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PubMed1979

The effects of opiate agonist and antagonist on serum prolactin in primates: possible role for endorphins in prolactin regulation.

Intravenous administration of the opiate receptor antagonist naloxone produced a significant reduction in basal serum PRL concentrations in four male Macaca arctoides. Significant decreases from basal levels were found 15, 30, 45, 60, 90, 120, 150, and 180 min after the iv injection of 0.05 and 0.25 mg/kg naloxone. The iv administration of 0.4 mg/kg morphine produced rapid and significant increases in PRL levels, while 0.04 mg/kg morphine or saline produced no change. Both the dopamine receptor-stimulating agent apomorphine (0.15 mg/kg) and naloxone (0.25 mg/kg) decreased basal serum PRL and blocked the morphine-induced increases in serum PRL. These data support the hypothesis that endorphins are involved in the stimulation of PRL secretion.

Animals↗
PubMed1980

Evidence that the dopaminergic prolactin-inhibiting factor mechanism regulates only the depletion-transformation phase and not the release phase of prolactin secretion during suckling in the rat.

We have compared the effectiveness of stalk-median eminence (SME) extracts, dopamine, and bromocriptine (CB-154) in inhibiting the release of PRL into the plasma during suckling when injected before depletion with that when the injections were given after the pituitary stores of PRL had been depleted and transformed by 10 min of suckling. We found that a single injection of either neutralized acidic extracts of SME at a dose of one or two SME equivalents per rat or 625 ng dopamine effectively prevented both the depletion of PRL within the pituitary and the subsequent rise in plasma PRL when given 1-3 min before the onset of suckling. Likewise, a single injection of bromocriptine (0.5 mg) given 20-30 min before the onset of suckling totally blocked pituitary depletion and the subsequent release of PRL into the circulation. However, the PRL concentration rose normally in the plasma in response to suckling when either SME extract or bromocriptine was given after PRL depletion had first been effected by prior short term (10 min) suckling. These data indicate that the depletion-transformation phase but not the release phase (into the circulation) of PRL secretion is under inhibitory control by a dopaminergic PRL-inhibiting factor system.

Animals↗
PubMed1980

Evidence that thyrotropin-releasing hormone and a hypothalamic prolactin-releasing factor may function in the release of prolactin in the lactating rat.

We have compared the effectiveness of TRH and a rat hypothalamic PRL-releasing factor (PRF; previously incubated with rat serum to destroy TRH) in stimulating the release of PRL into the plasma of conscious lactating rats when injected before and after pituitary PRL had been depleted and transformed into releasable PRL by 10 min of suckling. TRH (1.25 microgramsss) and PRF [equivalent to 2.5 stalk median eminence (SME) fragments] each caused a small increase (38 and 30 ng, respectively) in the plasma PRL concentration within 10 min when injected into nondepleted mothers. The levels then fell quickly. Suckling, by comparison, caused a sustained 175 ng/ml increase above basal levels. Though PRL depletion occurred, as expected, as a result of suckling, there was no measurable depletion within the pituitaries of TRH- or PRF-injected rats. By contrast, the iv administration of TRH (doses ranging from 2-250 ng) and hypothalamic PRF (doses ranging from 0.2-1.0 SME equivalent) after depletion-transformation had been effected by 10 min of suckling resulted in a rapid and, in most instances, a sustained elevation in the plasma PRL concentration comparable to that seen after suckling. Dose-response relationships, though, were not clearly evident with either PRF or TRH. Neither saline, 1.25 microgram TRH previously incubated in serum, 50 mU oxytocin, 1 microgram dopamine, 25 microgram LHRH, nor an extract of cerebral cortex prepared in the same manner as hypothalamic TRH caused plasma PRL to rise after PRL depletion. We conclude that TRH and possibly a separate hypothalamic PRF have a stimulatory action upon the releasable, but not upon the depletion-transformation, phase of PRL secretion in the lactating rat.

Animals↗
PubMed1981

Autofeedback regulation of prolactin (PRL) secretion: effect of prolactin before suckling on the subsequent nursing-induced release of PRL in the lactating rat.

