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PubMed2004

Neurotransmitters involved in the opioid regulation of prolactin secretion at the end of pregnancy in rats.

Using a pharmacological approach, we explored potential mechanisms for the regulation of prolactin secretion by opioid peptides at the end of pregnancy in rats. On day 19 of pregnancy, intracereboventricular administration of the mu-opioid receptor agonist (D-Ala2, NMe-Phe4, Gly-ol5)-enkephalin (DAMGO) or beta-endorphin (beta-END) induced a dose-related increase in serum prolactin levels 30 min later. Pretreatment with the opioid antagonist naloxone abolished the increase induced by DAMGO injection. At lower doses, DAMGO and beta-END did not modify the 3,4-dihydroxyphenylacetic acid/dopamine ratio, but at higher doses, the mu-agonists evoked a significant increase of the dopaminergic activity as compared with saline control. The time course of the effects of beta-END (2.5 microg/rat) showed a higher increase in serum prolactin levels at 15 min than at 30 min after treatment. The 3,4-dihydroxyphenylacetic acid/dopamine ratio increased 15 min after beta-END administration and was even higher 30 min later. Neither the selective kappa-agonist U50,488H nor the selective delta-agonist (D-Pen2, D-Pen5)- enkephalin were able to modify the serum prolactin levels at the doses studied. To evaluate potential neurotransmitters involved in the regulation of prolactin secretion at the end of pregnancy, we combined the administration of serotoninergic or GABAergic antagonists with the opioid agonist DAMGO. The serotonin 5-HT2 receptor antagonist ketanserin increased the serum prolactin levels and potentiated the effect of DAMGO. The intracerebroventricular administration of SR-95531 did not modify the serum prolactin concentration under basal conditions, but partially prevented the increase induced by DAMGO injection. The intracerebroventricular administration of the GABA(B) receptor antagonist phaclofen had no effect on the serum prolactin levels either in naive or DAMGO-treated rats. The present results support the proposal that activation of mu-opioid receptors stimulates prolactin secretion at the end of pregnancy. Although the exact mechanisms by which the opioid system modulates prolactin secretion at the end of pregnancy are unclear, these results suggest an interaction of the opioidergic system with serotoninergic and GABAergic systems, without ruling out a direct or indirect action on dopaminergic neurons. In conclusion, the opioid system may regulate prolactin secretion at the end of pregnancy through either stimulatory (present results) or inhibitory actions previously described.

Analgesics, Opioid↗
PubMed2006

Dopaminergic mechanisms involved in prolactin release after mifepristone and naloxone treatment during late pregnancy in the rat.

BACKGROUND/AIMS: During late pregnancy, the antiprogesterone mifepristone facilitates prolactin release. This effect is enhanced by administration of the opioid antagonist naloxone, suggesting an inhibitory-neuromodulatory role of the opioid system. Since hypothalamic dopamine (DA) is the main regulator of prolactin release, in this study we explored the role of DA on prolactin release induced by mifepristone and naloxone treatment. METHODS/RESULTS: Rats on day 19 of pregnancy were used. Naloxone treatment did not modify the 3,4-dihydroxyphenylacetic acid/DA (DOPAC/DA) ratio or serum prolactin concentration in control rats. After mifepristone treatment, DA activity diminished significantly without modifying serum prolactin levels. Naloxone administration to antiprogesterone-treated rats did not change the DOPAC/DA ratio but increased serum prolactin. Tyrosine hydroxylase (TH) expression in medial basal hypothalamus (MBH) protein extracts was lowered by pretreatment with mifepristone, with no additional effect of naloxone. While mifepristone decreased the intensity of TH immunoreactivity in the arcuate and periventricular nuclei and in fibers of the median eminence, naloxone treatment had no further effect. CONCLUSIONS: (1) A reduction of tuberoinfundibular dopaminergic (TIDA) neuron activity is suggested by the fall of the DOPAC/DA ratio and the low expression of MBH TH; (2) this reduction facilitates prolactin secretion by naloxone, indicating that progesterone stimulates DA neurons to maintain low serum prolactin; (3) naloxone action seems to depend on a previous decrease of DA tone induced by mifepristone, without involve a direct effect on neuronal DA activity, and (4) endogenous opioids may inhibit prolactin secretion through a non-dopaminergic neuronal system that regulates prolactin secretion in which as yet undetermined prolactin-releasing factors may participate.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1980

Regulation of prolactin and growth hormone secretion. Site and mechanism of action of thyrotropin-releasing hormone, L-dopa and L-5-hydroxytryptophan in unanesthetized dogs.

