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Involvement of calcium ions in dopamine inhibition of prolactin secretion from sheep pituitary cells.

The involvement of calcium in the regulation of prolactin secretion and a possible inhibitory mechanism of action for dopamine have been investigated. Basal prolactin secretion from cultured ovine pituitary cells was dependent on the concentration of calcium ions (Ca2+) in the medium and was inhibited by the presence of verapamil (10 microM). The divalent cation ionophore A23187 (1 microM) caused a rapid stimulation of prolactin release from the cells. The effect was essentially complete within 10 min and subsequently secretion of prolactin occurred at close to the basal rate. A23187 had no effect on cell cyclic AMP levels. Dopamine (0.1 microM) but not verapamil (10 microM) inhibited the A23187 (10 microM) induced release of prolactin. Inhibition of basal and A23187 (1 microM) stimulated prolactin secretion occurred over a similar range of dopamine concentrations. The dopamine receptor antagonist haloperidol (1 microM) reversed the inhibitory effect of dopamine (0.1 microM) on A23187-stimulated prolactin release. These results provide evidence to support the concept that control of Ca2+ handling by lactotrophs may be of fundamental importance in the regulation of prolactin secretion.

Animals↗
PubMed1987

Cyclic AMP inhibits the synthesis and release of prolactin from human decidual cells.

Exposure of human decidual cells for 0.5 h to dibutyryl cAMP, isobutyl-methylxanthine (IBMX), cholera toxin or forskolin caused a dose-dependent inhibition of prolactin release with maximal inhibition by each agent of 50-60%. Dibutyryl cAMP (5 mM), IBMX (0.5 mM), and cholera toxin (10 micrograms/ml) also inhibited prolactin synthesis to the same extent as prolactin release. Dibutyryl cAMP, IBMX, and cholera toxin, however, had no effect on the release of 35S-methionyl-prolactin from decidual cells preincubated for 24 h in medium with 35S-methionine. These agents, however, had no effects on the synthesis or release of TCA-precipitable 35S-decidual proteins and did not cause the degradation of intracellular or released prolactin. The demonstration that agents which increase intracellular cAMP levels inhibit the synthesis and release of decidual prolactin strongly implicates cAMP as a second messenger in the regulation of the synthesis and release of the hormone. The inhibitory effect of cAMP on prolactin release appears to be on the release from a rapidly releasable, newly synthesized intracellular prolactin pool.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Phosphorylated variant of bovine prolactin.

Bovine pituitary explants and cell cultures were incubated with [32P]orthophosphate. Extracts were prepared from the explants and analyzed by sodium dodecyl sulfate-containing acrylamide gel electrophoresis and autoradiography revealing a phosphoprotein that co-migrated with authentic bovine prolactin. Clonal antibodies to bovine prolactin were produced, purified and used to prepare affinity columns. Extracts of [32P]orthophosphate-labeled explants and cells or media were applied to prolactin affinity columns and a radiolabeled protein was eluted with a pH 2.8 wash. The eluted protein was identified as prolactin by co-migration with standard on gel electrophoresis and by amino acid analysis. Treatment of immunoaffinity-purified pituitary prolactin with alkaline phosphatase reduced the phosphate associated with prolactin in a time-dependent manner, indicating a covalent phosphate linkage. Autoradiography of gels revealed prolactin from explants, cells and their associated media to be a phosphoprotein. A phosphorylated variant of bovine prolactin is synthesized and secreted in both explant and cell cultures.

Animals↗
PubMed1994

DNA topology regulates rat prolactin gene transcription.

A cell-free transcription system was used to examine the effects of DNA negative supercoiling on transcription from rat prolactin promoters. The mRNA was faithfully transcribed from prolactin promoters that contained the DNA fragment spanning from -1960 to -10 base pairs upstream of the prolactin transcription start site. Prolactin promoters in supercoiled form, prepared from Escherichia coli, have a higher transcriptional efficiency than the promoter in the relaxed form. Deletion of DNA sequences containing the estrogen response element and putative non-B form DNA elements from the upstream region of the prolactin gene did not alter this effect of DNA topology on prolactin transcription. We further separated transcription into preinitiation and elongation steps by using sarkosyl and found that more preinitiation complexes were assembled on the supercoiled prolactin promoters than on the relaxed promoters. DNA supercoiling therefore plays an important role in controlling prolactin gene expression by facilitating the formation of preinitiation complexes on the promoters.

Animals↗
PubMed1979

Glucocorticoid modulation of prolactin receptors on mammary cells of lactating mice.

