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PubMed2002

Prolactin levels in cerebrospinal fluid of patients with infantile spasms.

Infantile spasms are an age-related epileptic syndrome of infancy and are characterized by the combination of clusters of epileptic spasms and specific electroencephalographic findings. The etiology and the pathogenesis of the disease is still unclear. Prolactin has been thought to be specifically related to epileptic seizures. To investigate the possible mechanism of prolactin secretion in infantile spasms cerebrospinal fluid prolactin levels were examined. Fifteen patients with infantile spasms (10 females and five males), 3-16 months of age, were evaluated and compared with age- and sex-matched control subject. Cerebrospinal fluid samples for prolactin were obtained before and after treatment. The mean prolactin levels in the cerebrospinal fluid of the patients before therapy (3.25 +/- 1.48 ng/mL) was higher than the control group (2.38 +/- 0.89 ng/mL), and the difference between the two groups was statistically significant (P < 0.001). The mean prolactin level in the cerebrospinal fluid of the patients after therapy (4.69 +/- 1.47 ng/mL) was demonstrated to be higher than the mean prolactin level before therapy (3.25 +/- 1.48 ng/mL) and the difference between the two groups was statistically significant (P = 0.037). Elevation of cerebrospinal fluid prolactin levels before and after treatment in patients with infantile spasms provided evidence that the cerebrospinal fluid prolactin level is related with neuronal injury.

Female↗
PubMed2005

Prolactin receptor mRNA expression in oocytes and preimplantation mouse embryos.

Prolactin was first identified as an anterior pituitary lobe hormone, responsible for the regulation of mammary gland growth and development. Prolactin receptors have been localized in a number of peripheral tissues, including tissues involved in reproduction. Studies with knockout animals have shown that prolactin receptor deficient mice present reproductive defects, whereas prolactin promotes the developmental potential of preimplantation mouse and rat embryos in vitro. To better understand the role of prolactin in the process of reproduction and early embryo development in mice, the expression of the four transcript variants of prolactin receptor was examined in the first stages of mouse embryo development. Prolactin long receptor mRNA was expressed in all stages examined, that is in cumulus cells, oocytes, zygotes, 2-cell embryos, 4-cell embryos, morulae and blastocysts. Prolactin receptor type S1 mRNA was observed only in cumulus cells, while S2 mRNA was present in cumulus cells, oocytes, zygotes and 2-cell embryos. S3 mRNA was expressed only in cumulus cells and oocytes. These results indicate that different isoforms of prolactin receptors may be present in the various stages of mouse preimplantation embryo and may play an important role in the control of its growth and development.

Animals↗
PubMed1999

Prolactin secretory bypath exposed in cultured lactotrophs.

In the present report, the prolactin secretory pathways were re-examined in cultured lactotrophs submitted to various experimental conditions of stimulation, inhibition and/or alteration of the intracellular flow of the synthesis and release of prolactin. Primary cultures of rat pituitary cells stimulated with thyrotropin-releasing hormone, or inhibited with either cycloheximide or dopamine in the presence or absence of 0.1 microg/ml brefeldin A, were used. The radioimmunoassay quantification of released and intracellular prolactin was correlated with ultrastructural and immunocytochemical studies. Brefeldin A diminished significantly the secretion and the intracellular content of prolactin 4 h after application, while morphological effects were seen starting from 30 min. The drug did not modify the response to thyrotropin-releasing hormone (120% increment). The simultaneous incubation of brefeldin A with cycloheximide or dopamine diminished the released prolactin concomitant with a lower (cycloheximide) or greater (dopamine) hormonal intracellular prolactin content with respect to brefeldin A. The combined treatment cycloheximide-dopamine inhibited prolactin secretion. The ultrastructural and immunocytochemical features of lactotrophs supported these radioimmunoassay data. These results revealed that prolactin release in vitro in the presence or not of brefeldin A is dependent on either: the neosynthesized hormone that can be inhibited by cycloheximide, and the hormone stored in granules, the exocytosis of which was blocked by dopamine, indicates the contribution of both constitutive and regulated pathways in the secretory process. The brefeldin A blockade of the intracellular transport also disclosed morphological evidence of an alternative pathway of prolactin secretion through vesicles originated in the rough endoplasmic reticulum bypassing the Golgi complex.