A heterologous radioimmunoassay for canine prolactin was developed and used to study the role of catecholamines and indoleamines in the regulation of prolactin secretion in dogs. Females dogs were found to have a higher plasma prolactin concentration than male dogs. Thyrotropin-releasing hormone (TRH) increased plasma prolactin in male and female trained conscious dogs. L-Dopa blocked the increase produced by TRH, but this effect could be reversed by pretreatment with carbidopa, an inhibitor of the conversion of L-dopa to catecholamines outside the blood-brain barrier. The intravenous administration of the immediate precursor of serotonin, L-5-hydroxytryptophan (5HTP), caused an increase in plasma prolactin and growth hormone. The administration of the serotonin receptor blocker, metergoline, 18 and 3 h before 5HTP, significantly augmented the growth hormone response to 5HTP. In contrast, metergoline diminished the prolactin response to 5HTP. Pretreatment with carbidopa did not change the prolactin or growth hormone responses to 5HTP. These observations indicate that the dog is similar to other mammals in that females have greater plasma prolactin concentrations than males and TRH increases plasma prolactin. L-Dopa appears to act at a site outside the blood-brain barrier to prevent the prolactin response to TRH. The data suggest that 5HTP increases plasma prolactin via a serotonergic mechanism, whereas it increases plasma growth hormone via a different, nonserotonergic mechanism.

5-Hydroxytryptophan↗
PubMed1992

Differential inhibition of dopamine and bromocriptine on induced prolactin release: multiple sites for the inhibition of dopamine.

Effects of dopamine and bromocriptine on TRH- or dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP)-induced prolactin release from primary cultured rat pituitary cells were studied using a perifusion system. TRH (100 nmol/l) stimulated prolactin release from basal concentrations of 33.8 +/- 0.5 to 151.2 +/- 28.0 ng/ml (net increase) or 447% increase. Dopamine inhibited the basal release of prolactin throughout the experiment, but TRH (100 nmol/l) was still able to stimulate prolactin release under the influence of dopamine. The increment in prolactin release was inversely proportional to the dopamine concentration. When TRH (100 nmol/l) was introduced during a perifusion period with bromocriptine 1 nmol/l, the prolactin concentration was increased to 110.9% of basal levels. The stimulatory effect of TRH under the influence of bromocriptine (1 nmol/l) was significantly lower than that without bromocriptine (control), although the higher concentrations of bromocriptine (10 and 100 nmol/l) did not further reduce the peak concentration of TRH-induced prolactin release. During a perifusion period with a low concentration of dopamine (1 nmol/l plus 0.1 mmol/l ascorbic acid), introduction of dbcAMP (3 mmol/l) stimulated prolactin release to 48% of basal concentration. A higher concentration of dopamine further reduced the stimulatory effect of prolactin release. Bromocriptine impeded the stimulatory effect of dbcAMP (3 mmol/l) on prolactin release in a similar manner as dopamine. Since a higher concentration of bromocriptine (10 and 100 nmol/l) did not further inhibit the TRH-induced prolactin release whereas a higher concentration of dopamine did, it is concluded that dopamine acts through additional mechanism(s) other than the D2 receptor transduction system.

Animals↗
PubMed1993

Activation of the adrenergic beta-receptor stimulates prolactin release from primary cultured pituitary cells.

