Showing papers on "Prolactin published in 1987"
TL;DR: Observed physiological patterns of fluctuating plasma hormone concentrations can be accounted for by distinct, highly delimited, random bursts of hormone release separated by intervals of secretory quiescence.
Abstract: To investigate patterns of endogenous hormone release, we have proposed a biophysical model in which measured hormone concentrations at any given instant reflect the operation of a suitable cumulation function (secretory input) convolved with an appropriate elimination mechanism (metabolic clearance). The cumulation function underlying a macroscopic hormone secretory burst can be represented by a random (Gaussian) distribution of instantaneous molecular secretory rates, which are centered with some finite and determinable standard deviation about a particular moment in time. The hormone elimination mechanism is described by a mono- or biexponential clearance function. The resultant convolution integral is solved by iterative nonlinear least-squares parameter estimation, in which all plasma hormone concentrations and their variances are considered simultaneously. Experiments with human endocrine time series revealed that the spontaneous secretory patterns of any of multiple distinct anterior pituitary hormones (luteinizing hormone, follicle-stimulating hormone, growth hormone, prolactin, thyrotropin, and adrenocorticotropic hormone) can be described effectively by this parsimonious model. In addition, endogenous hormone disappearance rates determined by deconvolution agreed well with those reported earlier that were determined after exogenous hormone injections. Moreover, this model predicted that durations of underlying secretory impulses are extremely brief; i.e., the standard deviations of the Gaussian distributions of instantaneous secretory rates range from 4.5 min (luteinizing hormone) to 16 min (growth hormone) compared to plasma hormone concentration peaks of 90-140 min in duration. Accordingly, we conclude that observed physiological patterns of fluctuating plasma hormone concentrations can be accounted for by distinct, highly delimited, random bursts of hormone release separated by intervals of secretory quiescence.
546 citations
TL;DR: Analysis of the deduced primary structure and additional biochemical characterization indicates that the protein is lactotransferrin, and the estrogenic stimulation in mouse uterus contrasts with the known prolactin dependence in mammary gland.
231 citations
TL;DR: The data suggest that IGF-II may act in an autocrine or paracrine fashion to stimulate the adrenal and gonadal growth stimulated by ACTH and gonadotropins, respectively.
Abstract: Insulin-like growth factors (IGFs) are single-chain polypeptides important for cell proliferation and growth. IGFs are produced in several tissues, suggesting that they function in a paracrine or autocrine fashion as well as functioning as endocrine hormones. We studied the hormonal regulation of IGF-I and IGF-II mRNA in human steroidogenic tissues. In cultured human ovarian granulosa cells, follicle-stimulating hormone, human chorionic gonadotropin, and dibutyryl cAMP increased IGF-II mRNA, but corticotropin [adrenocorticotropic hormone (ACTH)], chorionic somatomammotropin, growth hormone, prolactin, dexamethasone, estradiol, and progesterone had no effect. In cultured human fetal adrenal cells, ACTH and dibutyryl cAMP increased IGF-II mRNA accumulation, but human chorionic gonadotropin and angiotensin II did not. The same five size species of IGF-II mRNA were detected in transfer blots of RNA from granulosa cells and fetal adrenal cells, and all of these increased after hormonal stimuli. Dibutyryl cAMP also increased IGF-II mRNA accumulation in cultured human placental cells. Accumulation of mRNA for the cholesterol side-chain-cleavage monooxygenase [P450scc [corrected]; cholesterol, reduced-adrenal-ferredoxin:oxygen oxidoreductase (side-chain-cleaving), EC 1.14.15.6] was regulated in parallel with IGF-II mRNA in all these steroidogenic tissues. IGF-I mRNA was not detected in transfer blots of these RNAs, and the minimal amounts detected in dot blots showed no detectable change after any of the hormonal stimuli studied. The data indicate that the IGF-II gene is expressed in human steroidogenic tissues and is regulated by cAMP. These data suggest that IGF-II may act in an autocrine or paracrine fashion to stimulate the adrenal and gonadal growth stimulated by ACTH and gonadotropins, respectively.
229 citations
TL;DR: A first pregnancy leads to a long-term decrease in serum prolactin secretion, lasting at least 12 to 13 years, which is known to protect against subsequent breast cancer.
