that these amino acids exert a stimulatory action on hypophysial prolactin. Administration of a glutamate receptor agonist induces significant increase in prolactin release in rats, monkeys, and rams. In contrast, noncompetitive antagonists of N-methyl-D-aspartate receptors decrease plasma levels and attenuate the preovulatory surge of prolactin. It appears that the endogenous glutamatergic system participates not only in the regulation of basal secretion of prolactin, but also in the control of physiological prolactin responses induced by the suckling stimulus or by stress. Recent findings suggest that the glutamatergic innervation of the hypothalamic paraventricular nucleus is involved in the mediation of the neural signal of the suckling stimulus-induced prolactin release as well as in the mediation of the stress-induced release of prolactin.

Animals↗

PubMed2004

Annexin 5 inhibits thyrotropin releasing hormone (TRH) stimulated prolactin release in the primary culture of rat anterior pituitary cells.

Annexin 5, a novel calcium-phospholipid binding protein, is thought to be involved in hormone secretion by the anterior pituitary gland. Gonadotropin releasing hormone stimulates annexin 5 synthesis, which, in turn, enhances gonadotoropin secretion. On the other hand, annexin 5 was shown to inhibit prolactin release in vitro. To understand the nature of the opposing effects of annexin 5 on these two major pituitary hormones, the present study examines the inhibitory effect of annexin 5 on prolactin release in relation to thyrotropin stimulating hormone (TRH) using primary cultures of anterior pituitary cells of adult female rats. While recombinant rat annexin 5 was found to have little effect on basal prolactin release, it significantly inhibited TRH-stimulated prolactin release. Addition of specific anti-annexin 5 serum to the culture increased basal prolactin release in a concentration dependent manner, and no further increase in prolactin release was observed following application of TRH in the presence of anti-annexin 5. The enhanced basal prolactin release induced by anti-annexin 5 was reversed by the simultaneous administration of indomethacin, an inhibitor of cyclooxygenase. These results demonstrate that endogenous pituitary annexin 5 exerts an inhibitory effect on prolactin release and suggest that this is attained by suppression of eicosanoid synthesis in vitro.

Animals↗

PubMed1976

Prolactin release by synthetic luteinizing hormone-releasing hormone (LHRH) in thyroidectomized-androgenized adult rats.

Synthetic LHRH, at a dose of 5 mug/kg, induced a marked increase in the serum LH level but a marked decrease in the serum prolactin level when injected iv to normal adult female rats on the day of estrus. In adrogenized adult rats which had been showing persistent estrous vaginal smears, a less marked increase in the serum LH level was shown following injection of LHRH. Prolactin level decreased only slightly in these animals. Control level of serum prolactin in normal estrous and androgenized rats were 4.95 +/- 0.35 and 5.42 +/- 0.65 mIU/ml, respectively. Thyroidectomized-normal cycling rats responded to LHRH with a slight decrease in the serum prolactin level when injected on the day of diestrus. Prolactin level increased, however, 5 min after LHRH injection in thyroidectomized-androgenized adult rats, which were thyroidectomized at the age 4, 6 or 10-12 weeks and have retained a low prolactin level similar to that in the diestrous stage of normal cycling rats thereafter. The present results suggest that regulatory system of prolactin secretion became labile by androgenization and this status led to the release of prolactin by LHRH treatment after thyroidectomy.

Animals↗

PubMed1978

Prolactin binding in pregnancy-dependent mammary tumors in GR/A mice.

Prolactin binding in normal mammary glands and pregnancy-dependent mammary tumors and plasma prolactin levels were assayed near parturition in GR/A female mice. Mammary glands and tumors cut into 0.5-mm thick slices were incubated in Medium 199 containing 5 ng of 125I-labeled ovine prolactin at 37 degrees C for 2 hr, and specific prolactin binding was expressed in terms of the difference between total and nonspecific bindings per mg tissue. On day 19 of pregnancy, prolactin binding was low in both normal mammary glands and tumors. One day after parturition, the binding of nonlactating mammary gland was as low as that on day 19 of pregnancy. On the other hand, the binding of lactating glands was raised significantly. There was no difference in the binding of tumors between lactating and nonlactating animals and both were significantly higher on day 1 after parturition than on day 19 of pregnancy. The plasma prolactin level assayed by radioimmunoassay was significantly higher on day 19 of pregnancy than on day 1 after parturition regardless of lactation. No relations were observed between the plasma prolactin level and the prolactin binding of either normal or neoplastic mammary glands.