Prolactin release from primary cultured pituitary cells was investigated using a dynamic perifusion system. Although epinephrine (1 mumol/l) produced an elevation in the mean value of the prolactin concentration at the onset of the perifusion, the elevation was not statistically significant, and the overall effect of the epinephrine was to produce an inhibition of prolactin release. The alpha- and D2-receptors of the primary cultured cells were functionally removed by a pretreatment with phenoxybenzamine (0.1 or 1 mumol/l). Since phenoxybenzamine irreversibly inactivates both the adrenergic alpha- and the D2-receptors but does not block the beta-receptors, the enhanced stimulatory action of the epinephrine (1 mumol/l) on the phenoxybenzamine pretreated cells suggests the involvement of adrenergic beta-receptors in prolactin release. Perifusion of isoproterenol (1 mumol/l), a beta-receptor agonist, stimulated prolactin release. This stimulation was blocked by beta-receptor antagonism with propranolol (1 mumol/l) supporting the implication of the beta-receptor in prolactin release. In order to differentiate between beta 1- and beta 2-receptor involvement, we investigated the effects of ICI 118,551 (1 mumol/l) on isoproterenol-induced prolactin release. ICI 118,551, a selective beta 2-receptor antagonist, blocked the stimulatory action of isoproterenol on prolactin release indicating that the beta-receptor responsible for the stimulation of prolactin release belongs to the beta 2-receptor family. Moreover, the demonstration that salbutamol, a selective beta 2-receptor agonist, stimulated prolactin secretion offers further evidence in support of the role of the beta 2-receptor in the stimulation of prolactin release.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuterol↗
PubMed1998

Differential effects of estrogen and prolactin on autoimmune disease in the NZB/NZW F1 mouse model of systemic lupus erythematosus.

Estrogen and prolactin have been shown to modulate autoimmunity in the NZB/NZW F1 (B/W) mouse model of systemic lupus erythematosus (SLE). However, estrogen stimulates prolactin secretion. The goal of this study was to examine differential effects of estrogen and prolactin in the female B/W mouse model of SLE. B/W females were manipulated to create combinations of low and high concentrations of serum estrogen and prolactin. Hyperprolactinemic mice with either low or high serum estrogen levels had accelerated development of albuminuria at 24 and 32 weeks of age compared to normal and hypoprolatinemic mice. High estrogen/high prolactin mice also had a higher percentage of anti-DNA antibodies compared to mice in the low estrogen/low prolactin and the high estrogen/low prolactin groups. IgG levels were not significantly different between groups. Mean survival was shortest in the high estrogen/high prolactin group (34+/-1.0 weeks) and longest in the high estrogen/low prolactin group (42+/-1.2 weeks; P < 0.05). High levels of serum estrogen were associated with depressed in vitro lymphoproliferation and IL-2 production. This study suggests that high prolactin levels in either high or low serum estrogen states are associated with accelerated autoimmunity in the B/W mouse. This study further demonstrates that high estrogen levels do not accelerate murine SLE when the prolactin-stimulating property of estrogen is suppressed by bromocriptine. Further investigation of hormonal interactions in autoimmunity will provide a better understanding of hormonal immunoregulation and, perhaps, lead to improved clinical application of hormonal immunomodulation.

Animals↗
PubMed2006

Iron deficiency in infancy predicts altered serum prolactin response 10 years later.

Serum prolactin may reflect CNS dopaminergic function. Because iron deficiency (ID) alters brain dopamine in rats, serum prolactin levels were previously investigated in infants with varied iron status. High serum prolactin levels correlated with behaviors typical of chronic ID. The objective of this study was to determine the effect of infant iron status on serum prolactin levels after a stressor in early adolescence. One hundred fifty-nine of 191 children enrolled in infancy (chronic ID, n = 46; good iron comparison group, n = 113) had serum prolactin measurements after catheter placement at 11-14 y of age. Serum prolactin levels were compared by sex, pubertal status and infant iron status and the pattern of change over time was compared by infant iron status controlling for pubertal stage and background factors. Males and less mature adolescents had lower serum prolactin concentrations than females and more mature adolescents. Controlling for these factors, the serum prolactin response pattern differed significantly by infant iron status. Serum prolactin declined earlier for the chronic ID group. In conclusion, an altered serum prolactin response pattern was observed 10 y after chronic ID in infancy and may suggest a long-lasting effect of ID on the regulation of prolactin.

Adolescent↗
PubMed2006

Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats.