Abstract: An early first pregnancy is known to protect against subsequent breast cancer. We speculated that this effect may be mediated by a long-term depression of prolactin secretion after pregnancy. We therefore measured basal and post-stimulation serum levels of prolactin, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in two groups--15 women 18 to 23 years of age and 9 women 29 to 40--before and after a first full-term pregnancy, and in 40 appropriate nulliparous controls. We observed no significant change in basal levels of serum LH or FSH or in the levels stimulated by gonadotropin-releasing hormone in any group. A significant decrease was seen, however, in basal and perphenazine-stimulated levels of prolactin after pregnancy in both the younger and older first-pregnancy groups but not in the controls. In a separate cross-sectional study, we compared basal serum prolactin levels in 29 parous and 19 nulliparous women of similar age. The serum prolactin levels were significantly lower in the parous group but were not related to the number of pregnancies (one to three) or the time elapsed (12 to 150 months) since the last delivery. We conclude that a first pregnancy leads to a long-term decrease in serum prolactin secretion, lasting at least 12 to 13 years.
201 citations
TL;DR: It is suggested that the NPY induced changes in DA utilization in the tuberoinfundibular DA neurons may contribute to theNPY induced changed in PRL and TSH secretion.
166 citations
TL;DR: In perifused aggregates prepared from different gradient fractions from immature females, there was a negative correlation between the occurrence of FS cells and the magnitude of the PRL response to AII, and it is suggested that FS cells constitute an intercellular messenger system for local inhibitory control of pituitary hormone secretion.
Abstract: Dispersed anterior pituitary cells from adult female rats were separated by gradient sedimentation at unit gravity. The small-sized cell population on top of the gradient consisted of 65.6 ± (SE) 4.2% (n = 8) cells immunoreactive to antiserum against S-100 protein, a marker of folliculo-stellate (FS) cells in rat pituitary. The corresponding fraction derived from adult male or immature female rats were also enriched in S-100 positive cells but to a lower extent. Only small numbers of S-100 positive cells were found in medium- and large-sized cell populations. Coaggregating the S-100 cell-enriched populations from adult females with other pituitary cell populations resulted in a clear-cut inhibition of the GH response to rat GHreleasing factor and /3-adrenergic agents, of the PRL response to TRH and angiotensin II (All) and the LH response to LHRH. The magnitude of inhibition increased with the number of FS cells put into the coaggregates. In perifused aggregates prepared from different gradient fractions ...
162 citations
TL;DR: It is shown that two stressful stimuli, opiate withdrawal and intraperitoneal injection of hypertonic saline, both result in very rapid and marked increases in enkephalin mRNA in the parvocellular paraventricular nucleus, which may be important in the neuroendocrine response to stress.
Abstract: The median eminence of the pituitary is rich in opioid receptors, and exogenous opioids have major effects on the release of adrenocorticotropic hormone (ACTH), luteinizing hormone (LH), prolactin, growth hormone (GH) and thyrotropin. Stress results in similar changes in anterior pituitary hormone secretion. Enkephalin immunoreactivity has been reported in the medial parvocellular neurons of the hypothalamic paraventricular nucleus which project to the median eminence, the site where hypothalamic releasing factors are secreted into the portal blood and thence to the anterior pituitary gland. The endocrine response to stressful stimuli might therefore, at least in part, be mediated through the activation of hypothalamic enkephalinergic neurons. We show that two stressful stimuli, opiate withdrawal and intraperitoneal injection of hypertonic saline, both result in very rapid and marked increases in enkephalin mRNA in the parvocellular paraventricular nucleus. The activation of hypothalamic enkephalin neurons may be important in the neuroendocrine response to stress.
162 citations
TL;DR: In the rat, the activity of the tuberoinfundibular dopaminergic neurons is higher in the female than in the male, exhibits a characteristic cyclical pattern during the first half of pregnancy and is constantly high as a result of stimulation by placental lactogen during the last 9 days of pregnancy, and is reduced in lactating animals and acutely inhibited during suckling.