Animals↗

PubMed1996

The influence of cortisol on spontaneous and 5HT stimulated prolactin release in man.

The role of cortisol in influencing spontaneous and 5HT mediated prolactin release was investigated in 17 healthy male subjects who took part in 3 separate studies. Five of the subjects were treated for 24 h with metyrapone (the 11 beta-hydroxylase inhibitor which prevents the conversion of 11-deoxycortisol to cortisol) on one occasion and placebo for 24 h on another. On both test occasions their spontaneous prolactin was monitored before they underwent serotonergic-stimulated prolactin release using D-fenfluramine (30 mg). Treatment with metyrapone enhanced the spontaneous nocturnal prolactin surge and also the prolactin response to D-fenfluramine. Six of the subjects were treated for 24 h with hydrocortisone on one occasion or placebo on the other. With hydrocortisone treatment no nocturnal increase in prolactin was observed and the response to D-fenfluramine challenge was attenuated. To determine whether the influence of cortisol on prolactin release is at a pituitary or supra-pituitary site 6 subjects were tested with thyrotropin releasing hormone (TRH) which acts directly on the pituitary to bring about prolactin release. They were each tested twice, following either metyrapone or placebo treatment. The rise following metyrapone was significantly greater than that seen following placebo. The results suggest that cortisol influences both spontaneous and 5HT stimulated PRL release, probably acting at a pituitary level.

Adult↗

PubMed1981

Short- and long-term fluctuations in plasma prolactin concentration in normal subjects.

The physiological changes in plasma prolactin concentration were studied in 447 normal subjects, including 65 men, 75 pre-menopausal women and 307 post-menopausal women. The within-day and day-to-day variation as well as the circadian and circannual rhythm of plasma prolactin levels were determined. Furthermore, the relationship between changes in prolactin and oestradiol-17 beta levels during the normal menstrual cycle and in the climacteric was studied. Pre-menopausal women had significantly (P less than 0.01) higher basal plasma prolactin concentration than men and post-menopausal women. Furthermore, they had significantly (P less than 0.01) higher day-to-day variation than men. This suggests that prolactin in women is secreted in a pulsatile fashion. Only small seasonal variations in both sexes were seen. The levels of plasma prolactin during the ovulatory and the luteal phase in the cycle were significantly (P less than 0.02) higher than that of the follicular phase, and a positive correlation between changes in plasma concentration of oestradiol-17 beta and prolactin was found. Also in post-menopausal women a relationship between plasma concentration of prolactin and oestradiol-17 beta was seen. It is concluded that the assessment on the physiological variation recorded during sleep in both sexes. However, only in women day-to-day changes and the changes related to the menstrual cycle and the climacteric are of importance.

Adult↗

PubMed1981

The TRH-metabolic histidyl-proline-diketopiperazine (DKP) inhibits prolactin secretion in male rhesus monkeys.

Histidyl-proline-diketopiperazine (DKP) -- a stable degradation product of TRH -- has been shown to selectively inhibit prolactin secretion in vitro in rat pituitary tissue. In this study the effects of DKP on serum prolactin in intact and anaesthetized male rhesus monkeys and on TRH-stimulated prolactin levels have been investigated. In conscious monkeys 400 micrograms DKP significantly suppressed prolactin levels by 27%, and under ketamine anaesthesia, serum prolactin was suppressed in a dose-dependent manner by 150 and 400 micrograms DKP. The maximum prolactin response and the cumulative response to TRH (20 micrograms) was significantly and specifically inhibited by 400 micrograms DKP, while the lower dose was without effect. TSH levels were not affected by DKP in any instance. Hence DKP can specifically inhibit prolactin release in the rhesus monkey, and may be discussed as a possible regulatory factor in prolactin secretion.

Animals↗

PubMed1999

Stimulation of matrix-metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expression in rats by the preovulatory prolactin peak.

