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PubMed1982

On the mechanism by which dopamine inhibits prolactin release in the anterior pituitary.

An in vitro perfusion system was used to assess the effects of chloride channel blockers, dopamine (DA) receptor agonists and antagonists, and GABA receptor agonists and antagonists on prolactin release from the mouse anterior pituitary. Dopamine and muscimol inhibited prolactin release (IC50 = 6 X 10(-8)M and 10(-5)M respectively). The GABA receptor antagonist bicuculline blocked the inhibition of prolactin release by muscimol but not dopamine. The dopamine receptor antagonist chlorpromazine blocked the dopamine- but not muscimol-induced inhibition of prolactin release. Haloperidol, however, reversed both the muscimol and dopamine induced inhibition of prolactin release. Furthermore, the chloride channel blocker picrotoxinin blocked the inhibition of prolactin release elicited by both dopamine and muscimol. These later results suggest that the anterior pituitary dopamine receptor which mediates the inhibition of prolactin release may be coupled to a picrotoxinin sensitive chloride ionophore and that haloperidol may affect the function of both DA and GABA receptors in the anterior pituitary.

Animals↗
PubMed1987

Hepatic protein kinase C: translocation stimulated by prolactin and partial hepatectomy.

Prolactin stimulates a hepatotrophic response similar to that caused by phorbol esters or partial hepatectomy in rats. Since phorbol esters, which activate protein kinase C, mimic prolactin action in liver, the relationship between prolactin administration and subsequent hepatic protein kinase C translocation was assessed. Prolactin administration rapidly stimulated a 4-fold elevation of membrane protein kinase C activity. The effect of prolactin on hepatic protein kinase C was specific for lactogenic hormones but could be duplicated by phorbol esters. Further, an increase in serum prolactin was demonstrated subsequent to partial hepatectomy and preceding hepatic protein kinase C translocation. Therefore, translocation of hepatic protein kinase C appears important for hepatic proliferation in response to prolactin administration and to partial hepatectomy.

Animals↗
PubMed1987

Calmodulin modulates prolactin secretion in vitro: studies with calmodulin containing liposomes.

The control of prolactin secretion by Ca calmodulin and cyclic AMP was studied. Ca++ ionophore A23187 stimulated both cyclic AMP accumulation and prolactin release by primary culture of anterior pituitary cells in vitro. The increase of cyclic AMP formation by A23187 preceded that of prolactin release. To test the calmodulin involvement in these processes we used either selective calmodulin antagonist, the naphthalene sulphonamide derivative W7, or calmodulin containing liposomes. W7 dose dependently inhibited both basal or A23187 stimulated cyclic AMP accumulation and prolactin secretion. Insertion of Ca calmodulin within the cells stimulated prolactin secretion without modifying cyclic AMP accumulation. W7 inhibited the Ca calmodulin containing liposomes stimulation of prolactin release. These results suggest that calmodulin participates to the process of prolactin release.

Animals↗
PubMed1988

Time course of the insensitivity of prolactin release to morphine administration in the lactating female rat.

The effect of morphine on circulating levels of prolactin and growth hormone (GH) in the lactating female model was determined at various time intervals following the termination of suckling. Morphine administration did not produce an increase in prolactin levels when dams remained suckling. Four days after suckling was terminated, 50% of the dams tested showed a morphine induced prolactin increase. The prolactin secretory response to morphine gradually returned in dams, so that after 8 days of non-suckling, all animals tested showed a morphine induced prolactin increase. Consistent with the lack of prolactin stimulation, the tuberoinfundibular dopaminergic (TIDA) neurons, were insensitive to the morphine induced inhibition of activity during lactation. In contrast, circulating levels of GH were increased in these dams following morphine administration. These results suggest that the lactating female rat is insensitive to the mu mediated stimulation of prolactin release while suckling. However, sensitivity begins to return following at least 4 days of non-suckling.

Animals↗
PubMed1990

Dopamine antagonism does not potentiate the effects of oxytocin and vasopressin on prolactin secretion.