Animals↗
PubMed1997

Interactions of prolactin and growth hormone (GH) in the regulation of mammary gland function and epithelial cell survival.

The relative importance of GH and prolactin in mammary gland function varies between species with prolactin playing a major role in rodents and GH taking lead role in ruminants. In rodents, however, GH appears to play a vital role in maintaining a high-fat/low volume milk in the absence of prolactin and a similar finding has been demonstrated in goats where prolactin deficiency causes a more modest (15%) decrease in milk yield. Surprisingly GH-deficiency in goats induced no further decline in milk yield whereas exogenous GH or prolactin both stimulated milk output considerably. Although direct effects of prolactin on mammary epithelial cells are well-documented effects of GH are believed to be mediated indirectly via IGF-1 production from the liver. We have been unable to confirm this hypothesis in rats and believe this to be because it is too simplistic. By considering prolactin and GH to be survival factors for the mammary gland we now propose a mechanism by which they interact through the IGF system. Involution of the mammary gland involves apoptosis and, in rats, it is induced by prolactin-deficiency or milk accumulation. Coincidentally with this process mammary epithelial cells synthesize and secrete and IGF binding protein, IGFBP-5. We hypothesize that GH stimulates IGF-1 production, possibly from the mammary parenchyma. IGF-1 then acts as a survival factor for the mammary gland. Prolactin plays an essential role since it suppresses the secretion of IGFBP-5 which would otherwise inhibit IGF-1 action and lead to the induction of cell death.

Animals↗
PubMed2004

Prolactin acts as a potent survival factor for human breast cancer cell lines.

Human breast cancer is the leading cause of cancer death in women from Western societies, and a large study of the epidemiology demonstrated strong associations between human prolactin and risk of breast cancer. Using established models of apoptosis of human breast cancer cell lines, we assessed the role of prolactin in breast cancer cell growth and survival. We showed that prolactin had no effect on the metabolic activity or total cell number of any cell lines. We confirmed endogenous prolactin production by these cells and that the levels varied. In the presence of a prolactin-neutralising antibody, each of the cell lines responded with the induction of apoptosis as opposed to growth inhibition. The sensitivity of the cell lines to the physiological inducer of apoptosis, C2-ceramide, appeared relative to the levels of endogenous prolactin that they contained. We then showed that exogenously added prolactin acted as a potent survival factor against apoptosis in all the cell lines examined. In addition, we demonstrated that a prolactin-neutralising antibody in combination with C2-ceramide caused an anticipated, additive increase in cell death. This study demonstrated that prolactin protects human breast cancer cell lines against apoptosis and this may have important implications for cancer treatment.

Apoptosis↗
PubMed1976

Stimulation of prolactin synthesis and of adenosine 3':5'-cyclic phosphate formation by prostaglandins and thyroliberin in cultured rat pituitary cells.

1. The effects of prostaglandins E2 and F2alpha on prolactin synthesis were examined in a clonal strain of rat pituitary tumour cells, and compared with those of thyroliberin. 2. The prostaglandins and thyroliberin gave a dose-related and time-dependent stimulation of prolactin synthesis. The maximal effects (about twofold increases) were observed after 54h of treatment with 25nM-prostaglandin E2 and 2.5nM-prostaglandin F2alpha. A similar stimulation of prolactin synthesis was observed after 250nM-thyroliberin. The combined treatment with prostaglandins and thyroliberin did not increase prolactin synthesis over and above that obtained with each compound alone. 3. After removal of prostaglandins E2 and F2alpha there was a complete reversal of prolactin synthesis to pre-stimulation values 18h later (t1/2less than or equal to 9h). The rapid reversible effect of prostaglandins was in contrast with that of thyroliberin, where prolactin synthesis returned to control values with a t1/2 of about 42 h. 4. Prostaglandin E2 (5mum) and thyroliberin (5mum) increased cellular concentrations of cyclic AMP eight- and four-fold respectively. Maximal effects were observed after 2-5min of incubation. The increases in cyclic AMP were biphasic; normal values were obtained 60 min after the start of incubation with prostaglandin E2 or thyroliberin. 5. The dose/response curve showed that prostaglandin E2 caused maximal increase of cyclic AMP at 50nM. Concentrations of prostagland in E2 that caused half-maximal stimulation of cyclic AMP accumulation and of prolactin synthesis were 4 and 5nM respectively. 6. Combined treatment with prostaglandin E2 and thyroliberin in concentrations that separately caused maximal cyclic AMP increases did not result in a further increase in this cyclic nucleotide. 7. These results are consistent with a role of cyclic AMP in mediating the effects or prostaglandins and thyroliberin on prolactin synthesis. However, if cyclic AMP is involved as a common intracellular mediator of prolactin synthesis, it cannot alone explain all the effects of prostaglandins and thyroliberin in this cell system.