Since structural luteolysis involves deterioration of tissue, the gene expression of matrix-metalloproteinase-1 (MMP-1) and the respective tissue inhibitor of this metalloprotease (TIMP-1) were measured at various times on the day of pro-oestrus and in animals in which the preovulatory prolactin surge was blocked for the duration of 3 cycles by bromocriptine. An additional group of prolactin-blocked rats received a prolactin replacement injection on the afternoon of pro-oestrus. In spontaneously pro-oestrous rats, MMP-1 and TIMP-1 gene expression increased significantly (P<0.01) prior to the occurrence of the preovulatory LH surge but simultaneously with the onset of the preovulatory prolactin surge. When prolactin release was blocked by bromocriptine for 3 cycles, no such changes were observed during the afternoon of pro-oestrus. However, an intraperitoneal injection of bovine prolactin at the time when the preovulatory prolactin surge occurs normally, increased MMP-1 and TIMP-1 gene expression (P<0.01). These results indicate that MMP-1 and TIMP-1 gene expression are stimulated by the preovulatory prolactin surge. Previous work has shown that the preovulatory LH surge activates the enzymatic cascade which leads to increased collagenase activity.

Animals↗

PubMed1999

Dopamine agonists both stimulate and inhibit prolactin release in GH4ZR7 cells.

Prolactin secretion from the anterior pituitary gland is regulated by multiple factors including prolactin-release inhibiting factors (PIFs) and prolactin releasing factors. PIFs, however, usually dominate to exert a tonic inhibition in the biological system, and the physiological PIF is believed to be dopamine. However, there is accumulating evidence that dopamine can not only inhibit but also stimulate prolactin release. Many investigators believe that this is achieved by activating inhibitory and stimulatory subtypes of dopamine receptors. We tried to demonstrate that one subtype of dopamine receptors is capable of both inhibiting or stimulating prolactin release using GH(4)ZR(7) cells. GH(4)ZR(7) cells express only a short form of dopamine D(2) receptors (D(2s)). Low concentrations of three well-established D(2) receptor agonists (dopamine, apomorphine and bromocriptine) stimulated prolactin release from GH(4)ZR(7) cells while high concentrations inhibited the release. Haloperidol, a D(2) receptor antagonist, blocked the inhibitory action, but was unable to block the dopamine-induced stimulatory action. Pretreatment of cells with phenoxybenzamine, a receptor alkylating agent, abolished both the dopamine-induced stimulatory and inhibitory actions. Our results support the thesis that the stimulation of prolactin release induced by dopamine is mediated through dopamine D(2s) receptors since the GH(4)ZR(7) cells have only D(2s) receptors among dopamine receptors. We have concluded that the D(2s) receptor is capable of both stimulating and inhibiting prolactin release, probably via the activation of a G(s) protein by low concentrations and a G(i) protein by high concentrations of dopaminergic agents.

Alkylating Agents↗

PubMed2000

Role of phosphodiesterase and protein kinase G on nitric oxide-induced inhibition of prolactin release from the rat anterior pituitary.

OBJECTIVE: In order to determine the mechanism by which nitric oxide (NO) inhibits prolactin release, we investigated the participation of cGMP-dependent cAMP-phosphodiesterases (PDEs) and protein kinase G (PKG) in this effect of NO. METHODS: Anterior pituitary glands of male rats were incubated with inhibitors of PDE and PKG with or without sodium nitroprusside (NP). Prolactin release, and cAMP and cGMP concentrations were determined by RIA. RESULTS AND CONCLUSIONS: The inhibitory effect of NP (0.5 mmol/l) on prolactin release and cAMP concentration was blocked by EHNA (10(-4)mol/l) and HL-725 (10(-4)mol/l), inhibitors of cGMP-stimulated cAMP-PDE (PDE2). 8-Br-cGMP (10(-4) and 10(-3)mol/l), which mimics cGMP as a mediator of NP effects on prolactin release, also decreased cAMP concentration. Zaprinast (10(-4)mol/l), a selective inhibitor of specific cGMP-PDE (PDE5), potentiated the NP effect on cAMP concentration. Rp-8-[(4-chlorophenyl)thio]-cGMP triethylamine (Rp-8-cGMP, 10(-7)-10(-6)mol/l), an inhibitor of PKG, reversed the effect of NP on prolactin release. The present study suggests that several mechanisms are involved in the inhibitory effect of NO on prolactin release. The activation of PDE2 by cGMP may mediate the inhibitory effect of NO on cAMP concentration and therefore on prolactin release. NO-activated PKG may also be participating in the inhibitory effect of NO on prolactin release.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1981

Effect of TRH on the secretion of prolactin in ewes at various stages of pregnancy and in non-pregnant ewes during the breeding season and seasonal anoestrus.