Abstract: The secretion of prolactin from the adenohypophysis is tonically inhibited by dopamine that is released into the hypophysial portal blood from terminals of tuberoinfundibular neurons located in the external layer of the median eminence. These tuberoinfundibular neurons are unique among other dopaminergic neurons in the brain (including the well-characterized nigrostriatal neurons) in that they are not directly regulated by dopaminergic receptor-mediated mechanisms, but instead are selectively responsive to changes in prolactin concentrations in blood and cerebrospinal fluid. In the rat, the activity of the tuberoinfundibular dopaminergic neurons is higher in the female than in the male, exhibits a characteristic cyclical pattern during the first half of pregnancy and is constantly high as a result of stimulation by placental lactogen during the last 9 days of pregnancy, and is reduced in lactating animals and acutely inhibited during suckling.
161 citations
Journal Article•
TL;DR: Investigation of the hypothalamic-pituitary-gonadal axis in male patients with systemic lupus erythematosus found a decrease in the pituitary response to LH-RH stimulation; this low response could also be a hormonal manifestation of hyperprolactinemia.
Abstract: The hypothalamic-pituitary-gonadal axis was studied in 8 male patients with systemic lupus erythematosus (SLE), both before and after intravenous administration of luteinizing hormone-releasing hormone (LH-RH). We provide evidence herein that resting serum levels of estrone are increased and that resting serum testosterone (T) and dihydrotestosterone (DHT) levels are decreased in male patients with SLE. The decreased serum T levels were observed even after the IV administration of 25 micrograms of LH-RH. The high basal serum prolactin (PRL) levels observed in these patients with SLE is a novel finding not previously reported that could explain why serum T and DHT levels are low in this syndrome. We observed a decrease in the pituitary response to LH-RH stimulation; this low response could also be a hormonal manifestation of hyperprolactinemia. Furthermore, it has been suggested that PRL plays a role in immunocompetence, and therefore it could have influence either directly or indirectly in the altered immunoregulation observed in SLE.
155 citations
TL;DR: Pituitary adenomas originating from cells producing glycoprotein hormones are common, but are difficult to recognize clinically because of the absence of characteristic endocrine syndromes and defective hormone biosynthesis and secretion.
Abstract: Approximately 25% of patients with pituitary adenomas have no clinical or biochemical evidence for excess hormone secretion and are classified as having null cell or nonfunctioning adenomas. To characterize the cell type of these tumors, we analyzed pituitary hormone gene expression in clinically nonfunctioning pituitary adenomas using specific oligonucleotide probes for the messenger (m)RNAs encoding growth hormone, prolactin, ACTH, and the glycoprotein hormone subunits, alpha, luteinizing hormone (LH)beta, follicle-stimulating hormone (FSH)beta, and thyroid-stimulating hormone (TSH)beta. Expression of one or more of the anterior pituitary hormone genes was found in 12/14 (86%) of the patients with clinically classified nonfunctioning adenomas. Expression of one or more of the glycoprotein hormone genes (alpha, LH beta, FSH beta, TSH beta) was identified most commonly (79%) with expression of multiple beta-subunit genes in many cases. Expression of alpha-subunit mRNA was found in each of the adenomas from patients expressing one of the beta-subunit mRNAs and in three patients with no detectable beta-subunit mRNA. Although FSH beta and LH beta mRNAs were found with similar frequencies in nonfunctioning adenomas, expression of FSH beta mRNA was generally much more abundant. TSH beta mRNA was detected in only one adenoma. The levels of glycoprotein hormone subunit mRNAs were variable in different adenomas, but the lengths of the mRNAs and transcriptional start sites for the alpha- and beta-subunit genes were the same in the pituitary adenomas and in normal pituitary. Growth hormone and prolactin gene expression were not observed in the nonfunctioning adenomas, but ACTH mRNA was found in a single case. Immunohistochemistry of the adenomas confirmed production of one or more pituitary hormones in 13/14 (93%) nonfunctioning tumors, with a distribution of hormone production similar to that of the hormone mRNAs. These data indicate that pituitary adenomas originating from cells producing glycoprotein hormones are common, but are difficult to recognize clinically because of the absence of characteristic endocrine syndromes and defective hormone biosynthesis and secretion.