Orphanin FQ/nociceptin (OFQ/N), the most recently identified endogenous opioid peptide, stimulates prolactin secretion in both male and female rats. OFQ/N, however, did not elicit this stimulatory effect through the mu-, delta-, or kappa-opiate receptor subtype. The role OFQ/N plays in prolactin regulation under physiological conditions and its mechanism of action are not known. The purpose of these studies was to determine the physiological significance and pharmacological specificity of the prolactin secretory response to OFQ/N. In addition, the role of the tuberoinfundibular dopaminergic (TIDA) neurons in mediating this response was examined. Opioid receptor-like-1 (ORL-1) receptors were blocked by pretreatment with compound B (Comp B), a purported OFQ/N antagonist, or receptor synthesis was disrupted by pretreatment with ORL-1 receptor antisense oligonucleotides. The prolactin secretory response to OFQ/N administration in diestrous females was measured. Furthermore, the suckling-induced prolactin response was also determined after Comp B pretreatment. TIDA neuronal activity was quantified in diestrous female rats to determine whether OFQ/N stimulates prolactin release by inhibiting TIDA neurons. OFQ/N significantly inhibited the TIDA neurons by 1 min, preceding the prolactin secretory response. Both Comp B and antisense pretreatment blocked the stimulatory effects of OFQ/N on prolactin release, and Comp B abolished the suckling-induced prolactin response. These studies indicate that OFQ/N is a potent stimulus for prolactin secretion in female rats and that it mediates this effect by rapid and transient inhibition of TIDA neuronal activity. Furthermore, OFQ/N plays a physiologically significant role in the regulation of prolactin secretion during lactation, and it mediates its effects via actions at the ORL-1 receptor subtype.

Animals↗
PubMed1977

Termination of pseudopregnancy following hypothalamic implantation of prolactin.

Pseudopregnancy (PP) in the rat is characterized by maintenance of the corpora lutea and twice daily surges of prolactin at 1500-2100 h and 0100-0900 h. Four days after PP was induced by cervical stimulation with a glass rod, rats were cannulated via the right carotid artery and one day later received an implant of ovine prolactin (200-250 mg) or albumin (controls) into the median eminence of the hypothalamus. Forty-five of 54 rats implanted with prolactin showed a termination of PP within 4 days. Ova were recovered from 19 of these rats whereas all of the controls remained pseudopregnant and did not ovulate. Ovarian and uterine weights were increased in rats implanted with prolactin. Plasma prolactin levels in the rats implanted with prolactin were lower each day (45-89%) at 0100, 0300 and 1800 h compared to controls. Plasma LH levels rose gradually after prolactin implantation, and in those rats in which ovulation occurred, a preovulatory LH rise was detected at 1800 h on the previous day. It is concluded that daily surges of prolactin play an essential role in maintaining PP in the rat, and that implantation of prolactin into the median eminence results in inhibition of prolactin. The stimulation of LH secretion, which led to ovulation, may be the result of a direct neural action of prolactin on the LH release mechanism or may simply result from the termination of PP.

Animals↗
PubMed1975

Mechanism of the effects of hypothalamic deafferentation on prolactin secretion in the rat.

Male rats with complete hypothalamic deafferentation had consistently lower serums prolactin concentrations than controls when the blood samples were obtained under other anesthesia. However, when rats were decapitated, both groups had similar low prolactin levels. Posterolateral deafferentation was as effective as complete deafferentation in preventing the stress-induced prolactin release, whereas anterior frontal deafferentation had only a small effect, L-Dopa (100 mg/kg body wt, ip) decreased prolactin titers in both control and deafferented animals, whereas reserpine (1 mg/kg body wt, ip) had the opposite effect. Since both drugs inhibited prolactin release from pituitaries in vitro, the decrease of prolactin levels following L-dopa in vivo might have been caused not only by stimulation of PIF release but also at least partly by the direct effect of the drug on the pituitary. However, the increase of serum prolactin following reserpine was in all probability caused by inhibition of PIF secretion. Electrolytic lesions in the median eminence of deafferented rats caused an elevation of serum prolactin which was more marked in female than in male rats. On the contrary, deafferentation in the females affected prolactin levels less than in males. It is concluded that hypothalamic deafferentation prevents ether-induced release of prolactin and that the "low" levels of the deafferented animals are probably due to a tonic release of prolactin-inhibiting factor (PIF) from the isolated island. It is though that this continuous release of PIF might be maintained by persisting autonomous activity of the adrenergic, presumably dopaminergic, neurons contained in the isolated island.

Animals↗
PubMed1975

Effects of acute stress on serum LH and prolactin in intact, castrate and dexamethasone-treated male rats.