The roles of oxytocin and vasopressin on prolactin secretion were studied. Adult female Sprague-Dawley rats ovariectomized for two weeks and treated with a long-acting estrogen, polyestradiol phosphate for one week were used. Hormone administration and serial blood sampling were accomplished through indwelling intra-atrial catheters which were implanted two days before the experiment. Both oxytocin (20 micrograms/rat) and vasopressin (5 micrograms/rat) stimulated prolactin secretion within 10 min after injection and the effects were diminished by 30 min. In animals pretreated with a small dose of dopamine antagonist, sulpiride (1 microgram/rat), the effect of TRH on prolactin secretion was repeatedly shown to be potentiated. Same pretreatments with two different time intervals (30 and 60 min) between sulpiride and oxytocin/vasopressin administration, however, had no effect on oxytocin- or vasopressin-stimulated prolactin secretion. A vasopressin analog, 1-deamino-[D-Arg8]-vasopressin (dDAVP), with antidiuretic but no vasopressor activity was also used in the study. It was found that unlike vasopressin, dDAVP had no effect on prolactin secretion. In conclusion, both oxytocin and vasopressin can have a stimulatory effect on prolactin secretion when given in vivo. Unlike TRH, however, the action of oxytocin or vasopressin was not augmented by pretreatments of dopamine antagonist. The action of vasopressin on prolactin secretion may be a side effect of its vasopressor activity.

Animals↗
PubMed1995

Attenuation of the magnitude of suckling-induced prolactin release with advancing lactation: mechanisms.

To study why suckling-induced plasma prolactin levels decline in magnitude with advancing lactation, we examined prolactin release in lactating rats following suckling and pharmacologic manipulations during early, mid- and late lactation. On day 2 of lactation, litters were adjusted to 8 pups. On day 3, dams were implanted with an atrial catheter and experiments were conducted on lactation days 5, 11 and 17. To examine suckling-induced prolactin release, pups were removed at 0800 h, an extension was attached to the catheter at 1100 h, and pups returned to dams at 1200 h. Blood samples were obtained before, and at 10, 30, 60, 90 and 120 min after suckling started. Prolactin responses to sulpiride and thyrotropin releasing hormone (TRH) administration were studied in lactating rats separated from their litters for 4 hours. Blood samples were obtained before, and at 10, 30, 60 and 90 min after sulpiride (10 or 40 micrograms/kg BW) and 5, 10, 20 and 30 min after TRH (1 or 4 micrograms/kg BW) in rats pretreated with sulpiride. Prolactin release in response to suckling, administration of sulpiride or sulpiride and TRH diminished as lactation advanced. From these results, we conclude that refractoriness in anterior pituitary lactrotropes to prolactin-releasing stimuli is at least partially responsible for the decline in suckling-induced prolactin release with advancing lactation.

Animals↗
PubMed1978

Evidence for autonomous secretion of prolactin in some alcoholic men with cirrhosis and gynecomastia.

Prolactin responses to provocative thyrotropin releasing hormone (TRH) stimulation were evaluated in 20 cirrhotic men with gynecomastia. Fifteen of these cirrhotic men had normal responses with a minimum doubling of the prolactin concentration above basal in response to TRH. Five had abnormal (autonomous) responses in that they failed to double their basal level or had a paradoxical decrease from basal in response to TRH. Moreover, these same five men failed to have a sleep-related increase in plasma prolactin. Three of them also failed to respond to chlorpromazine stimulation. Such abnormal responses are generally associated with the presence of a prolactin secreting pituitary tumor. Basal plasma levels of prolactin were measured in all 20 men studied. The five men who failed to respond to TRH had significantly greater basal prolactin concentrations (80.5 +/- 18.7 ng/ml) than did the 15 men who responded normally (33.7 +/- 4.3 ng/ml) (p less than 0.01), although all 20 had increased prolactin levels relative to that of controls (10.8 +/- 0.9 ng/ml) (both p less than 0.01).

Gynecomastia↗
PubMed1993

Nursing-induced changes in pain sensitivity, prolactin, and somatotropin in the pig.

Suckling by piglets led to increases in prolactin and somatotropin in the sow. Failed nursing attempts, which did not result in milk ejection, also led to elevations of prolactin and somatotropin, suggesting that massage of the udder is sufficient and milk ejection is not necessary for these hormonal changes to occur. Prior treatment with the opioid antagonist, naloxone, blocked the nursing-induced increases in prolactin and somatotropin. Tail-flick latencies of the sows were significantly elevated after a nursing, suggesting reduced pain sensitivity. This was blocked by naloxone, suggesting that nursing directly increases endogenous opioid activity. Removing piglets for 2 h led to a drop in prolactin and somatotropin. When the piglets were returned, the nursing-induced increase in prolactin and somatotropin tended to be higher than following a normal nursing interval (1 h). However, prolactin concentrations remained at a significantly lower level following the extended nursing interval. A reduction in nursing frequency seems likely to lead to reduced prolactin levels and altered patterns of somatotropin secretion.