Animals↗
PubMed1998

Influence of adrenal glands on the modulation of prolactin gene expression by the endogenous benzodiazepine ligand octadecaneuropeptide in the male rat pituitary gland.

Recently, an 86-amino acid polypeptide with high affinity for diazepam binding sites, termed diazepam-binding inhibitor (DBI), has been found in the rat brain. DBI, as well as a peptide derived from DBI, the octadecaneuropeptide DBI[33-50] (ODN), interacts with the GABA(A) receptor complex. To investigate the role of these endogenous ligands for GABA(A) receptors on prolactin gene expression, we studied the effects of acute intracerebroventricular administration (4 h before sacrifice) of ODN on prolactin mRNA levels in the male rat. Because, in some neuropeptidergic systems, glucocorticoids play a role in the response to ODN, we also studied the influence of adrenal glands and the effect of dexamethasone administration in the response of prolactin gene expression to ODN. ODN injection produced an increase in prolactin mRNA levels. Adrenalectomy performed 5 days before sacrifice resulted in an increase in prolactin gene expression and also potentiated the stimulating effect of ODN. Because castration has been shown to decrease prolactin gene expression in the male rat, we used castrated and adrenalectomized animals to study the role of dexamethasone in the response of lactotrophs to ODN. In these steroid-deprived animals, dexamethasone treatment (for 4 days) decreased prolactin mRNA levels but did not modify the response to ODN. These data indicate that an endogenous neuropeptide interacting with the GABA(A) receptor complex can stimulate prolactin gene expression and suggest that the adrenal glands may produce factor(s) capable of decreasing prolactin mRNA. On the other hand, it does not appear that glucocorticoid hormones play a role in the effect of ODN on lactotroph activity.

Adrenal Glands↗
PubMed1998

Hypothalamic dopamine D1 receptors are involved in the stimulation of prolactin secretion by high environmental temperature in the female sheep.

Recent evidence suggests that dopamine, acting via its D1 receptors, may function as a neurotransmitter in intrahypothalamic pathways involved in the stimulation of prolactin secretion. Functional dopamine D1 receptors are present in the ventromedial hypothalamic nucleus (VMH) and we hypothesized that they might be part of a prolactin-stimulatory pathway activated by stress. We tested this hypothesis in a series of experiments on sheep involving two different forms of stressors, audiovisual (barking dog) and high environmental temperature. We attempted to block the stimulation of prolactin secretion by infusion into the VMH of an antagonist specific for the D1 receptor. Ovariectomised, oestradiol-implanted merino ewes were surgically implanted with bilateral guide tubes directed at the VMH. After a 180 min pretreatment period, the ewes either were or were not exposed to a stressor (30 min of barking dog or 120 min at 35 degrees C, 65% relative humidity). D1 receptor antagonist, SCH23390 or vehicle (0.9% saline) was infused into the VMH (1.7 microliters/h, 120 nmol/h) for 60 min prior to and during the stressor period. Blood was sampled every 15 min via jugular cannulae and the plasma was assayed for prolactin, cortisol and growth hormone (GH). Both stressors significantly increased prolactin concentrations over control levels. SCH23390 infusion significantly attenuated the prolactin response to high environmental temperature, but had no effect on the prolactin response to audiovisual stress. Cortisol concentrations were significantly increased by audiovisual stress only and were not affected by SCH23390. GH concentrations were not changed by either stressor or infusion. Drug infusion alone did not affect the concentration of the hormones. The data suggest that the VMH D1 receptors are involved in a prolactin stimulatory pathway in response to high environmental temperature. The inability of the D1 antagonist to affect the response to the barking dog indicates that this pathway is stress-specific, implying that there is more than one mechanism or pathway involved in the prolactin response to different stressors.

