Showing papers on "Prolactin published in 1990"
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TL;DR: Data imply that both transcriptional and post-transcriptional regulation of Pit-1 gene expression and combinatorial actions with other classes of transcription factors activated in distinct temporal patterns, are required for the mature physiological patterns of gene expression that define distinct cell types within the anterior pituitary gland.
Abstract: Development of the anterior pituitary gland involves proliferation and differentiation of ectodermal cells in Rathke's pouch to generate five distinct cell types that are defined by the trophic hormones they produce. A detailed ontogenetic analysis of specific gene expression has revealed novel aspects of organogenesis in this model system. The expression of transcripts encoding the c~-subunit common to three pituitary glycoprotein hormones in the single layer of somatic ectoderm on embryonic day 11 establishes that primordial pituitary cell commitment occurs prior to formation of a definitive Rathke's pouch. Activation of Pit-1 gene expression occurs as an organ-specific event, with Pit-1 transcripts initially detected in anterior pituitary cells on embryonic day 15. Levels of Pit-1 protein closely parallel those of Pit-1 transcripts without a significant lag. Unexpectedly, Pit-1 transcripts remain highly expressed in all five cell types of the mature pituitary gland, but the Pit-I protein is detected in only three cell types--lactotrophs, somatotrophs, and thyrotrophs and not in gonadotrophs or corticotrophs. The presence of Pit-1 protein in thyrotrophs suggests that combinatorial actions of specific activating and restricting factors act to confine prolactin and growth hormone gene expression to lactotrophs and somatotrophs, respectively. A linkage between the initial appearance of Pit-1 protein and the surprising coactivation of prolactin and growth hormone gene expression is consistent with the model that Pit-1 is responsible for the initial transcriptional activation of both genes. The estrogen receptor, which has been reported to be activated in a stereotypic fashion subsequent to the appearance of Pit-l, appears to be capable, in part, of mediating the progressive increase in prolactin gene expression characteristic of the mature lactotroph phenotype. This is a consequence of synergistic transcriptional effects with Pit-l, on the basis of binding of the estrogen receptor to a response element in the prolactin gene distal enhancer. These data imply that both transcriptional and post-transcriptional regulation of Pit-1 gene expression and combinatorial actions with other classes of transcription factors activated in distinct temporal patterns, are required for the mature physiological patterns of gene expression that define distinct cell types within the anterior pituitary gland.
607 citations
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TL;DR: Findings demonstrate a central site of PRL action in the stimulation of maternal responsiveness and point to the medial preoptic area as a key neural site for PRL regulation of maternal behavior.
Abstract: A series of experiments were conducted to determine whether and under what conditions central prolactin (PRL) administration would stimulate the onset of maternal behavior in female rats and to identify possible neural sites of PRL action. In each experiment ovariectomized, nulliparous rats whose endogenous PRL levels were suppressed with bromocriptine were tested for maternal behavior toward foster young. In experiments 1, 2, and 4, females were also exposed to pregnancy-like levels of progesterone (days 1-11) followed by estradiol (days 11-17). In experiment 1 infusions (days 11-13) of four doses of ovine PRL (400 ng, 2 micrograms, 10 micrograms, or 50 micrograms, but not 80 ng) into the lateral ventricle resulted in a rapid onset of maternal behavior (behavioral testing, days 12-17). The stimulatory action of these doses of PRL appears to be central, since subcutaneous injections of 50 micrograms of ovine PRL failed to affect maternal responsiveness (experiment 2). Experiment 3 indicated that the stimulatory effect of intracerebroventricularly administered PRL is steroid dependent. Infusions of either 10 micrograms of ovine PRL or 10 micrograms of rat PRL failed to induce maternal behavior in nonsteroid-treated animals. In the final experiment (no. 4) bilateral infusions of 40 ng of ovine PRL into the medial preoptic area of steroid-treated rats resulted in a pronounced stimulation of maternal behavior. These findings demonstrate a central site of PRL action in the stimulation of maternal responsiveness and point to the medial preoptic area as a key neural site for PRL regulation of maternal behavior.
319 citations
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01 Apr 1990
TL;DR: A histologic and immunocytochemical study of 69 autopsy-obtained pituitaries from women who died during pregnancy, after abortion, or in the postpartum period revealed an accumulation of large chromophobic to slightly acidophilic and periodic acid-Schiff-negative pregnancy cells that were immunoreactive for prolactin but not for other pituitary hormones.