Animals↗
PubMed1992

Pyrularia thionin increases arachidonate liberation and prolactin and growth hormone release from anterior pituitary cells.

Pyrularia thionin is a 47 amino acid peptide isolated from the nuts of Pyrularia pubera. This peptide does not have intrinsic phospholipase A2 activity, but it increases the liberation of arachidonate from several tissues. Exposure of anterior pituitary cells to this toxin increases the liberation of arachidonate, increases the cellular levels of lysophospholipids, and decreases cellular phospholipids. Thus, phospholipase A2 is involved in the liberation of arachidonate stimulated by this peptide. Because this toxin also increases stearate liberation from the pituitary cells, either diacylglycerol lipase, phospholipase A1 or lysophospholipase may be directly or indirectly activated by this toxin. In addition to increasing fatty acid liberation, Pyrularia thionin increases the release of prolactin and growth hormone from anterior pituitary cells over the identical concentration ranges that this toxin liberates the fatty acids. Pyrularia thionin increased arachidonate liberation and prolactin release from perifused pituitary cells within 2 min, and following withdrawal of the toxin, arachidonate liberation and prolactin release returned to near basal levels within 6 min. Dopamine, a physiological inhibitor of prolactin release that closes calcium channels, decreased prolactin release stimulated by Pyrularia thionin. However, dopamine had no effect on the arachidonate liberation stimulated by this peptide. Similarly, D-600, an organic calcium channel blocker, decreased the prolactin and growth hormone release stimulated by the toxin without affecting the toxin-stimulated arachidonate liberation. Therefore, Pyrularia thionin increases arachidonate liberation through the rapid activation of phospholipase A2 by a mechanism that is not dependent on calcium uptake via D-600-inhibitable calcium channels. In contrast, the prolactin and growth hormone release stimulated by this toxin requires calcium uptake via D-600 inhibitable calcium channels.

Animals↗
PubMed1976

The possible mode of action of prostaglandins: X. Antagonism between prostaglandin F2a and prolactin or human chorionic gonadotropin: a comparative study.

A comparative assessment of the efficacy of prolactin or HCG in reversing the luteolytic property of a single dose (2.0 mg/kg) of PGF2a was conducted in pregnant (day 10) rats. It was found that prolactin maintained pregnancy in 90% of the test animals. HCG though found to maintain pregnancy in 70% of the PGF2a-treated pregnants, the fetal survival rate was, however, recorded to be 62% against the control value of 98%. Conversely, prolactin replacement maintained the fetal survival rate as high as 93.4%. Moreover, the growth of the fetuses, placentae and corpus luteum in the pregnants having prolactin in conjunction with PGF2a was also found to be greater compared to the animals which had a combined regimen of PGF2a and HCG, but identical to controls. On the other hand, similar combined regimen when applied to hysterectomized pregnant rats, it was observed that though the vaginal diestrus was maintained by the prolactin or HCG in the presence of PGF2a, the prolactin regimen was found to be superb compared to HCG in the maintenance of luteal weight and functional activity. It was concluded that the antifertility effect of PGF2a in the rat is primarily the consequence of luteolysis and prolactin seems to be a much more appropriate hormonal replacement compared to HCG, a long-acting LH, in antagonizing the luteolytic property of PGF2a.

Animals↗
PubMed1984

Acute effects of natural and synthetic cannabis compounds on prolactin levels in human males.

Plasma prolactin levels were determined in 23 adult males prior to and following administration of delta 9-tetrahydrocannabinol (THC) (17.5 mg orally), a synthetic cannabis compound, Nabilone (2 mg orally), a 1-g marihuana cigarette containing 1.83% THC, smoked under controlled conditions and placebo capsules and cigarettes for each of the active cannabis compounds. In order to control for possible influence of previous cannabis use history on prolactin response, three groups of subjects were studied--regular (daily) marihuana users, intermittent (weekly) marihuana users, and occasional (monthly) marihuana users. Each subject served as his own control for each drug condition. Double blind studies were conducted on a residential research ward. All baseline prolactin values were within the normal range for healthy adult males. There were no statistically significant differences in plasma prolactin levels among the three subject groups prior to administration of THC, Nabilone, marihuana or their respective placebos. There were no statistically significant changes in prolactin levels following TCH, Nabilone or marihuana smoking. Only placebo administration to regular and occasional marihuana users was followed by a significant increase in plasma prolactin levels. These findings indicate that acute administration of cannabis compounds, either orally or via smoking, does not significantly affect plasma prolactin levels in adult human males.