Acoustic Stimulation↗
PubMed2001

Short-term modulation of prolactin secretion by melatonin in anestrous ewes following dopamine- and opiate receptor blockade.

This study tested the hypothesis that the dopaminergic and opioidergic systems are not involved in the short-term stimulatory action of melatonin (MLT) on the secretion of prolactin in anestrous ewes. Thus, MLT should stimulate prolactin release after blockade of either dopamine (DA) or opiate receptors with specific antagonists at the level of the pituitary gland and central nervous system (CNS), respectively. During afternoon intracerebroventricular (icv.) infusion of MLT, the mean plasma prolactin concentration increased significantly (P < 0.001) as compared with the concentrations noted before and during the infusion of the vehicle (veh.). As a result of subcutaneous (s.c.) injection of sulpiride (SULP, DA antagonist), an increase in plasma prolactin concentration was observed, followed by a gradual decrease during the icv. infusion of the vehicle. MLT infused icv. significantly increased (P < 0.001) the secretion of prolactin in SULP + MLT-treated ewes, as compared with the concentration of prolactin noted during infusion of the vehicle in SULP + veh.-treated ewes. Naloxone (NAL, opioid antagonist) infused icv. did not significantly affect the secretion of prolactin, however, a significant (P < 0.01) increase in the concentration was observed after the infusion. In MLT + NAL-treated ewes, the plasma prolactin concentration increased significantly (P < 0.001) during the infusion, as compared with the concentration noted before and that in NAL-alone infused ewes. These results demonstrate that melatonin stimulates prolactin release after the pharmacological exclusion of the dopaminergic input with the DA antagonist sulpiride and also despite the presence of DA activity in the hypothalamus after NAL treatment. Secondly, endogenous opioid peptides are not a major component of this melatonin action.

Anestrus↗
PubMed2004

Differences in platelet activation by prolactin and leptin.

Hormones such as prolactin and leptin have recently been recognized as potent platelet aggregation co-activators, and have therefore been postulated as an additional risk factor for both arterial and venous thrombosis. Clinical situations exist that are known to be associated with higher leptin and/or prolactin levels (obesity, pregnancy, prolactinomas and anti-psychotic therapy respectively) and increased venous thrombosis or atherosclerosis risk. Therefore, we compared the impact of both hormones on platelet activation in vitro and in vivo. First, we investigated platelet aggregation and P-selectin expression after stimulation with 1,000 mU/l prolactin or 100 ng/ml leptin in five healthy volunteers in vitro. Prolactin revealed significant higher levels of P-selectin expression and platelet aggregation than leptin in all subjects. We also compared the correlation of prolactin and leptin values with the P-selection expression on platelets. Previously, we detected a significant correlation between prolactin values and ADP-stimulated P-selectin expression on platelets in pregnant women, patients with pituitary tumours, and patients on anti-psychotic therapy. In contrast, leptin did not correlate with P-selectin expression in all subject groups investigated. However, leptin correlated with body mass index in the subjects investigated. Our data indicate that prolactin has a stronger effect on platelet activation as leptin in vitro and in vivo. Moreover, our data suggest that the stronger effect of prolactin on ADP-stimulated platelet aggregation, compared to leptin, depends on higher stimulation of CD62p expression by prolactin.

Antipsychotic Agents↗
PubMed1982

Loss of hypothalamic dopaminergic control of prolactin secretion in the hyperprolactinaemic rat.