141 citations
TL;DR: Data presented here suggest that most apparently nonfunctioning pituitary tumors contain immunoreactive hormones and the majority of these are subunits of the glycoprotein hormones.
Abstract: ✓ Pituitary tumors in which no excess hormone secretion can be identified clinically have been considered as nonfunctioning or null-cell adenomas. Immunocytochemical data presented here suggest that many of these tumors contain subunits of the glycoprotein hormones. Of 160 patients referred for pituitary surgery, 37 (23%) had no evidence of excess hormone secretion on preoperative endocrine evaluation. Immunocytochemical staining of these tumors was carried out using antibodies specific for prolactin, growth hormone, adrenocorticotropic hormone, the beta subunits of luteinizing hormone (β-LH), follicle-stimulating hormone (β-FSH), and thyroid-stimulating hormone (β-TSH), and the alpha subunit. One or more of these pituitary hormones were detected in 73% of cases. The alpha and beta subunits were detected most frequently, being found in 68% of cases; 27% had staining for one or more beta subunits and 37.9% had staining for both alpha and beta subunits. The incidence was: β-FSH in 58%, β-LH in 47%, β-TSH in...
TL;DR: Circulating progesterone concentrations in both strains of rat were significantly higher during pregnancy than in virgin controls, except at term in the SD group, and there was little variation in the circulating corticosterone concentration except in pregnant rats at term when levels fell.
Abstract: Plasma samples were obtained throughout pregnancy and pseudopregnancy from Sprague-Dawley (SD) rats and during pregnancy from rats of the Munich Wistar (MW) strain. The concentrations of progesterone, oestradiol, prolactin, plasma renin activity (PRA), aldosterone and corticosterone were measured by radioimmunoassay to establish hormonal profiles in the two strains of rat. Circulating progesterone concentrations in both strains of rat were significantly higher during pregnancy than in virgin controls, except at term in the SD group. The hormonal pattern for pseudopregnancy was similar to that of the first half of pregnancy. Oestradiol concentrations were similar to, or lower than, those in virgin controls throughout pseudopregnancy and for the first 2 weeks of pregnancy in both strains of rat. Increased concentrations of steroid were seen only in the pregnant groups towards term. In SD rats, highest prolactin concentrations were apparent during the first half of pregnancy and pseudopregnancy, and at term in the pregnant group. Pregnant MW rats showed a different profile for this hormone, with low levels throughout pregnancy except at term. In all groups PRA rose to a peak at day 9 and decreased to day 16. Pregnant SD rats also showed a significant increase at term. Aldosterone concentrations were significantly increased at several stages of pregnancy in both strains of rat, particularly during the second half of gestation. Pseudopregnant animals showed a different hormone profile, with no significant changes until day 16 when lower concentrations were recorded. There was little variation in the circulating corticosterone concentration except in pregnant rats at term when levels fell. These findings are discussed in relation to the known renal changes of pregnancy and pseudopregnancy.
TL;DR: Depressed patients have different types of abnormal 5-hydroxytryptamine-mediated neuroendocrine responses that correlate with the presence or absence of severe weight loss and cortisol hypersecretion, and these abnormalities are central to the depressive disorder or have implications for treatment response.
Abstract: • The increases in plasma levels of prolactin (PRL) and growth hormone (GH) following intravenous administration of the 5-hydroxytryptamine precursor tryptophan (100 mg/kg) were assessed in 30 depressed patients and 30 control subjects. In depressed patients who lost less than 10 lb, PRL responses were significantly reduced compared with controls. In contrast, the PRL responses of patients with weight loss exceeding 10 lb were significantly greater than those of either controls or the other depressed patients. Growth hormone responses to tryptophan were significantly decreased in patients who lost less than 10 lb. Prolactin, but not GH, responses correlated significantly with the postdexamethasone plasma cortisol concentration; however, an apparent relationship between GH and PRL responses and suicidal behavior was probably due to the common factor of weight loss. The results suggest that depressed patients have different types of abnormal 5-hydroxytryptamine—mediated neuroendocrine responses that correlate with the presence or absence of severe weight loss and cortisol hypersecretion. Further investigations are needed to establish if these abnormalities are central to the depressive disorder or have implications for treatment response.