The concentrations of prolactin in plasma were measured before and after the injection of TRH in pregnant ewes and in non-pregnant ewes during the breeding season and seasonal anoestrus. During the first 80 days of pregnancy basal concentrations or prolactin were low and stable but thereafter increased progressively to reach maximum values at Day 140. During a comparable time of year (December-April) basal concentrations of prolactin in non-pregnant ewes were not significantly different from those found between Days 20 and 120 of pregnancy. At other times of the year basal concentrations of prolactin in non-pregnant ewes were elevated during anoestrus and declined markedly at the onset of the breeding season. In pregnant and non-pregnant ewes the responsiveness of the pituitary gland to stimulation with TRH was significantly correlated with the basal concentration of prolactin in plasma: the raised concentration of prolactin at Day 140 of pregnancy and in July in non-pregnant ewes was associated with the greatest release of prolactin from the pituitary gland. A change in the responsiveness of the pituitary gland may play an important role in the overall control of prolactin secretion in the ewe.

Anestrus↗

PubMed1984

Prolactin as a factor in the uterine response to progesterone in rabbits.

The direct effect of prolactin on uteroglobin production and on uterine endometrial oestrogen and progesterone receptor concentrations was tested by using ovariectomized rabbits (at least 12 weeks) treated with prolactin; prolactin + progesterone; prolactin + oestradiol + progesterone; oestradiol + progesterone; or progesterone alone. Prolactin treatment produced a significant (P less than 0.05) increase in the concentration of cytosolic oestrogen and progesterone receptors, restoring the concentrations to values found at oestrus. However, the concentration of nuclear receptors remained low. In the remaining treatment categories there was no significant (P greater than 0.05) increase in the concentration of oestrogen and progesterone receptors compared with those in ovariectomized controls. However, the sequential treatment of ovariectomized animals with prolactin + progesterone stimulated uteroglobin production to a concentration equal to that found in intact rabbits on the 5th day of pregnancy. This was not achieved by prolactin or progesterone alone or with oestradiol. These results suggest that prolactin acts as an essential factor in the rabbit uterine response to progesterone, perhaps by the modulation of progesterone receptor activity.

Animals↗

PubMed1990

Effects of prostaglandin and prolactin on luteolysis and parturient behaviour in the non-pregnant tammar, Macropus eugenii.

In Exp. 1 non-pregnant female tammars were injected, on Day 26 (the day parturition would normally occur) after removal of pouch young, with saline, 200 micrograms ovine prolactin or 5 mg PG and changes in plasma concentrations of progesterone, prolactin, PGF-2 alpha metabolite (PGFM), oestradiol-17 beta and LH were determined. Luteolysis occurred in females treated with prolactin alone, while treatment with PG first induced a rapid rise in prolactin and subsequently a significant decrease in plasma progesterone. After prolactin treatment the oestradiol peak, oestrus and the LH surge were advanced significantly compared to the saline-treated females. In Exp. 2 the effects of the same treatments as used in Exp. 1 were determined on Day 23 and again on Day 26 after removal of pouch young in non-pregnant females. On Day 23 both prolactin and PG induced significant elevations in plasma progesterone, but luteolysis did not occur. On Day 26 the treatments initially induced significant elevations in plasma progesterone but these were followed by luteolysis within 8-12 h after treatment. PG treatment induced parturient behaviour in the non-pregnant females within 3-21 min and this persisted during the period that plasma concentrations of PGFM were elevated. The results show that PG induces birth behaviour and the release of prolactin, while prolactin first induces an elevation of plasma progesterone concentrations and, in the mature CL on Day 26, subsequently induces luteolysis.