The possibility that chronic hyperprolactinaemia results in loss of the ability of hypothalamic dopamine activity to inhibit prolactin secretion was studied in rats. Two degrees of hyperprolactinaemia (moderate and gross) were induced in the animals following the chronic administration of two different doses of oestradiol valerate. In rats with high chronic serum prolactin concentrations (approximately 20 times normal) there was a profound increase in prolactin secretion following inhibition of brain dopamine (DA) synthesis by 3-iodo-L-tyrosine, indicating intact and highly active hypothalamic DA-inhibitory control of prolactin release. However, the degree of hypothalamic inhibition of prolactin release relative to normal controls was significantly reduced. In animals with grossly elevated chronic serum prolactin concentrations (approximately 100 times normal) a prolactin response to DA synthesis inhibition was absent despite a highly significant reduction in hypothalamic DA concentrations induced by 3-iodo-L-tyrosine. These observations show that chronic and gross hyperprolactinaemia in the rat results in loss of hypothalamic DA inhibitory control of prolactin secretion. The use of 3-iodo-L-tyrosine to block brain DA synthesis in these studies has provided significant new data relating to prolactin control in hyperprolactinaemic states and indicates that this compound could be a useful clinical tool in the study of human hyperprolactinaemia.

Animals↗
PubMed1980

Absolute requirement of glucocorticoid for expression of the casein gene in the presence of prolactin.

Second thoracic mammary glands of immature BALB/c female mice were stimulated to pregnancy-like lobuloalveolar (LA) development aftr 6 days of incubation in a corticosteroid-free step I culture medium containing insulin, prolactin, estradiol, progesterone, and growth hormone. A low basal level (0.0009%) of casein mRNA (mRNAcsn) sequences was detectable in the LA glands by a specific cDNA probe. Subsequent incubation of the LA glands for 3 days in medium containing insulin and prolactin or insulin and cortisol failed to elicit mRNAcsn above the basal level, indicating that neither prolactin nor cortisol alone can support casein gene expression. However, an increase in mRNAcsn levels was observed when the 3-day incubation with insulin and cortisol or insulin and prolactin was followed by 3 days of culture in presence of insulin, prolactin, and cortisol. When a 3-day incubation with insulin and prolactin was followed by 3 days in insulin and cortisol medium, mRNAcsn levels in the gland remained similar to the basal level. However, a 20-fold increase in the mRNAcsn levels ensued when the LA glands were sequentially incubated for 3 days in insulin and cortisol and then for another 3 days in insulin and prolactin medium. After a preincubation in insulin and cortisol medium, the LA glands retained residual cortisol during subsequent incubation in insulin and prolactin medium, and the mRNAcsn levels in these glands were related to the level of residual cortisol present. When mRNAcsn and the residual cortisol level reached a minimum, addition of fresh cortisol to the medium caused a 20-fold increase in the mRNAcsn levels. This indicates that cortisol is a limiting factor in insulin and prolactin medium and its presence is absolutely required for casein gene expression.

Animals↗
PubMed1988

Use of antiserum to neurotensin reveals a physiological role for the peptide in rat prolactin release.

Previous studies have indicated that the brain peptide neurotensin can stimulate prolactin release by direct action on the pituitary gland, whereas its action within the hypothalamus is inhibitory. The inhibitory action is mediated by the release of dopamine into the hypophyseal portal veins, which deliver the neurotransmitter to the anterior pituitary gland to inhibit prolactin release. Our experiments were done to evaluate the physiologic significance of these neurotensin actions by injecting the globulin fraction of highly specific neurotensin antiserum either intravenously or intraventricularly. Injection into the third ventricle of either 1 or 3 microliter of neurotensin antiserum significantly increased plasma prolactin concentrations in (i) ovariectomized and (ii) ovariectomized estrogen- and progesterone-primed rats within 1 hr of injection. The response was more pronounced in the ovariectomized than in the ovariectomized estrogen- and progesterone-treated animals and was dose related. Intraventricular injection of these doses of neurotensin antiserum also evoked elevations in plasma prolactin in intact males, which were significant but smaller in magnitude than those seen in female rats. To evaluate the effect of the antiserum on the pituitary directly, the antiserum was injected intravenously at a dose of 40 microliter, which was sufficient to block the blood pressure-lowering effect of neurotensin. After the intravenous injection of antiserum, a highly significant suppression of plasma prolactin occurred, detectable when first measured at 1 hr after injection in both ovariectomized and ovariectomized estrogen- and progesterone-treated animals; however, the intravenous injection of antiserum had no significant effect on the prolactin release in males. These data indicate the physiological significance of the hypothalamic inhibitory actions of neurotensin on prolactin release, which are probably mediated by its stimulation of dopamine release that in turn, inhibits prolactin secretion by the lactotropes. The direct stimulatory effect of the peptide on prolactin release after its presumed release into portal vessels also appears to be physiologically significant in female but not in male rats.