TL;DR: Data indicate a role for IGF-I in negative feedback of GH gene expression and provide evidence for the direct transcriptional regulation of the GH gene by IGF- I in primary rat anterior pituitary cells.
Abstract: We have previously shown that insulinlike growth factor I (IGF-I) inhibits growth hormone (GH) secretion and messenger RNA (mRNA) levels in pituitary cells. The effects of IGF-I on new GH mRNA synthesis rates in primary monolayer rat pituitary cells were therefore examined by nuclear runoff transcription assays. IGF-I (1.3 nM) treatment for 1 h inhibited GH gene transcription to 60% of controls. IGF-I (3.25 nM) maximally suppressed GH gene transcription to 30% of control values after 4 h. After 24 h treatment, GH transcription was suppressed to 48% of controls by 3.25 nM IGF-I. IGF-I (3.25 nM) also inhibited the twofold growth hormone-releasing hormone (GHRH) (10 nM)-stimulated GH gene transcription by 30% after 4 h. Transcription of the prolactin (PRL) gene was not suppressed in these cells by IGF-I. Relatively high doses of insulin (200 nM) also suppressed GH gene transcription, but epidermal growth factor and fibroblast growth factor did not change GH mRNA synthesis. The results show that IGF-I exerts a rapid and selective suppression of basal and GHRH-stimulated GH gene transcription. These data indicate a role for IGF-I in negative feedback of GH gene expression and provide evidence for the direct transcriptional regulation of the GH gene by IGF-I in primary rat anterior pituitary cells.
Journal Article•
TL;DR: The results clearly demonstrate that, under the proper conditions of culture, the human breast cancer cell line MCF-7 is highly responsive to growth stimulation by homologous lactogenic hormones, and affords an excellent model for further studies on the possible role of prolactin in growth and maintenance of human Breast cancer.
Abstract: MCF-7 human breast cancer cells, grown in long-term tissue culture, were found to be highly responsive to prolactin in terms of growth even in the presence of serum. Human prolactin, placental lactogen, and growth hormone (50–250 ng/ml) stimulated MCF-7 cells to grow when added to culture medium of cells in the presence of charcoal-stripped serum. Within 3 days of the hormone addition, a 4.4-fold increase in cell number was achieved with human prolactin at 100 ng/ml in the presence of 10% charcoal-stripped serum. Under these same conditions, estradiol-17β at 10 -8 m achieved only a 2-fold increase. After 6 days of culture, both estradiol-17β and prolactin gave a total 5-fold increase in cell number. No prolactin effect was achieved in the presence of 10% fetal bovine serum. Stripping fetal bovine serum with dextran-coated charcoal removes as much as 85% of the endogenous lactogens. Removal of these hormones is essential for demonstration of subsequent prolactin-induced growth response in MCF-7 cells, since bovine prolactin binds effectively to lactogen receptors on the surface of the cells but does not transmit a growth signal. When added simultaneously with human prolactin, bovine prolactin blocks the growth response to the former hormone. These results clearly demonstrate that, under the proper conditions of culture, the human breast cancer cell line MCF-7 is highly responsive to growth stimulation by homologous lactogenic hormones. This then affords us an excellent model for further studies on the possible role of prolactin in growth and maintenance of human breast cancer.
TL;DR: The results indicate that NPY may have central effects on neuronal release of GnRH, and that ovarian factors are critical in the directional mode of these NPY actions.
Abstract: Neuropeptide Y (NPY) is present in large quantities in the hypophysiotropic areas of the brain and has a similar distribution pattern as gonadotropin-releasing hormone (GnRH). The aim of this study wa
TL;DR: The results indicate that interleukin‐1 can act in minute doses, presumably on structures near the third ventricle, to stimulate growth homone and prolactin release and to inhibit TSH releas.