Prolactin receptors were monitored by measuring 125I-labeled prolactin binding to collagenase-dissociated mammary epithelial cells of lactating BALB/c mice. Specific receptors for iodine-labeled prolactin with an apparent dissociation constant (Kd) of 0.99 . 10(-9) M were present on the dissociated mammary cells. The binding was inhibited by ovine prolactin, human growth hormone and human placental lactogen but not by follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone, bovine growth hormone or insulin. Adrenal ablation of nursing mothers caused a reduction of the number of prolactin receptors and this effect was preventable by hydrocortisone therapy. Hydrocortisone injections to mothers 3 days after adrenalectomy also induced a replenishment of the prolactin receptors on the mammary cells. Injections of progesterone failed to sustain the high level of mammary cell prolactin receptors in adrenalectomized animals. Stimultaneous injections of hydrocortisone and progesterone to animals 3 days after adrenalectomy caused a partial suppression of the stimulatory action of hydrocortisone alone. The results suggest that hydrocortisone can exert a modulatory influence on mammary cell prolactin receptors in non-hypophysectomized post-partum mice without altering the dissociation constant (Kd) of the receptors.

Adrenal Glands↗
PubMed1979

Relationship of prolactin receptors to concanavalin A binding.

Concanavalin A, which binds to specific carbohydrate determinants on the cell surface, was used to investigate the binding of prolactin to its receptors in liver membranes from female rats. The binding of 125I-labeled ovine prolactin to receptors was sharply inhibited by concanavalin A. This effect was reversed by the competitive sugar alpha-methyl-D-mannopyranoside and thus required the presence of specifically bound lectin. Concentrations of concanavalin A of up to 50 mu/ml caused a progressive decrease in the apparent affinity of the prolactin receptor for hormone. When higher concentrations were used, the number of available binding sites decreased. Concanavalin A-resistant receptors, about 30% of the total, had the same dissociation constant (Kd) as the controls. The binding of 125I-labeled concanavalin A in the same membrane preparations showed the presence of two distinct types of concanavalin A binding. At low concentrations, the lectin bound with high affinity (Kd approximately equal to 6.6 . 10(-8) M. At high lectin concentrations, low affinity (Kd approximately equal to 6.7 . 10(-5) M) binding predominated. Since high affinity concanavalin A binding was saturated at 50 microgram/ml, this class of binding most likely alters the affinity of the prolactin receptor for hormone; low affinity concanavalin A binding may mask prolactin receptors, making them inaccessible to the hormone. Binding sites for concanavalin A and prolactin appear to be independent but closely related since (i) concanavalin A did not displace bound prolactin from its receptor, and (ii) detergent-solubilized 125I-labeled prolactin-receptor complexes bound to concanavalin A-Sepharose and were eluted by alpha-methyl-D-mannopyranoside.

Animals↗
PubMed1986

Proteolytic modification of rat prolactin by subcellular fractions of the lactating rat mammary gland.

The current study explored prolactin proteolysis by rat lactating mammary gland. 125I-labelled rat prolactin was incubated with tissue fractions of lactating mammary gland and the extent of prolactin degradation and fragment formation was visualized and densitometrically quantitated from autoradiographs derived from SDS-polyacrylamide gel electrophoresis under reducing conditions. At pH 4.5, the 25 000 X g pellet of mammary gland converted intact prolactin (23 kDa band) to proteolytic fragments (8-16 kDa bands) in a time- and tissue concentration-dependent fashion similar to that reported previously for rat ventral prostate. The prolactin-degrading and -fragmenting activity in lactating mammary gland was 5-10-times that observed for ventral prostate, the most active male tissue. This activity at acid pH was also demonstrable in other fractions of mammary gland but appeared to predominate in the cytosol. The above activities in mammary gland virtually disappeared at pH 7.4, appeared sensitive to aspartate and sulfhydryl proteinase inhibitors, and insensitive to serine and metalloenzyme proteinase inhibitors. The distribution of this activity could not be correlated with a particular enzyme marker. These characteristics of mammary gland activity differed significantly from those reported previously for prostate. When electrophoresis was conducted under non-reducing conditions, prolactin proteolysis in prostate and mammary gland was primarily associated with the formation of a more slowly migrating product (24 kDa band) with little spontaneous 8-16 kDa fragment formation. Re-electrophoresis of the 24 kDa band under reducing conditions resulted in the appearance of the 8 and 16 kDa fragments. In conclusion, prolactin is proteolytically modified by prostate and lactating mammary gland to a variant of intact hormone (24 kDa band) with a cleavage site in its large loop, by two or more widely distributed, acid-dependent proteinases. Lactating mammary gland, the principal target for prolactin, has the capacity to cleave the hormone in its loop at rates higher than any other tissue examined to date.