The effects of handling, ether vapor anesthesia and blood sampling on serum LH and prolactin were determined in intact, castrate and dexamethasone-treated male rats. Cage removal and transport to an adjacent room increased LH and prolactin levels by 10 and 15 min after the initial animal disturbance. Intact male rats subjected to repeated ether anesthesia and blood sampling showed a more rapid increase in serum LH and prolactin than the preceding rats, since serum LH and prolactin was increased by 4, 8 and 15 min after initial cage disturbance. In a group of rats subjected to serial blood sampling over a longer time interval, both prolactin and LH levels remained higher than 90 min after initial animal handling. At 90 minutes after a single blood sampling, blood prolactin concentration remained higher than in controls. Serum LH levels returned to control levels 90 min after the stress of a single blood sampling. Although serum prolactin was increased in the castrate group subjected to serial anesthesia and blood sampling, LH concentrations were reduced under the same conditions. Injection of 5 and 50 mug of dexamethasone/100 g body wt for 8 days markedly reduced adrenocortical responsiveness to the stress of serial anesthesia and blood sampling at 1, 4, 8 and 15 min after initial rat disturbance. The 50 mug dexamethasone treatment reduced the stress-stimulated increase in serum prolactin at all blood sampling intervals. The dexamethasone-treated groups also showed smaller increases in serum LH at 8 and 15 min after first animal handling than the control rats. These results indicate that serum LH and prolactin concentrations are consistently increased by acute stress in intact male rats, the duration of the stress stimulation of LH and prolactin is at least 90 min under the conditions of this study, serum LH levels of castrate male rats are decreased by acute stress and dexamethasone administration lowers stress stimulation of LH and prolactin release.

Anesthesia↗
PubMed1975

The nyctohemeral rhythm of plasma prolactin: effects of ganglionectomy, pinealectomy, constant light, constant darkness or 6-OH-dopamine administration.

In male rats maintained on a 12 h light-dark schedule (6 AM-6 PM), there is a nyctohemeral cycle of plasma prolactin which consists of a nadir at 11:30 AM and an apogee at approximately 11:30 PM. In rats exposed to constant darkness, this rhythm persists for 7 days. Seven days of constant light, however, reverses this diurnal variation such that plasma prolactin levels peak at 11:30 AM and reach a nadir at approximately 11:30 PM. In animals maintained on a 12 h light-dark cycle, ganglionectomy and lateral ventricular injections of 6-OH-dopamine (250 mug) also appear to reverse the diurnal variation of plasma prolactin, whereas a single injection of 6-OH-dopamine (250 mug) into the third ventricle decreases plasma prolactin values at all times intervals but does not alter the diurnal rhythm. Both sites of 6-OH-dopamine administration markedly deplete hypothalamic dopamine and norepinephrine, but injection of 6-OH-dopamine into the lateral ventricle destroys the catecholaminergic terminals in the pineal, whereas injection of 6-OH-dopamine into the third ventricle does not. Pinealectomy slightly increases the early morning values of plasma prolactin, but otherwise has no effect on the diurnal variation of prolactin. Five conclusions appear to be justified: 1) there is a nyctohemeral rhythm of plasma prolactin, which is reversed by constant light; 2) the pineal gland probably plays no role in the diurnal regulation of plasma prolactin secretion; 3) the diurnal rhythm of plasma prolactin is controlled by sympathetic input into the brain via the superior cervical ganglion; 4) a rhythm of plasma prolactin develops in constant light which is the exact opposite of the normal diurnal variation; 5) there appears to be a noradrenergic pathway in the hypothalamus or brainstem which stimulates release of prolactin.

Animals↗
PubMed1975

Characteristics of the prolactin stimulation of uridine metabolism in mammary gland explants.

Experiments were carried out to characterize the prolactin stimulation of labeled uridine uptake into mammary gland explants which were initially preincubated for 2 days in medium containing insulin plus hydrocortisone. Prolactin was found to enhance labeled uridine uptake after 4 h but not after 2 h when uridine concentrations ranging between 0.1 muM and 1 mM were tested. The effect of prolactin on labeled uridine uptake also appears to require ongoing RNA and protein synthesis since incubation with a variety of inhibitors of RNA and protein synthesis abolished the prolactin effect. It was further discovered that prolactin stimulates the labeling of the cellular pools of the phosphorylated derivatives of uridine while the quantity of label present in the uridine and uracil pools was not affected. It is thus possible that the effect of prolactin on labeled uridine uptake may be caused by the enhanced phosphorylation of the uridine. It was also found that the onset of the effect of prolactin on the phosphorylation of uridine to UTP was not different from the onset of the effect of this hormone on labeled uridine uptake and its incorporation into RNA. Additional studies were carried out to determine if the effect of prolactin on RNA synthesis could be dissociated from its effect on the uptake of precursor substances. For this purpose the effect of prolactin on the uptake of radiolabeled phosphate and its incorporation into RNA was studied. Prolactin stimulated the incorporation of phosphate into RNA after 4 h but the uptake of phosphate was not affected by the hormone at that time. Further, the effect of prolactin on phosphate incorporation into RNA was temporally identical to the hormonal effect on the incorporation of 3H-uridine into RNA.