PRL can have an inhibitory effect upon its own release. The present investigation assessed quantitative and temporal relationships among exogenously raised systemic PRL concentrations, PRL discharged in situ, and PRL negative feedback control of PRL release. Lactating rats were administered PRL in amounts designed to increase systemic plasma PRL concentrations to levels that either exceed (3 mg ovine PRL injected sc) or fall within (five iv injections of 400 or 800 ng rat PRL given at 1-min intervals) the range of PRL concentrations normally produced by suckling stimulation. The 800-ng iv or 3-mg sc dose of PRL did not block the suckling-induced rise of plasma PRL concentration when given 30 min before suckling. When administered 4 h beforehand, however, 3 mg PRL reduced both the suckling- and ether-stimulated rises of plasma PRL. Although the 400- or 800-ng iv dose of PRL increased systemic plasma PRL concentrations to levels (280 and 389 ng/ml, respectively) that approximate those of the suckled rat, neither dose inhibited the suckling-induced release of PRL when given 4 h before nursing. These data indicate that high concentrations of PRL are required before PRL from the systemic circulation can activate PRL autoregulatory mechanisms, and that these mechanisms are not activated as an immediate response to rising plasma PRL titers. The suckling-induced release of PRL was also inhibited by 3 mg PRL given 16 h before nursing. The PRL discharged in situ by 15 min of nursing was not effective, however, in blocking the suckling-induced release of PRL 16 h later. Since large amounts of PRL can presumably reach PRL regulatory mechanisms during in situ release via retrograde pituitary secretion, we conclude that the functional significance of autofeedback control of PRL release may be limited to conditions where PRL secretion is prolonged or at an abnormally high rate.

Animals↗
PubMed1982

Effects of somatostatin and urotensin II on tilapia pituitary prolactin release and interactions between somatostatin, osmotic pressure Ca++, and adenosine 3',5'-monophosphate in prolactin release in vitro.

Both somatostatin (SRIF) and urotensin II, a dodecapeptide from the teleost caudal neurosecretory system, inhibit PRL release from the organ-cultured rostral pars distalis of the tilapia, Sarotherodon mossambicus, in a dose-related manner. The inhibitory action of SRIF on PRL release was completely prevented by the presence of the calcium ionophore A23187. PRL release was also blocked when Ca++ was excluded from the incubation medium, even in the presence of the ionophore. Both dibutyryl cAMP (dbcAMP) and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, alone or in combination, stimulated PRL release during incubation in high osmotic pressure medium. The effect of dbcAMP appeared to be dose related. Together, dbcAMP and 3-isobutyl-1-methylxanthine were also effective in preventing the inhibition of PRL release by SRIF. These results are consistent with the notion that Ca++, and possibly cAMP, may be important mediators of PRL secretion, and it is likely that SRIF may inhibit PRL release by blocking a Ca++- or cAMP-mediated mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Thyroid hormone specifically inhibits prolactin synthesis and decreases prolactin messenger ribonucleic acid levels in cultured pituitary cells.

Electrophoretic analysis of soluble proteins from pituitary cells pulse labeled with [35S]methionine demonstrated that 10 nM T3 inhibited PRL synthesis, but did not affect the synthesis of most other pituitary proteins. The effects of T3 were somewhat slow, requiring about 3 days for a 50% reduction in PRL synthesis. PRL synthesis slowly returned toward control levels after the removal of T3 from the culture medium. In serum-free medium, a concentration of about 0.6 nM T3 was required for half-maximal inhibition of PRL synthesis. In medium containing 5% fetal calf serum, only slightly higher concentrations of T3 were required to inhibit PRL synthesis. The Kd for the binding of [125]T3 to pituitary cell nuclei was 0.2 nM. Analysis of PRL mRNA levels by hybridization of total cellular RNA to PRL cDNA demonstrated that there was a good correspondence between T3 effects on PRL synthesis and PRL mRNA. These findings demonstrate that T3 can specifically inhibit PRL synthesis and PRL mRNA levels in cultured pituitary cells and suggest that T3 may have a physiological role in the regulation of PRL synthesis.

Animals↗
PubMed1983

Adenosine 3',5'-monophosphate (cAMP) and calcium-calmodulin interrelation in the control of prolactin secretion: evidence for dopamine inhibition of cAMP accumulation and prolactin release after calcium mobilization.