Animals↗
PubMed1985

Habituation of the prolactin response in rats to psychological stress.

It is well known that stress is a stimulant for prolactin release. However, relatively few studies have investigated the role of psychological factors in prolactin secretion, and investigators have typically used one-time exposure and a single collection period in their studies. In our studies, attempts were made to carefully characterize the prolactin response to different psychological stressors by serially sampling blood from an indwelling cannula and to determine if repeated exposure to the stressor leads to habituation of the prolactin response. Exposure of the male rats to different novel situations such as being placed in a new cage, being placed on a platform in water, or being handled resulted in increased prolactin levels. As the rats habituated behaviorally to repeated exposure to similar situations, the prolactin response also attenuated. These findings show that psychological factors do play a role in influencing prolactin secretion and are consistent with the idea that as the psychological stress imposed by a stimulus becomes habituated, the prolactin response to that stimulus also becomes habituated.

Animals↗
PubMed1987

The effect of prolactin on glutamate decarboxylase activity and GABA concentration in hypothalamic slices.

The effect of prolactin on the activity of GABA-related enzymes and GABA concentrations were studied in hypothalamic slices incubated in vitro. After short periods of incubation (up to 40 min), prolactin (0.25 micrograms/ml) added to the incubation medium produced a significant increase (21% at 20 min of incubation) in glutamic acid decarboxylase (GAD) activity in the hypothalamic slices. A higher concentration of prolactin (1.0 micrograms/ml) produced a slight but significant decrease (8% at 20 min of incubation) in hypothalamic GAD activity. However, after longer periods of incubation (over 8 hr), both doses of prolactin induced a sustained increase in hypothalmic GAD activity, a response which depends upon protein synthesis. No changes were observed in GABA-transaminase (GABA-T) activity of hypothalamic slices incubated in the presence of prolactin. Prolactin decreased GABA concentration in the hypothalami incubated for 10 hr and, at the same time, increased GABA release into the medium. These results indicate that prolactin modifies the synthesis and release of hypothalmic GABA and suggest the existence of a feedback mechanism that prolactin may exert directly at the hypothalamic level.

Animals↗
PubMed1981

Changes in prolactin release caused by GABA and endogenous GABA increase in rats.

GABA and gamma-acetylenic-GABA (GAG), a GABA-Transaminase inhibitor, were used in this study to determine the influence of GABA on the release of prolactin. In unrestrained male rats, intraventricular (IVT) injection of GABA in high doses (500 microgram) markedly increased plasma prolactin levels. On the contrary, GABA at low doses (10 microgram) and GAG (100 microgram, IVT), were non effective. Systemic. GABA administration (25,50,100 and 200 mg/kg IP) lacked action. Both IVT and systemic GAG (100 mg/kg) slightly decreased plasma prolactin levels. The stimulation of prolactin release by histamine was prevented, and the proestrus prolactin surge was blunted by GAG injected IP (100 mg/kg at 1300 hr) or IVT (100 microgram). GABA (500 microgram, IVT) exhibited a similar action on the histamine response. Results suggest that GABA in basal condition has a pharmacological ability to increase prolactin release. In contrast, the parallel inhibitory effects of GABA and GAG on the histamine effect, and on the proestrus prolactin surge give evidence in favor of a physiological inhibitory role of GABA in the control of prolactin. GABA might act in these conditions as a modulatory transmitter.

Alkynes↗
PubMed1996

Inverse agonism at dopamine D2 receptors. Haloperidol-induced prolactin release from GH4C1 cells transfected with the human D2 receptor is antagonized by R(-)-n-propylnorapomorphine, raclopride, and phenoxybenzamine.

Our earlier observation that the antipsychotic drug haloperidol in the absence of dopamine increases cAMP formation and prolactin release in two prolactin-producing cell lines expressing rat dopamine D2 receptors (GH3, GH4ZR7), but not in similar cells devoid of D2 receptors (GH4C1), prompted us to suggest that haloperidol may act as an inverse (or negative) agonist, rather than as a neutral antagonist, at the D2 receptor (Nilsson and Eriksson 1993). In the present study it is shown that haloperidol elicits a dose-dependent increase in prolactin release also in prolactin-producing GH4C1 cells transfected with the human dopamine D2 receptor (short isoform) (GH4C1-hD2s); in addition, it is shown that another antipsychotic drug, flupenthixol, also causes prolactin release per se in this cell line. The effect of haloperidol on prolactin release in GH4C1-hD2s is calcium dependent and counteracted by pretreatment either with the D2 receptor agonist R(-)-n-propylnorapomorphine or with a D2 receptor antagonist that does not affect prolactin release per se (raclopride). In addition, pretreatment with the alkylating compound phenoxybenzamine at a concentration causing a marked reduction of D2 receptor density in GH4C1-hD2s cells significantly counteracted haloperidol-induced prolactin release.