Animals↗

PubMed1994

Increased LH receptor mRNA and extended corpus luteum function induced by prolactin and indomethacin treatment in vivo in hysterectomized pseudopregnant rats.

To assess the effects of prostaglandins and prolactin on corpus luteum function and regression, sterile-mated adult pseudopregnant rats hysterectomized on day 5 after mating were injected with indomethacin or prolactin. Daily samples of blood were collected via the tail, from day 12 to day 21, and assayed for serum concentrations of progesterone, 20 alpha-dihydroprogesterone and LH, whereafter corpora lutea and the remainder of ovaries were separated and the tissue content of PGF2 alpha, PGE2 and LH receptor mRNA were measured. Injections of prolactin (8 iu) s.c. or a low dose of indomethacin (200 micrograms kg-1) s.c. were administered twice a day, beginning on day 13 after mating. Both indomethacin and prolactin significantly increased serum progesterone concentrations (P < 0.05; n = 8), and extended the period of functional corpora lutea when compared with controls. Indomethacin, but not prolactin, lowered the concentration of serum 20 alpha-dihydroprogesterone. In the corpora lutea of indomethacin-treated animals, collected on day 21, both prostaglandins measured were reduced in concentration by 50% or more, compared with controls (P < 0.05; n = 8), whereas prolactin had no effect. Both prolactin and indomethacin treatment caused a substantial (tenfold) increase in the concentration of LH receptor mRNA, confined solely to the luteal compartment. These findings in vivo provide further evidence for a luteolytic role of locally synthesized prostaglandins in the rat ovary. Furthermore, prolactin can sustain corpus luteum function by exerting a luteotrophic effect during the late luteal phase, as judged by the stimulation of progesterone synthesis and the expression of LH receptors.

20-alpha-Dihydroprogesterone↗

PubMed2000

Effects of a 3beta-hydroxysteroid dehydrogenase inhibitor on monocyte-macrophage infiltration into rat corpus luteum and on apoptosis: relationship to the luteolytic action of prolactin.

The administration of prolactin to hypophysectomized rats results in regression of the corpora lutea, accompanied by immune-inflammatory events such as infiltration of monocytes and macrophages. Recent reports indicate an autocrine role for progesterone during the lifespan of the corpus luteum. In the present study, an inhibitor of 3beta-hydroxysteroid dehydrogenase, Trilostane, was used to investigate the hypothesis that a decrease in luteal tissue steroids precipitates the cascade of immune-inflammatory events leading to luteal regression in prolactin-treated hypophysectomized rats. Immature rats were induced to ovulate by administering eCG-hCG, and hypophysectomized on the day after ovulation (at 32 days of age). Rats were injected s.c. 9-11 days after hypophysectomy with (a) Trilostane (80 mg kg(-1) day(-1)), (b) ovine prolactin (500 mg day(-1)), (c) Trilostane plus prolactin, or (d) vehicle. Plasma and luteal tissue progesterone and 20alpha-dihydroprogesterone ('progestin') were quantified; luteal tissue monocytes-macrophages and apoptotic nuclei were counted, and luteal wet mass was determined. Rats treated with prolactin alone showed the expected markers of luteal regression: decreased plasma progestin, increased numbers of monocytes-macrophages and apoptotic nuclei in luteal tissue, and decreased luteal wet mass; however, progestin concentration in luteal tissue was unchanged. Treatment with Trilostane reduced plasma and luteal tissue progestin, but did not result in an infiltration of monocytes-macrophages or increased numbers of apoptotic nuclei in the corpora lutea, or any change in luteal wet mass. Trilostane in combination with prolactin reduced plasma and luteal tissue progestin and produced the expected markers of regression, with the exception of luteal tissue mass, which remained unchanged. In conclusion, inhibition of steroidogenesis does not initiate luteal regression or augment prolactin-induced luteal regression in hypophysectomized rats. Prolactin-induced infiltration of monocytes-macrophages is not accompanied by a decrease in luteal tissue progestin, at least in the early stages of luteal regression.

3-Hydroxysteroid Dehydrogenases↗

PubMed2002

Prolactin family miniarray: a tool for evaluating uteroplacental-trophoblast endocrine cell phenotypes.