Animals↗
PubMed1975

On the mechanism of prolactin and estrogen action in 7,12 dimethylbenz(A)anthracene-induced mammary carcinoma in the rat. II. In vivo tumor responses and estrogen receptor.

In order to test the in vivo effect of prolactin on estrogen receptor (ER) binding capacity in tumors induced by 7,12 dimethylbenz(a)anthrancene (DMBA-tumor), growth of the tumors from changes in prolactin and estrogen levels was compared retrospectively with cytoplasmic ER levels. It was demonstrated that some tumors required prolactin, some needed prolactin-estrogen during their growth period anda small number were not influenced by hormonal milieu. ER was present in hormonally dependent tumors but was low or absent in hormonaly-independent tumors. Deletion of hormones by endocrine ablation in the host rat resulted in tumor regression loss of ER. Replenishment of ER and subsequent tumor growth were accomplished by injection of prolactin or prolactin-estrogen in endocrine ablated rats but were not achieved in rats bearing tumors exposed to prolactin-nafoxidine. Our results demonstrate that both estrogen and prolactin were essential for growth of hormonally dependent DMBA-tumors. Tumor growth was also prevented when cytoplasmic ER was not replenished , indicating that ER may be an indispensable prerequisite for growth. Prolactin, independently of or cooperatively with estrogen, stimulated ER binding capacity. These results support the hypothesis that there may exist a prolactin regulatory mechanism of estrogen action at the tumor site. The interactions of estrogen and prolactin in situ in modulating hormonal receptor binding capacities may contribute to the overall stimulatory effect of these two hormones on DMBA-tumors.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

A "critical period" for cervically-stimulated prolactin relase.

To investigate the role of ovarian steroids in the initiation and maintenance of the prolactin surges typical of pseudopregnancy in the rat, the pattern of plasma prolactin concentrations resulting from cervical stimulation of long-term ovariectomized rats was determined. Cervical stimulation of rats, ovariectomized 2-4 weeks previously, at 1900 h (lights on 0600-1800 h) resulted in a surge of prolactin which was initiated 4-6 h later and which was similar in timing and duration to the nocturnal prolactin surge of intact, pseudopregnant rats. Daily prolactin surges continued for 6 days but declined thereafter. Because plasma progesterone levels were elevated significantly after cervical stimulation, the experiment was repeated iin adrenalectomized-ovariectomized rats. Prolactin surges were still observed, demonstrating that ovarian and adrenal steroids are required neither for initiation nor maintenance of prolactin surges after cervical stimulation. Cervical stimulation at different times of the day (1900 h, 2400 h or 0400 h) always resulted in a surge of prolactin which peaked at 0300-0700 h. The latency from cervical stimulation in the peak of the prolactin surge was 8 h for the 1900 h group, 5 h for the 2400 h group, and 3 h for the 0400 h group. Thus, the appearance of prolactin surges is related to the time of day rather than to the time cervical stimulation is applied, demonstrating the existence of a "critical period" for cervically-induced prolactin release.

Adrenalectomy↗
PubMed1976

[Plasma prolactin and thyroid-stimulating-hormone (TSH) in patients with breast cancer (author's transl)].