Animals↗
PubMed2005

Circadian variations in plasma concentrations of melatonin and prolactin during breeding and non-breeding seasons in yak (Poephagus grunniens L.).

Circadian variations of plasma melatonin and prolactin concentrations were determined during breeding as well as non-breeding seasons in yak. Blood samples (5 ml) were collected during different phases of estrous cycle, viz. early (0-6 days), mid (7-12 days) and late luteal (13-19 days) at 2 h interval for 24 h from eight yaks during one breeding month (November); the same yaks were bled at 2 h interval during one non-breeding month (February) for 24 h. Plasma melatonin concentrations rose sharply (P < 0.01) after sunset to record peak concentrations between midnight and 2 a.m. declining sharply thereafter in both breeding as well as non-breeding seasons. Basal melatonin concentrations were recorded between 0600 and 1600 h. Stage of luteal phase did not influence the diurnal hormone change (P < 0.01). In the breeding season, mean plasma prolactin concentrations displayed circadian variations with maximum value at 0400 h (41.22+ /- 1.5 ng/ml) and minimum at 1400 h (12.0 +/- 4.02 ng/ml). In the non-breeding season plasma prolactin concentrations showed circadian variation with maximum value at 0000 h (59.9 +/- 10.5 ng/ml) and minimum at 1200 h (32.13 +/- 3.2 ng/ml). A positive correlation in breeding (r = 0.75) and in non-breeding season (r = 0.65) between circadian changes in mean plasma prolactin and melatonin concentrations were seen. Circadian changes of mean plasma melatonin concentrations during breeding and non-breeding seasons were not different (P > 0.05). However, mean plasma prolactin concentrations were found to be higher (P < 0.01) in the non-breeding season. Three conclusions were drawn from the study: (i) melatonin and prolactin concentrations followed a circadian pattern of secretion (ii) melatonin and prolactin secretion may be closely interrelated and (iii) higher prolactin concentrations during the non-breeding season could be due to nutritional and environmental stress and hence might be contributing to lack of cyclicity.

Animals↗
PubMed2006

Twenty-four hour rhythm of plasma prolactin in female rabbit pups. Correlation with hypothalamic and adenohypophysial dopamine, serotonin, gamma-aminobutyric acid and taurine content.

Lactation in the rabbit is a nocturnal activity, extremely short and regular, that can be a strong synchronizer for the development of circadian rhythmicity in the pups. In the present study, 24-h rhythmicity of plasma prolactin and median eminence and anterior pituitary content of dopamine (DA), serotonin (5HT), gamma-aminobutyric acid (GABA) and taurine were examined in 11 days old female pups kept under 16 h light:8 h dark photoperiods (lights on at 08:00 h). Groups of six to seven female rabbit pups were killed by decapitation at six different time points throughout a 24-h cycle, starting at 09:00 h. Plasma prolactin levels changed significantly throughout the day, showing two peaks, one at first half of rest span (at 13:00 h) and another one at the beginning of the scotophase (at 01:00 h), just preceding doe visit. Median eminence DA content changed in a bimodal way as a function of time of day, displaying two maxima, at the beginning of the rest span and of the activity phase. Median eminence DA and plasma prolactin correlated significantly in an inverse way. Two maxima in median eminence 5HT levels were found, about 4 h in advance to the prolactin peaks. Circulating prolactin correlated inversely with median eminence 5HT content and directly with adenohypophysial 5HT content. Median eminence GABA content reached its maximum at the beginning of the scotophase and correlated significantly with plasma prolactin concentration. A positive correlation between plasma prolactin and adenohypophysial taurine content was observed. These results show that the circadian rhythmicity in prolactin secretory mechanisms in female rabbit pups develops during the early neonatal life.

Aging↗
PubMed2004

A regulatory role of prolactin, growth hormone, and corticosteroids for human T-cell production of cytokines.