Abstract: In order to determine the possible effects of interleukin-1 on the release of pituitary hormones by direct action on the brain, the peptide was injected into the third brain ventricle of conscious, unrestrained male rats and the effects on hormone release were compared with effects on rectal temperature. The procedure of blood sampling and intraventricular injection resulted in a significant decline in body temperature and a decrease in plasma growth hormone without alteration in the plasma level of thyroid stimulating hormone (TSH) and prolactin. Interleukin-1 injected intraventricularly at a dose of 5 ng (0.3 pmol) prevented the decline in body temperature that occurred in the saline-injected controls and resulted in a significant elevation of plasma growth hormone levels that became apparent within 15 min of injection, as well as a highly variable but significant elevation of plasma prolactin and a significant decline in plasma TSH that was observed at 30 min. The results were similar when areas under the release curves for the various hormones were calculated. On the other hand, the higher dose of 25 ng (1.5 pmole) of interleukin-1, although producing a frank pyrexia, was associated with smaller changes in hormone values, which were no longer significant for any of the three hormones. The results indicate that interleukin-1 can act in minute doses, presumably on structures near the third ventricle, to stimulate growth hormone and prolactin release and to inhibit TSH release. Apparently when frank febrile responses occur, these hormonal responses are muted for reasons that are yet to be determined. In view of the minute doses injected we favor a hypothalamic site for these effects.
TL;DR: The PIP gene is useful in studying the molecular actions of the prolactin/growth hormone polypeptide hormone family and the interaction with androgen, in mammary and other potential target cells.
TL;DR: The results suggest that the physiological significance of IL-1 as a tissue CRF is indeed questionable and should be further clarified.
Abstract: The present study was performed mainly to determine whether interleukin-1 (IL-1), a polypeptide produced by immunologically activated monocytes, plays a physiological role in the regulation of adrenocorticotropic hormone (ACTH) using primary monolayer cultures of rat anterior pituitary cells. Neither human IL-1 alpha nor IL-1 beta stimulated the ACTH release from normal pituitary cells in concentrations ranging from 0.01 to 10 nM. IL-1 beta caused a slight, but significant, increase in ACTH release at a concentration of 100 nM, while IL-1 alpha did not, even at the highest dose tested. IL-1 beta exhibited a synergistic action with corticotropin-releasing factor (CRF) in ACTH secretion at 10 and 100 nM of CRF, but the interaction was not striking. Both of the monokines failed to cause any change in the secretions of growth hormone, prolactin, follicle-stimulating hormone and luteinizing hormone throughout concentrations ranging from 0.01 to 100 nM. The effects of possible sex-related differences and prolonged preincubation of cultured pituitary cells in serum-free medium prior to assay incubation were also tested, providing no significantly different findings. These results suggest that the physiological significance of IL-1 as a tissue CRF is indeed questionable and should be further clarified.
TL;DR: The data show that prolactin can stimulate the immune system in a biphasic manner and that a reduction in the basal levels of this hormone results in an attenuated immune response.
TL;DR: T‐cells and NK cells from aged rats are not inherently defective because their proliferative responses to lectins and cytolytic activity can be augmented by exogenous GH, and these effects are not as apparent as thos observed in immunocompromised aged animals.
Abstract: Growth hormone (GH) appears to play a major role in a reciprocal axis that has been postulated between the thymus and pituitary glands. Our previous studies showed that thymic structure, as well as T-cell proliferation and IL-2 synthesis, could be restored in aged female Wistar-Furth rats by the implantation of GH3 pituitary adenoma cells. These cells secrete GH and some prolactin. We have now used three different approaches to determine whether GH affects a variety of immune events in vivo in both old and young rodents, and whether GH3 cells can directly affect progenitor T-cells in nude rats that congenitally lack a thymus gland. To test the effects of GH in aged rats, 750 μg of pituitary-derived ovine GH was injected 2× daily into 26-month-old Fischer 344 rats for 5 weeks. This approach demonstrated that GH augments splenocyte proliferation to T-cell lectins as well as natural killer (NK) activity at low effector: target ratios even though morphologic characteristics of the thymus were not altered. To assess the effect of GH in young rodents, mice were studied that were transgenic for the rat metallothionein-GH gene. Histologic evaluation of thymus glands revealed that the amount of adipose tissue and the number of epithelial cells and Hassall's corpuscles are augmented in transgenic mice. Splenocyte proliferation at suboptimal mitogen doses is greater in transgenic than in control littermate mice, but neither IL-2 synthesis nor antibody synthesis to sheep erythrocytes is affected. The role of pituitary hormones on progenitor T-cells was then explored by implanting GH3 cells into Rowett nude rats. GH3 cells are unable to augment proliferation to T-cell lectins, IL-2 synthesis, antibody production to sheep erythrocytes, or NK activity in nude rats. Collectively, these experiments show that T-cells and NK cells from aged rats are not inherently defective because their proliferative responses to lectins and cytolytic activity can be augmented by exogenous GH. If GH affects progenitor T-cells, these effects are not apparent in nude rats. Finally, GH can also augment T-cell proliferative responses in young rodents, but the immunoenhancing effects are not as apparent as thos observed in immunocompromised aged animals.