In order to investigate plasma prolactin and thyroid-stimulating-hormone (TSH) concentration and pituitary reserve of these two hormones in patients with breast cancer, following examinations were carried out. Plasma prolactin concentration was measured before and 15, 30, 60, 90 minutes after the 500mug of thyrotropin-releasing-hormone (TRH) i.v. injection in 22 patients with breast cancer and 4 patients with benign breast disease. All patients did not take any hormonal therapy and any medication inducing prolactin secretion. Ten healthy females were also tested as controls. Plasma prolactin concentration was estimated by a double antibody radioimmunoassay (RIA) technique using hPRL RIA kit provided by NIAMDD. The basal prolactin concentration in patients with breast cancer was 18.6 +/- ng/ml (Mean +/- SEM), and it was slightly higher than the control group (14.7 +/- 2.2 ng/ml), but not statistically significant. In 6 out of 22 patients with breast cancer, high plasma prolactin concentrations more than 25 ng/ml were observed. The maximal plasma prolactin concentration following the TRH injection was obtained at 15-30 minutes after TRH in most patients with breast cancer. The maximal value was 87.4 +/- 9.2 ng/ml, and it was near the upper limit of normal range of prolactin response, and not significantly higher than the maximal value in the control group (59.7 +/- 5.7 ng/ml). In 7 patients with breast cancer, the maximal prolactin values more than 100 ng/ml were obtained after TRH injection. There was no statistically significant difference between early breast cancer group (TNM: stage I & II, N=14) and advanced breast cancer group (TNM: stage III & IV, N=6) in both the plasma prolactin concentration and the pituitary prolactin reserve...

Adult↗
PubMed1976

Origin of prolactin cells in the pituitary autografts in the renal capsule of young male and female rats.

Origin of the prolactin cells in the pituitary grafts autotransplanted into the renal capsule was electron microscopically investigated in young male and female rats. Prolactin cells may mainly originate from the completely degranulated acidophils after grafting in both sexes. The comprehensive degranulation of acidophils may be essential condition for the development of prolactin cells. Formation of initial prolactin granules is related to the Golgi apparatus in 3 and 6 days in the males. Even prolonged transplantation for the duration of 10 and 20 days failed to develop the typical prolactin cells storing large polymorphic granules in the grafts in the males. In the females, however, the population of prolactin cells became higher (20-30%) and their granulation was more rapidly advanced than in the male. Nine and 16 days after grafting quite numerous typical prolactin cells, characterized by the pronounced vesiculation of ER stored large polymorphic granules in the females. Progressive vesiculation of ER in degranulated acidophils may be the second necessary condition for establishing the prolactin cells. Thus, the entire course of cell conversion of acidophils into prolactin cells was observed in this study. All the graft cells including prolactin cells finally turned into the cells losing the respective individuality (10 days in the males; 32 days in the females). This fine structural similarity was striking in the males. We could not, however, deny the possibility of origination of prolactin cells from the follicular cells or their adjoining undifferentiated cells.

Animals↗
PubMed1987

Effects of H2-receptor antagonists on prolactin secretion: specificity and mediation of the response.

The effects on prolactin secretion of histamine H2-receptor antagonists infused intracerebroventricularly were studied in urethane anaesthetized male rats. A dose of 1.6 mumol cimetidine stimulated basal prolactin secretion and did not affect the histamine-induced release, whereas 0.4 mumol cimetidine inhibited basal and histamine-stimulated prolactin secretion. 0.1 mumol cimetidine had no effect. The more potent H2-receptor antagonist ranitidine at doses of 0.1, 0.4, 1.6 mumol had no effect on basal prolactin secretion, whereas 0.4 and 1.6 mumol inhibited the histamine-stimulated secretion completely. SKF-92408, a compound resembling cimetidine in chemical structure but devoid of H2-receptor antagonist activity, stimulated basal prolactin secretion at a dose of 1.6 mumol, but had no effect on the histamine-induced release or at a dose of 0.4 mumol. The H2-receptor antagonists metiamide and oxmetidine (1.6 mumol) stimulated basal prolactin secretion and did not prevent the response to histamine. A dose of 0.4 or 1.6 mumol imidazole (the ring structure contained in cimetidine, SKF-92408, metiamide, and oxmetidine) had no effect on basal or histamine-stimulated prolactin secretion. The findings indicate that cimetidine stimulates prolactin secretion by a non-specific action when infused centrally at high doses. In contrast, when infused at lower doses cimetidine inhibits the basal and histamine-stimulated secretion by blockade of H2-receptors. The prolactin-stimulatory action of cimetidine was not due to an H2-agonist effect, since ranitidine did not prevent the response. Cimetidine did not stimulate prolactin secretion via an effect on the dopaminergic system, since the drug had no effect on the dopamine concentration in hypophysial portal blood or in hypothalamic tissue and since inhibition of the dopamine synthesis by alpha-methyl-p-tyrosine did not prevent the cimetidine-induced prolactin release.

Animals↗