The release of the pituitary hormones, prolactin and growth hormone (GH), and of adrenal corticosteroids is subject to a profound regulation by sleep. In addition these hormones are known to be involved in the regulation of the immune response. Here, we examined their role for in vitro production of T-cell cytokines. Specifically, we hypothesized that increased concentrations of prolactin and GH as well as a decrease in cortisol, i.e., hormonal changes characterizing early nocturnal sleep, could be responsible for a shift towards T helper 1 (Th1) cytokines during this time. Whole blood was sampled from 15 healthy humans in the morning after regular sleep and was activated in vitro with ionomycin and two concentrations of phorbol myrestate acetate (PMA, 8 and 25 ng/ml) in the absence or presence of prolactin, prolactin antibody, GH, glucocorticoid receptor (GR) antagonist RU-486, or mineralocorticoid receptor (MR) antagonist spironolactone. Hormones were examined at physiological concentrations. Production of T-cell derived cytokines was measured at the single cell level using multiparametric flow cytometry. Generally, effects were more pronounced after stimulation with 8 rather than 25 ng/ml PMA. The following changes reached significance (p <.05): prolactin (versus prolactin antibody) increased tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) producing CD4+ and CD8+ cells and interleukin-2 (IL-2) producing CD8+ cells. Compared with control, prolactin antibody decreased, whereas GH increased IFN-gamma+CD4+ cells. RU-486 increased TNF-alpha, IFN-gamma, and IL-2 producing CD4+ and CD8+ cells. Surprisingly strong effects were found after MR blocking with spironolactone which increased TNF-alpha, IFN-gamma, and IL-2 producing CD4+ and CD8+ cells. No effects on IL-4+CD4+ cells were observed, while the IFN-gamma/IL-4 ratio shifted towards Th1 after spironolactone and after RU-486 plus GH. Results suggest that enhanced prolactin and GH concentrations as well as low cortisol levels during early nocturnal sleep synergistically act to enhance Th1 cytokine activity.

Adrenal Cortex Hormones↗
PubMed2004

Noradrenergic regulation of prolactin secretion at the level of the paraventricular nucleus of the hypothalamus: functional significance of the alpha-1b and beta-adrenergic receptor subtypes.

Previous research has demonstrated that in the Siberian hamster, both photoperiod and estrous cyclicity alter the profile of noradrenergic activity with the paraventricular nucleus of the hypothalamus (PVN), and that noradrenergic activity is correlated with changes in circulating levels of prolactin. Work from our laboratory has demonstrated an inhibitory role for norepinephrine (NE) acting at the alpha-2 receptor subtype within the PVN on serum prolactin levels; however, the functional significance of other adrenergic receptor subtypes on this system is unknown. The purpose of this study was to investigate the functional significance of the alpha-1b and beta-adrenergic receptor subtypes at the level of the PVN on circulating levels of prolactin. These experiments were performed in male Siberian hamsters using reverse microdialysis coupled with serial blood sampling. In Experiment 1, infusion of l-phenylephrine hydrochloride (alpha-1b agonist) initiated a dose-dependent increase in circulating prolactin, whereas infusion of chloroethylclonidine (alpha-1b antagonist) induced a significant dose-dependent decline in prolactin. In Experiment 2, intraparaventricular administration of propranolol (beta antagonist) initiated a significant increase in prolactin levels in a dose-dependent manner, whereas isoproterenol (beta agonist) induced a dose-dependent decline in prolactin. The results of this study indicate that both the alpha-1b and beta-adrenergic receptor subtypes have a significant role in regulating circulating levels of prolactin at the level of the PVN in the Siberian hamster.

Adrenergic alpha-Agonists↗
PubMed2005

Role of steroid hormones and prolactin in canine mammary cancer.

In several animal studies, prolactin has been found to be essential for mammary epithelial development, and its administration has been consistently shown to increase the rate of mammary tumours. High levels of steroid hormones have also been suggested to enhance mammary cancer development. The present study investigates the levels of the following hormones in serum and in tissue homogenates in dogs bearing canine mammary tumours: prolactin (PRL), progesterone (P4), dehydroepiandrosterone (DHEA), androstenedione (A4), testosterone (T), 17beta-estradiol (17beta-E2) and estrone sulfate (S04E1). Eighty mammary tumours (40 dysplasias and benign and 40 malignant tumours) from 32 female dogs, and 10 normal mammary glands from eight female dogs without history of mammary tumours, were analysed. Prolactin and steroid hormones in serum and tissue homogenates, were analysed by enzyme immunoassays (EIA) techniques, previously validated for this animal species. Levels of prolactin in tissue homogenates were significantly different between malignant and benign mammary tumours (p<0.01). Serum prolactin concentrations were lower in the control group as compared with the group of dogs with benign tumours and in dogs with malignant tumours (p=0.01). Serum prolactin levels in dogs with benign lesions were not significantly different than those obtained from dogs with malignant tumours. Levels of steroid hormones were significantly higher in malignant tumours compared with the benign tumours and normal mammary glands (p<0.01) both in serum and homogenate determinations. Our results suggest that the canine neoplastic mammary gland could be a source of prolactin. Our hypothesis is that both prolactin and steroid hormones are involved in the growth of canine mammary cancer, and that they might have an autocrine/paracrine role in the maintenance of this disease.