Adult↗
PubMed1988

Prolactin and growth hormone stimulate food intake in ring doves.

Ingestive behavior and body weight were measured in male and female ring doves given twice daily subcutaneous injections of ovine prolactin (7 mg/kg/day) or vehicle and in male doves given daily intracerebroventricular (ICV) injections of ovine prolactin at doses ranging from 0.1 to 2.0 micrograms/day. Changes induced by ICV administration of turkey prolactin, turkey growth hormone, ovine growth hormone, human growth hormone, and vehicle were also examined. Subcutaneous injections of ovine prolactin markedly increased food intake and body weight in both sexes. Similar effects occurred in dose-related fashion in male doves given ICV injections of ovine prolactin. The three growth hormone preparations also increased feeding and body weight significantly, but turkey prolactin was ineffective in this regard. Changes in drinking generally paralleled feeding patterns but were less pronounced and may have been secondary to feeding changes. We conclude that feeding in this species is strongly stimulated by some prolactin and growth hormone preparations. However, the physiological mechanisms underlying these effects remain to be clarified.

Animals↗
PubMed1988

Prolactin-induced yawning behavior requires an intact nigro-striatal dopamine system.

Herein, we evaluate the importance of the nigro-striatal dopamine system in prolactin-, apomorphine-, and physostigmine-induced yawning behavior. Bilateral 6-OH-dopamine lesions of the substantia nigra were performed on male rats (2-4 months old). The lesioned as well as control rats were injected with either physiological saline, physostigmine (200 micrograms/kg), apomorphine (50 micrograms/kg), or ovine prolactin (0.25 micrograms/kg) 72 hours after the surgical procedure. The results show that bilateral lesions of the substantia nigra did not affect physostigmine-induced yawning whereas both apomorphine- and prolactin-induced yawning were reduced by the lesion. Following the observation period the caudate nuclei were removed and analyzed for dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) content. The lesions reduced DA and DOPAC content in all treatment groups compared to the respective intact groups. Also, both DA and DOPAC concentrations were lower in the intact apomorphine and prolactin treated groups compared to intact saline controls, at times that were temporally related to the display of yawning behavior suggesting a decrease in dopamine activity following apomorphine and prolactin treatment. Interestingly, DA and DOPAC concentrations were higher in the lesioned apomorphine group compared to lesioned saline controls; however, in the lesioned prolactin group only the DA concentrations were higher when compared to lesioned saline controls. These results indicate that prolactin- and apomorphine-induced yawning require an intact nigro-striatal dopamine system and that these substances induce yawning by different mechanisms.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Inhibitory effects of putative dopamine D3 receptor agonists, 7-OH-DPAT and quinpirole, on prolactin secretion in rats.

The present experiments were performed to investigate effects of (+/-)-2-(dipropylamino)-7-hydroxy-1,2,3,4-tetrahydronaphthalene (7-OH-DPAT) or quinpirole (LY 171555), putative dopamine (DA) D3 receptor agonists, on serum prolactin levels in male rats. Basal prolactin levels were reduced dose-dependently by SC administration of 7-OH-DPAT or quinpirole at respective doses of 10-100 micrograms/kg and 25-250 micrograms/kg. Daily treatment with estradiol, 35 micrograms/kg/day for 3 days, increased serum prolactin levels to fourfold higher levels than those of nonprimed rats. Intraperitoneal injection of alpha-methyl-p-tyrosine (alpha-MT), 300 mg/kg, also increased serum prolactin levels. 7-OH-DPAT or quinpirole at a dose of 50 micrograms/kg caused a marked reduction in serum prolactin levels in both the estradiol- and alpha-MT-induced hyperprolactinemia. The 7-OH-DPAT- and quinpirole-induced decreases in serum prolactin levels were antagonized by the administration of the DA D2 receptor antagonist, spiperone, at 0.5 mg/kg. The results indicate that 7-OH-DPAT and quinpirole decrease prolactin levels in rats by stimulation of the D2 receptor.

Animals↗
PubMed1990

Prolactin shifts after neuroleptic withdrawal.