Calcium (Ca2+) ionophore A23187 increased the intracellular cAMP content and PRL release in normal rat anterior pituitary cells. Cotreatment with dopamine reduced both control and A23187-stimulated cAMP accumulation and PRL release. The dopamine antagonist spiperone restored the response of cAMP to ionophoric stimulation after pretreatment with dopamine in the greatest concentration used. Penfluridol, a compound with Ca2+-calmodulin-blocking properties, decreased control and A23187-stimulated cAMP content and PRL release. W7, a selective calmodulin-blocking agent, reduced basal cAMP and PRL release, whereas W5, a W7 analog with only 20% of its calmodulin-blocking ability, did not affect cAMP or PRL secretion. These data indicate that the Ca2+-calmodulin and cAMP systems are interrelated in the regulation of PRL secretion. They are also consistent with the hypothesis that the inhibition of PRL release by dopamine occurs after Ca2+ is mobilized and when or before it stimulates adenylate cyclase activity.

Animals↗
PubMed1984

Does prolactin modify testosterone feedback in the hamster? Suppression of plasma prolactin inhibits photoperiod-induced decreases in testosterone feedback sensitivity.

The hormonal changes during the photoperiodically driven annual reproductive cycle of the male golden hamster can be explained partially by a change in the sensitivity of the hypothalamo-pituitary axis to negative feedback by testosterone (T). The present studies test the hypothesis that the increases in plasma levels of LH and FSH that follow photo-stimulation are due to decreasing feedback sensitivity and examine if this change in sensitivity is dependent upon increasing PRL levels. Adult males were exposed to a lighting schedule of 5 h of light, 19 h of darkness (5:19) for 12 weeks to induce gonadal regression. The animals were castrated; treated with an inhibitor of PRL release, bromocriptine (CB-154), or oil; and received a Silastic capsule that was empty or filled with T. Subsequently, the animals were transferred to 14:10 and killed 9 or 31 days later. There were no significant changes in FSH and LH in animals receiving oil injections and empty implants between days 9 and 31, suggesting no steroid-independent changes in gonadotropin secretion during this time period. However, 4-mm T implants were more effective in suppressing LH and FSH levels on day 9 than on day 31. This suggests that there is a gradual decrease in feedback sensitivity to T following photostimulation. T was more effective in inhibiting LH and FSH levels in CB-154-treated than in oil-treated animals on both day 9 and day 31. Thus, increases in PRL release are instrumental in causing decreases in feedback sensitivity following photostimulation.

Animals↗
PubMed1985

Ontogeny of prolactin cells in neonatal rats: initial prolactin secretors also release growth hormone.

Reverse hemolytic plaque assays and immunocytochemistry were used to monitor the ontogeny of individual hormone-secreting and hormone-containing cells in rats. Monodispersed anterior pituitary cells from fetal rats (sex unspecified) and neonatal rats of each sex were cultured for 24 h and then subjected to immunocytochemistry or plaque assays for PRL or GH. PRL secretors first appeared in appreciable numbers in cultures from 4-day-old animals, and by day 5, they accounted for 8-12% of all cells in culture. The percentage of GH secretors rose to a peak on day 5 (comprising approximately 40% of all cells), when the values were slightly higher than those observed previously in adults. The percentage of cultured cells from 4- to 5-day-olds that released PRL or GH was not influenced by the sex of the donor animal and was consistent with immunocytochemical estimates. Using a sequential plaque assay that enabled the detection of both GH and PRL release from the same cells, we found that of every 100 pituitary cells from 5-day-old males that released PRL and/or GH 62.5 released GH only, 1.7 released PRL alone, and the remaining 35.8 released both hormones. Almost identical proportions were found for females. These findings were confirmed using an additional variation of the plaque assay and by double staining immunocytochemistry. Taken together, these results indicate that mammosomatotropes, cells that release both GH and PRL, appear early in the neonatal development of both sexes and raise the possibility that PRL-secreting cells arise from GH-secreting cells.

Animals↗
PubMed1989

Prolactin messenger ribonucleic acid concentrations in 4-day cycling rats and during the prolactin surge.