TL;DR: Understanding the mechanisms that stimulate mammary epithelial cell numbers has the potential to lead to new methods for increasing efficiency of milk production.
TL;DR: Findings indicate that central galanin has a stimulatory role in pituitary PRL secretion via the hypothalamus in the rat and that VIP may be involved in rat PRL release induced by galanIn, a newly identified neuropeptide.
TL;DR: It is clear that postpartum administration of exogenous prolactin during the period of lactation prior topeak milk yield or after peak milk yield does not alter lactational performance in high producing dairy cows.
TL;DR: The LOBEX-lactating rat is not refractory to PRL-releasing stimuli other than suckling and its hypothalamic DA and serotonergic systems are functionally intact.
Abstract: The aim of this study was to determine the role of the posterior pituitary in the regulation of PRL release during suckling. Lactating rats were subjectd to posterior pituitary lobectomy (LOBEX) or sham surgery (SHAM) and separation from pups in the evening; experimental manipulations and blood collection were performed the next morning. In the first experiment rats were divided into three groups: SHAM, LOBEX, and LOBEX treated with a vasopressin analog, l-desamino-8-Darginine vasopressin and oxytocin. Plasma PRL levels in SHAM rats increased 20- to 25-fold upon introduction of pups and remained elevated for the duration of suckling. In contrast, basal plasma PRL levels in LOBEX rats were 3- to 4-fold higher than in SHAM but suckling failed to induce a further increase. Treatment of LOBEX rats with l-desamino-8-D-arginine vasopressin and oxytocin reduced water consumption and allowed for milk ejection and milk intake by the pups but did not restore the suckling-induced rise in PRL. The second experiment t...
TL;DR: The results show that intraventricular injections of galanin in the awake and unrestrained male rat produce rapid increases of prolactin and growth hormone secretion but no effects on serum luteinizing hormone, thyroid stimulating hormone or on corticosterone levels.
Abstract: Galanin-catecholamine interactions have been analysed within the hypothalamus and the anteromedial frontal cortex of male rats by means of quantitative histofluorimetrical and biochemical measurements of catecholamine fluorescence in discrete catecholamine nerve terminal systems and measurements of serum levels of adenohypophyseal hormones and corticosterone using radio-immunoassay determinations. 125I-galanin binding sites were analysed and related to the distribution of galanin-immunoreactive neuronal structures in the median eminence and paraventricular hypothalamic nucleus. The results show that intraventricular injections of galanin in the awake and unrestrained male rat produce rapid increases of prolactin and growth hormone secretion but no effects on serum luteinizing hormone, thyroid stimulating hormone or on corticosterone levels. These changes in neuroendocrine function were associated with a selective reduction of the catecholamine stores in the medial palisade zone of the median eminence at the 20 min time interval. 125I-galanin binding sites were found throughout the hypothalamus including the median eminence and the magnocellular part of the paraventricular hypothalamic nucleus with a good correspondence with galanin immuno-reactivity. It is suggested that the enhancement of prolactin secretion induced by galanin involves an interaction between galanin and dopamine in the medial palisade zone leading to a reduced synthesis and/or release of dopamine and thus to a reduced prolactin inhibitory activity and to increases in prolactin secretion. A possible involvement of hypothalamic catecholamines in the galanin-induced changes of growth hormone secretion remains to be established.