Androgens↗
PubMed2006

Tibolone and metabolites induce prolactin production in human endometrial stromal cells in vitro: evidence for cell-specific metabolism.

In this study, we assessed the effects of tibolone and its metabolites on the production of a progesterone sensitive parameter, prolactin, in human endometrium stroma cells in vitro. In addition, the metabolism of the compounds by isolated stromal and epithelial cells was evaluated. The reference compounds, progesterone, Org 2058, and DHT all induced prolactin production. Oestradiol also slightly induced prolactin production and enhanced the response to Org 2058. Tibolone and Delta4-tibolone were similar with regard to potency to induce prolactin levels in the culture supernatant. Their potency was lower than that of Org 2058, similar to that of progesterone and higher than that of DHT. The efficacies of tibolone, Delta4-tibolone and Org 2058 were similar (approximately 200-fold induction). The estrogenic tibolone metabolites 3alpha- and 3beta-OH tibolone also significantly stimulated prolactin production. Their potency, however, was low since significance was reached only at the highest concentrations tested. The PR antagonist Org 31710 inhibited both tibolone- and Delta4-tibolone-induced prolactin production. The responses of tibolone and Delta4-tibolone were not affected by co-incubation with the androgen receptor antagonist OH-flutamide. The effect of tibolone, but not Delta4-tibolone, was antagonized approximately 50% in combination with the highest dose (1 microM) estrogen receptor antagonist, ICI 164384. The induction of prolactin by 3alpha- and 3beta-OH tibolone was antagonized most potently by Org 31710, but also by ICI 164384 and OH-flutamide. Tibolone is metabolized differently in epithelial and stromal cells of the human endometrium. The epithelial cells mostly produce the progestagenic/androgenic Delta4-tibolone. The stromal cells produce predominantly the 3beta-OH tibolone, and some Delta4-tibolone, but the net effect observed with regard to prolactin production is progestagenic. When the metabolites 3alpha-OH, 3beta-OH, and Delta4-tibolone were added to the cultures no conversions were observed. The HPLC analyses showed no evidence for the production of sulfated metabolites. In conclusion, the net effects on endometrial stromal cells are predominantly progestagenic. Tibolone is converted by epithelial cells into Delta4-tibolone which displays progestagenic and androgenic activities, whereas in stromal cells also the estrogenic metabolites 3alpha- and 3beta-OH tibolone are formed.

Cells, Cultured↗
PubMed2006

Gender differences in prolactin elevation induced by olanzapine in Japanese drug-naïve schizophrenic patients.

We investigated the effect of gender on plasma prolactin levels in 20 Japanese drug-naïve schizophrenic patients [10 male, 10 female, aged 25.4+/-10.3 (mean+/-S.D.), range = 12-46 years] treated with olanzapine. Plasma prolactin levels were measured at baseline, and weeks 3 and 8 after starting titration of olanzapine. Comparisons of plasma prolactin levels between baseline and week 3, and between baseline and week 8 were made by repeated analysis of variance (ANOVA) and paired t-test. Two-way ANOVA showed a significant difference in olanzapine-induced prolactin changes between male and female patients (P = 0.037). In male patients (n = 10), the plasma concentration of prolactin at week 3 was significantly higher than at baseline (P = 0.016), but there was no significant difference between the plasma concentration of prolactin at week 8 and at baseline or week 3 (P = 0.191). In female patients (n = 10), there was a significant change of prolactin between baseline and week 3 (P = 0.005), and between baseline and week 8 (P = 0.047). Our results indicate the possibility of gender differences in prolactin elevation induced by olanzapine in Japanese drug-naïve schizophrenic patients. These gender-based findings may be helpful for clinicians when deciding the frequency of follow-up visits once a patient starts olanzapine therapy.

Adolescent↗