Neuroleptic-induced alterations in serum prolactin levels may have important clinical implications. Twenty-two stable schizophrenic patients, taken off medication over a 3-week period, were followed for 40 weeks or until the neuroleptic was reinstituted. Serum prolactin levels were measured during neuroleptic treatment and during the neuroleptic-free period. When serum prolactin levels were plotted over time, 55% of the subjects showed shifting prolactin levels in the shape of a "V" (i.e., a fall in prolactin level preceding an increase in the level) in the early weeks following withdrawal. Subjects with the "V" shape had significantly lower prolactin levels during neuroleptic treatment than those without the "V" shape. The pathophysiological significance of the prolactin "V" pattern is uncertain. It is consistent, however, with transient dopaminergic hyperactivity following neuroleptic withdrawal.

Adult↗
PubMed1986

Cloning and sequence analysis of cDNA for mouse prolactin.

The present study was undertaken to find out whether or not sexual dimorphism in biological activities and amino acid compositions of mouse prolactin might be due to heterogeneity in mRNA for mouse prolactin Cloned cDNAs for mouse prolactin were first isolated from a mouse pituitary cDNA library by hybridization with a rat prolactin cDNA. Then, one clone of about 140 positive clones obtained from 2000 transformants was subjected to nucleotide sequence analysis and verified to contain a nearly full length of cDNA sequence coding for mouse prolactin precursor. The deduced complete amino acid sequence indicates that the precursor molecule consists of 31 amino acids as the signal peptide and 197 amino acids of prolactin, in which two amino acids were found to be different from the amino acid sequence previously published elsewhere. S1 nuclease mapping analysis using male and female pituitary RNAs indicates that mouse preprolactin is encoded by two mRNAs in both sexes. The two mRNAs differ from each other based upon the deletion of three nucleotides in the coding region for the signal peptide determined by the nucleotide sequence analysis in other cDNA clones. In the present study, no sexual difference was revealed in murine prolactin mRNA.

Amino Acid Sequence↗
PubMed1984

Polyamine requirement for prolactin action on macromolecular synthesis in the MCF-7 human mammary epithelial cell line.

The actions of insulin, hydrocortisone, prolactin and growth hormone on the synthesis of macromolecules in MCF-7 cells was determined in a serum-free defined medium. The inclusion of the polyamine spermidine in the medium was shown to enhance the insulin stimulation of the rate of [3H]uridine incorporation into RNA in a manner similar to that demonstrated for hydrocortisone. Spermidine, in addition to insulin and hydrocortisone, was also essential for prolactin to manifest a stimulation of the rate of [3H]uridine incorporation; this effect of spermidine was optimal with spermidine concentrations between 1 and 5 mM. Prolactin also stimulated the rate of [3H]leucine incorporation into total cellular protein and into an isoelectrically precipitable (pH 4.6) phosphoprotein fraction. The actions of prolactin on total protein and phosphoprotein synthesis were only expressed if spermidine, in addition to insulin and hydrocortisone, was contained in the culture medium. All of the prolactin responses were observed employing physiological concentrations of prolactin. Specificity of the prolactin responses was established by demonstrating that porcine growth hormone had no effects on RNA or phosphoprotein synthesis in the MCF-7 cells.

Breast↗
PubMed1980

Effects of lysomotropic agents, and of microfilament- and microtubule-disrupting drugs on the activation of casein-gene expression by prolactin in the mammary gland.

The organ-culture technique was used to investigate the effects of lysomotropic agents (NH4Cl and chloroquine) and of modifiers of microfilaments (cytochalasin B) and microtubules (colchicine) on the induction of casein synthesis and the accumulation of casein mRNA by prolactin in the rabbit mammary gland. Neither chloroquine nor NH4Cl altered the lactogenic action of prolactin. Cytochalasin B attenuated the response to prolactin in terms of casein synthesis. However, this drug did not hamper the accumulation of casein mRNA. Colchicine exhibited a marked specific inhibitory effect on the induction of casein synthesis. It also prevented the accumulation of casein mRNA. These results suggest that a putative degradation of the internalized prolactin--receptor complex by lysosomes is not strictly involved in prolactin action. In addition, the integrity of the microfilaments seems unnecessary in the process of casein-gene activation by prolactin. By contrast, the integrity of the microtubule network seems absolutely necessary to ensure the transmission of prolactin information to the nucleus.

Ammonium Chloride↗