Pituitary PRL mRNA concentrations were measured during the 4-day rat estrous cycle. Adult female Sprague-Dawley rats were killed at 3-h intervals throughout the cycle and hourly between 1000 and 2400 h on proestrus (n = 5-12). Serum PRL was increased on the afternoons of proestrus (P) and estrus (E), with peak concentrations at 1700 h (P, 624 +/- 126; E, 261 +/- 107 ng/ml). PRL mRNA concentrations were elevated during the evening on P and E (2300 h: P, 14.4 +/- 1.5; E, 16.1 +/- 1.3 ng cDNA bound/100 micrograms pituitary DNA) to values 2-fold higher than those at 0800 h on each respective day. On diestrus (D) PRL mRNA levels decreased abruptly during the morning (1100 h, 1.7 +/- 0.3 ng cDNA bound), followed by a 6- to 7-fold increase between 1700 and 2000 h on the same evening. In contrast, PRL mRNA levels were elevated at 0800 h on metestrus (M). The changes in PRL mRNA concentrations obtained on M and D were not associated with increased PRL secretion. A more detailed examination of P revealed that PRL mRNA levels increased during the morning (1000 h, 9.9 +/- 2.6 ng cDNA bound), then decreased abruptly at 1100 h (4.9 +/- 1.2). The morning rise in mRNA concentrations was followed by a 2-fold rise in pituitary PRL content. As serum PRL rose during the afternoon surge, a coincident decrease in pituitary PRL content and an increase in PRL mRNA levels were observed. The relationship between PRL secretion and gene expression was further examined in ovariectomized estradiol-replaced rats receiving either bromocriptine (1.2 mg/day, sc) or vehicle control sc. The vehicle-treated group expressed a characteristic afternoon PRL surge between 1500 and 2100 h. Pituitary PRL decreased during the surge to 10% of morning values, and PRL mRNA levels increased 2-fold beginning 2 h after initiation of the surge. These changes in serum PRL, pituitary PRL, and PRL mRNA levels were abolished by bromocriptine administration. These data reveal that alterations in PRL mRNA concentrations occur on a daily basis during the rat estrous cycle. Increases occur during the evenings of P and E at the time of the increase in PRL secretory activity. The effect of blocking the PRL surge in ovariectomized estradiol-replaced rats suggests a regulatory interaction between secretion and gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Regulation of prolactin secretion in the human B-lymphoblastoid cell line IM-9-P3 by dexamethasone but not other regulators of pituitary prolactin secretion.

We examined whether the ectopic production of human(h) PRL by the human B-lymphoblastoid cell line IM-9-P3 is under hormonal control. We demonstrate that PRL secretion in this cell line is regulated by dexamethasone but not by other hormones known to modulate PRL secretion in the pituitary or decidua. Dexamethasone caused a reduction of secretion rates to 30% of control values after 3 day paralleled by a decrease in hPRL mRNA levels, without affecting cell viability. Half-life determinations of hPRL mRNA in control and dexamethasone-treated cells revealed a reduction of t1/2 from 16 to 4 h. PRL secreted by IM-9-P3 cells did not control its own secretion in an autocrine loop, nor did it serve as an autocrine growth factor.

Antibodies, Monoclonal↗
PubMed1990

A nonoxytocinergic prolactin releasing factor and a nondopaminergic prolactin inhibiting factor in bovine neurointermediate lobe extracts: in vitro and in vivo studies.

Several peptidergic PRL-releasing factors (PRFs) have been described; however, none have been proven to be of primary physiological importance in the control of hormone release. Similarly dopamine withdrawal alone cannot completely explain the profiles of PRL secretion observed under a variety of conditions. We describe here the isolation in semipurified form of both a PRF and a PRL-inhibiting factor (PIF) from bovine neurointermediate lobe (NIL) extracts. Acid extracts of bovine NILs stimulated, in a dose-related manner, PRL release from cultured anterior pituitary cells, even after immunoabsorption of endogenous oxytocin from the extract. PIF and PRF activities were semipurified from NIL extracts by Sephadex chromatography and detected by in vitro and in vitro bioassays. The PRF material could be separated from oxytocin by gel sieving and was active in the presence of dopamine in vitro unlike synthetic oxytocin and in cell preparations in which the oxytocin-responsive lactotrophs had been removed by selective cytotoxin cell targeting using an oxytocin-ricin A chain cytotoxic conjugate. The PRF material stimulated PRL secretion in a dose-dependent fashion in conscious male rats after iv injection. The PIF material comigrated on sizing gel chromatography with immunoreactive oxytocin and was active in vitro during dopamine blockade with domperidone and in vivo in the presence of endogenous dopaminergic tone. These data suggest that novel factors present in the NIL might exert physiologically relevant control over lactotroph function and add to the growing literature on the presence of a PRF in the NIL.

Animals↗