The prolactin family represents a group of hormones and cytokines that participate in the control of maternal and fetal adaptations to pregnancy. The aim of this study was to develop a simple assay for monitoring patterns of prolactin family gene expression in rats and mice. Prolactin family cDNAs were spotted on to nylon membranes. Total RNA was extracted from tissues or cells. cDNAs were generated, radiolabelled using reverse transcriptase, and used as probes to hybridize with the prolactin family miniarrays. Pituitary, uterine decidual tissue and placenta each expressed a unique profile of prolactin family members. Placental tissues exhibited regional- and temporal-specific patterns of expression. Prolactin family gene expression differed markedly in mid-pregnant versus late gestation placental tissues and between the junctional and labyrinthine zones of the chorioallantoic placenta. Marked changes in prolactin family gene expression were also observed in cultured trophoblast cells undergoing differentiation. In conclusion, the prolactin family miniarray assay is an effective method for evaluating the endocrine phenotype of the uterus, placenta and trophoblast cells.

Animals↗

PubMed1990

Adenosine and its analogue (-)-N6-R-phenyl-isopropyladenosine modulate anterior pituitary adenylate cyclase activity and prolactin secretion in the rat.

The effect of adenosine and its analogue (-)-N6-R-phenylisopropyladenosine (PIA) on both anterior pituitary adenylate cyclase activity and prolactin secretion was examined in the rat. Adenosine inhibited basal adenylate cyclase activity in a dose-dependent manner and also reduced the stimulation of the enzyme by vasoactive intestinal peptide (VIP). Likewise, in primary cultures of anterior pituitary cells, adenosine decreased prolactin secretion in both basal and VIP-stimulated conditions. In perifusion experiments, adenosine also inhibited prolactin release in both basal and TRH-stimulated conditions. PIA produced a biphasic pattern of response of basal adenylate cyclase activity, being inhibitory at low and stimulatory at high concentrations. In VIP-stimulated conditions, low concentrations of PIA inhibited both adenylate cyclase activity and prolactin release from primary cultures of pituitary cells, while no additive stimulatory effect was seen at high concentrations. Similarly, low concentrations of PIA reduced both basal and TRH-stimulated prolactin release from perifused pituitaries, while increasing PIA concentrations restored prolactin release. These data show that adenosine affects basal and stimulated prolactin secretion from anterior pituitary cells. Adenosine receptors seem to be coupled to the adenylate cyclase system in the anterior pituitary gland, suggesting a possible relationship between the effect of adenosine on adenylate cyclase activity and prolactin secretion.

Adenosine↗

PubMed1996

Expression of a prolactin-like factor in preneoplastic and neoplastic mouse mammary gland and cells.

Prolactin is a member of the growth hormone family and is required for the growth and terminal differentiation of the mammary gland. Ectopic production of this hormone has been reported in several species, including rat, sheep, goat and human mammary tissues. In this study, mouse mammary cell lines, xenographs in the mammary gland from these cell lines and from hyperplastic alveolar nodules, spontaneous tumours, and normal tissues were studied for de novo production of this growth factor. Prolactin transcripts were found by reverse transcriptase PCR in some neoplastic and preneoplastic tissues and in mouse mammary cell lines, NOG8 and CDNR4, but were not detected in the normal mouse mammary gland. Northern analysis revealed a 1 kb transcript for both cell lines that co-migrated with the prolactin pituitary transcript. Conditioned medium from NOG8 cells was positive for prolactin bioactivity by the Nb2 rat lymphoma cell proliferation assay, and Western analysis revealed the presence of immunoreactive proteins at M(r) 14,000 and 60,000. Prolactin-like bioactivity was not detected in conditioned medium from CDNR4 cells, but an immunoreactive protein of M(r) 60,000 was detected by Western analysis. The mouse mammary cell line, Comma D, was negative for prolactin transcripts; however, adenocarcinomas derived from inoculation of Comma D cells into the cleared mammary fat pad were positive by reverse transcriptase PCR in two of four cases. Hyperplastic outgrowths maintained in the cleared mammary fat pad as well as spontaneous tumors were positive for prolactin transcripts in one of four cases. These results suggest that prolactin can be produced ectopically by the neoplastic mouse mammary gland.

Animals↗