Animals↗
PubMed2002

Serum prolactin and response to treatment among cocaine-dependent individuals.

Considerable evidence indicates that dopaminergic mechanisms may modulate the central effects of cocaine. We investigated whether basal serum prolactin, a measure of central dopamine activity, differed between cocaine-dependent subjects and controls, and whether prolactin levels among cocaine patients were related to their response to treatment. Eighty-six African-American cocaine-dependent outpatients and 35 African-American controls were studied. Prolactin concentrations in fasting blood samples were assayed by radioimmunoassay. The outcome measures were: number of negative urine drug screens, retention in treatment, counselor ratings of improvement and discharge status. Chi-square tests and independent t-tests were used for data analyses. The basal prolactin(ng/ml) among cocaine patients (9.12 +/- 4.12) was significantly higher compared to controls (7.14 +/- 3.36) (t = 2.52, p < 0.02). Furthermore, the higher prolactin subjects (median prolactin = 7.71) had significantly fewer negative urine screens (p < 0.05) and received less favorable ratings of improvement by counselors (p < 0.01) compared to the lower prolactin group. However, the two groups did not differ significantly in treatment retention (p = 0.13) or discharge status (p = 0.08). The higher basal prolactin among cocaine patients relative to controls may reflect changes in DA activity among cocaine patients. Moreover, higher prolactin seems to be related negatively with certain measures of response to treatment among cocaine patients.

Adult↗
PubMed1970

Production of both prolactin and growth hormone by clonal strains of rat pituitary tumor cells. Differential effects of hydrocortisone and tissue extracts.

Several established clonal strains of rat pituitary cells which produce growth hormone in culture have been shown to secrete a second protein hormone, prolactin. Prolactin was measured immunologically in culture medium and within cells by complement fixation. Rates of prolactin production varied from 6.6 to 12 microg/mg cell protein per 24 hr in four different cell strains. In these cultures ratios of production of prolactin to growth hormone varied from 1.0 to 4.1. A fifth clonal strain produced growth hormone but no detectable prolactin. Intracellular prolactin was equivalent to the amount secreted into medium in a period of about 1-2 hr. Both cycloheximide and puromycin suppressed prolactin production by at least 94%. Hydrocortisone (3 x 10(-6)M), which stimulated the production of growth hormone 4- to 8-fold in most of the cell strains, reduced the rate of prolactin production to less than 25% of that in control cultures. Conversely, addition of simple acid extracts of several tissues, including hypothalamus, to the medium of all strains increased the rate of production of prolactin six to nine times and decreased growth hormone production by about 50%. We conclude that multifunctional rat pituitary cells in culture show unusual promise for further studies of the control of expression of organ-specific activities in mammalian cells.

Animals↗
PubMed1979

On the mechanism of 5-bromodeoxyuridine induction of prolactin synthesis in rat pituitary tumor cells.