TL;DR: Results demonstrate that activation of the mu receptors produces an inhibition of LH secretion and a stimulation of PRL release; activation ofThe delta receptors produces a inhibition of RH secretion but has no effect onPRL release, and activation ofthe kappa receptors producesAn inhibition ofRH release and a variable stimulation ofPRL secretion.
Abstract: With the recent development of highly specific ligands for the µ, δ and Kopioid receptors it was of interest to define the effects of activation of each of these receptor types on LH and prolactin (PRL) secretion. The compounds were infused (10 µl/h) at various concentrations into the third cerebroventricle of unanesthetized, ovariectomized rats. The µ agonist, DAGO, at both 1 and 10 µg/h caused a significant suppression of LH secretion and a significant stimulation of PRL release. DPDPE, the δ agonist, had no effect on either hormone at 1 µg/h but inhibited LH secretion at 10 µg/h. There was still no effect of this high dose of DPDPE on PRL release. The Kagonist, U50,488H, had no effect on either hormone at 10 µg/h, but at 100 µg/h produced a significant suppression of LH release and a highly variable increase in PRL. Coinfusion of 100 µg/h of naloxone with the high dose of each of the agonists completely blocked the responses of both hormones to each of the agonists with one exception: the highly variable stimulation of PRL by U50,488H was not affected, thus indicating a nonspecific effect of U50,488H on PRL secretion. These results demonstrate that: (1) activation of the µ receptors produces an inhibition of LH secretion and a stimulation of PRL release; (2) activation of the δ receptors produces an inhibition of LH secretion but has no effect on PRL release, and (3) activation of the Kreceptors produces an inhibition of LH release and a variable stimulation of PRL secretion.
TL;DR: Hyperprolactinaemia may be a causative factor in the impairment of OT stress responses observed in lactating rats, and plasma levels of vasopressin were not significantly modified in either control or immobilized rats of any experimental groups.
Abstract: The plasma oxytocin (OT) response to acute stress was compared between virgin, lactating, and hyperprolactinaemic female rats. In virgin rats, brief immobilization was associated with a significant elevation of plasma OT to 24.7 +/- 3.7 pmol/l compared with 7.7 +/- 1.1 pmol/l in controls. In contrast, the stress response was absent in lactating (6 days post-partum) animals: control OT 9.4 +/- 2.2, immobilized OT 9.0 +/- 1.1 pmol/l. Hyperprolactinaemia produced by treatment with either dopamine antagonists (domperidone or haloperidol) or ovine prolactin was also associated with an impairment of the OT stress response in intact females, whereas domperidone treatment failed to modify the response in ovariectomized (OVX) rats. Following ovarian steroid replacement with oestradiol and progesterone, the inhibitory effect of domperidone was observed in OVX rats: control OT 11.1 +/- 2.5, immobilized OT 16.0 +/- 3.7 pmol/l. Treatment of OVX rats with oestradiol and progesterone, either separately or combined, did not modify the OT stress response. Plasma levels of vasopressin were not significantly modified in either control or immobilized rats of any experimental groups. The results indicate that hyperprolactinaemia may be a causative factor in the impairment of OT stress responses observed in lactating rats.
TL;DR: Some alterations in endocrine function were detected prior to the cessation of menstrual periods and there were changes in prolactin, cortisol, TSH and triiodothyronine in relation to menopausal status as well as in ovarian steroids and gonadotrophins.
TL;DR: It is suggested that dieting alters brain 5-HT function in women but not in men, and biological factors as well as greater psychosocial pressures to diet may contribute to the high prevalence of eating disorders amongst women.
Abstract: The increase in plasma prolactin which follows intravenous administration of L-tryptophan (LTP) was used to assess changes in brain 5-hydroxytryptamine (5-HT) function in normal male and female subjects, following a three week period of dieting. In women, but not men, there was a marked increase in the prolactin response to LTP, suggesting that dieting had caused alterations in brain 5-HT-mediated responses. In contrast, dieting did not alter the prolactin response to thyrotropin releasing hormone in either men or women, indicating that the changes in response to LTP could not be attributed to an increase in pituitary reserve of prolactin. These findings suggest that dieting alters brain 5-HT function in women but not in men. Biological factors as well as greater psychosocial pressures to diet may contribute to the high prevalence of eating disorders amongst women.