GH12C1, a clonal strain of rat pituitary tumor cells in culture (GH cells), does not produce detectable amounts of prolactin. 5-Bromodeoxyuridine (BrdUrd), the thymidine analogue, at sublethal concentrations (3-5 microgram/ml) induces prolactin synthesis in these cells. BrdUrd also induces prolactin synthesis in F1BGH12C1 cells, a BrdUrd resistant (BrdUrdr) substrain isolated from GH12C1 cells. The F1BGH12C1 strain is not drug dependent, but its resistance to BrdUrd is a stable phenotype. The significant features of the induction of prolactin synthesis in the BrdUrdr strain are the increased net synthesis of prolactin and the shortening of the lag period of prolactin induction. As BrdUrd concentration in the growth medium is increased, the rise in prolactin synthesis parallels the increased incorporation of BrdUrd into DNA. Prolactin synthesis is first detected when BrdUrd replaces 20-25% of the thymidine in DNA. BrdUrd can replace up to 75-80% of the thymidine within 2 d of treatment. Partial starvation of these cells under specified growth conditions does not affect the general growth pattern of the cells, general protein synthesis, and thymidine uptake, but does affect DNA synthesis. When cells are cultured under conditions in which DNA synthesis is preferentially inhibited, BrdUrd does not induce prolactin synthesis, suggestive of a DNA-mediated mechanism of action for the drug.

Animals↗
PubMed2005

Risperidone-induced prolactin elevation in a prospective study of children, adolescents, and adults with mental retardation and pervasive developmental disorders.

OBJECTIVE: Risperidone is widely prescribed for aggression and self-injury in children, adolescents, and adults with mental retardation (MR) and pervasive developmental disorders (PDD). Risperidone elevates prolactin more than other atypical antipsychotic medications. Females may show greater prolactin elevation than males. METHOD: In this relatively long-term study of risperidone efficacy and safety for aggression and self-injury in children, adolescents, and adults with MR and PDDs, serum prolactin was measured in a 21-subject subset during the course of a double-blind, placebo-controlled trial. Prolactin was measured in ng/mL at baseline, once during acute treatment, and once during maintenance. RESULTS: In children and adolescents (n=10), mean age of 12.5 years, prolactin increased from mean 13.2+/-8.6 at baseline to 31.0+/-11.6 acutely and remained elevated at 37.9+/-10.4 in maintenance. In adults, mean age of 35.3 years, prolactin increased more markedly from 11.6+/-7.4 baseline (n=11) to 93.3+/-54.2 acutely but decreased to 67.8+/-62.9 in maintenance (n=7). Prolactin remained significantly elevated above normal in all subjects for at least 26 weeks. Mean prolactin of adult females, while similar to that of adult males at baseline, was 2.2 times male levels acutely and 3.7 times greater in maintenance. CONCLUSION: In this small subset, mean prolactin elevation persisted for at least 26 weeks. In adults, females showed significantly greater elevations than males.

Adolescent↗
PubMed2001

Dependence on prolactin of the luteolytic effect of prostaglandin F2alpha in rat luteal cell cultures.

Luteal regression is a multistep, prolonged process, and long-term luteal cultures are required for studying it in vitro. Cell suspensions from ovaries of superovulated rats were enriched with steroidogenic cells, seeded on laminin or fibronectin, and maintained in defined medium for up to 10 days. Progesterone secretion was much lower than that of 20alpha-dihydroprogesterone, a product of 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD). Prolactin added throughout the incubation period gradually increased the percent progesterone out of total progestins to fourfold, while reducing 20alpha-HSD mRNA by 73%. Luteinizing hormone accelerated the establishment of higher percent progesterone by prolactin but by itself had no effect. Prolactin did not increase total progestin production or cytochrome P450 side-chain cleavage (P450(scc)) mRNA. Cell viability was unaffected by prolactin and/or LH. Prostaglandin F2alpha (PGF2alpha) was added 7-8 days after seeding. In prolactin-treated cells, PGF2alpha reduced steroidogenesis after 4-45 h, and at 45 h total progestins and P450(scc) mRNA were reduced by 45%. At 8-45 h PGF2alpha reduced the percent progesterone out of total progestins, and at 45 h 20alpha-HSD mRNA was doubled. In contrast, in prolactin-deprived cultures, PGF2alpha had little effect on total progestins or 20alpha-HSD mRNA but doubled P450(scc) mRNA. Phospholipase C activity was stimulated by PGF2alpha regardless of prolactin. Thus, when prolactin-treated, our cultures are a good model for mature corpora lutea challenged with PGF2alpha; the finding that without prolactin PGF2alpha has an alternative set of actions could help in identifying the signaling pathways of PGF2alpha responsible for its luteolytic effects.

20-Hydroxysteroid Dehydrogenases↗