Abstract: A histologic and immunocytochemical study of 69 autopsy-obtained pituitaries from women who died during pregnancy, after abortion, or in the postpartum period revealed an accumulation of large chromophobic to slightly acidophilic and periodic acid-Schiff-negative pregnancy cells that were immunoreactive for prolactin but not for other pituitary hormones. This increase in the number of prolactin cells was confirmed by cell counts. Thus, pregnancy cells are capable of prolactin production. The finding of mitotic figures in such cells supports the view that they arise by multiplication from preexisting prolactin cells. With use of "mirror section" techniques, no mammosomatotrophs (cells immunoreactive for growth hormone and prolactin) were identified. Hyperplasia of prolactin cells was evident at 1 month of pregnancy and gradually disappeared within several months after delivery or abortion; the process of involution seemed to be retarded in the one lactating patient investigated. In some pituitaries, the accumulation of prolactin cells was so extensive that the hyperplastic foci resembled microadenomas. Another striking change in the pituitaries of pregnant women was appreciable reduction of immunostaining of gonadotropic cells, a process that was reversible as soon as 1 month after delivery. Among the 69 pituitaries studied, 8 noninvasive microadenomas (12%) were encountered (7 contained prolactin only and 1 was plurihormonal). Prolactin-producing adenomas were no more numerous or larger than were similar tumors encountered in nonpregnant women or normal men; thus, pregnancy neither initiates formation of pituitary adenomas nor accelerates their growth. In the pituitaries that harbored prolactin-producing adenomas, massive pregnancy cell hyperplasia was evident outside the tumor; thus, prolactin production by adenoma cells did not seem to suppress the proliferation of prolactin-containing pregnancy cells.
235 citations
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TL;DR: The spatial and temporal correlation between the appearance of GHF-1 protein and growth hormone gene activation suggests that GHF, the pituitary-specific transcription factor, is responsible for this very last step in the specialization of somatotrophic cells.
207 citations
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TL;DR: The data indicate that extracellular prolactin is requisite for T-cell proliferation and suggest that the effects of prolactIn are exerted in the nucleus, and indicate that the results of interleukin 2 stimulation induced the translocation of Prolactin into the nucleus and prolACTin receptor to the nuclear periphery.
Abstract: The requirement for prolactin in interleukin 2-driven T-cell proliferation was evaluated. Addition of an anti-prolactin antiserum resulted in the specific inhibition of T-cell proliferation in a time- and dose-dependent manner. Synthesis of prolactin and its mRNA, however, did not occur during interleukin 2 stimulation. Instead, previously internalized prolactin, presumably from fetal bovine serum, appears to serve as the source of prolactin under serum-free conditions. A 7-fold increase in a prolactin receptor occurred as a function of cell cycle progression; accumulation of a 1.6-kilobase prolactin receptor mRNA increased approximately 2-fold. Interleukin 2 stimulation induced the translocation of prolactin into the nucleus and prolactin receptor to the nuclear periphery. These data indicate that extracellular prolactin is requisite for T-cell proliferation and suggest that the effects of prolactin are exerted in the nucleus.
197 citations
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TL;DR: From a flounder pituitary cDNA library, cDNA clones encoding a 28-kDa glycoprotein produced by the pars intermedia of the pituitaries were isolated and characterized and found to be distantly and similarly related to growth hormone and prolactin.
Abstract: From a flounder pituitary cDNA library, cDNA clones encoding a 28-kDa glycoprotein produced by the pars intermedia of the pituitary were isolated and characterized. Nucleotide sequencing demonstrated a precursor of the 28-kDa protein, which consisted of 231 amino acid residues, to be cleaved into a signal peptide (24 amino acids) and a mature protein (207 amino acids) containing one N-glycosylation site. By comparison of amino acid sequences, the 28-kDa protein was found to be distantly and similarly related to growth hormone and prolactin. Consequently, it was named somatolactin. Somatolactin mRNAs were specifically expressed as 1.2 and 1.8 kb poly(A)+ RNAs in flounder pituitary.
188 citations
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TL;DR: It is proposed that in vivo exposure of PRL, under certain physiological conditions, may prime a pool of splenocytes to express IL-2 cell surface receptors, allowing these cells to be responsive to variations in local concentrations ofIL-2.
Abstract: A case for the involvement of PRL in the regulation of the immune system is strong. However, no mechanism by which PRL exerts this regulation has yet been identified. We studied the in vitro effects of PRL on splenocytes from ovariectomized (OVX) rats and discovered that PRL induced the formation of interleukin-2 (IL-2) cell surface receptors. However, PRL did not induce IL-2 secretion. This response, which was dependent on the concentration of PRL, also depended upon the estrogen status of the splenocyte donor; thus, splenocytes from OVX rats or rats in diestrus responded to PRL, whereas those from estrogen-treated OVX rats or rats in estrus did not. We propose that in vivo exposure of PRL, under certain physiological conditions, may prime a pool of splenocytes to express IL-2 cell surface receptors, allowing these cells to be responsive to variations in local concentrations of IL-2. (Endocrinology 126: 88–94,1990)
173 citations
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TL;DR: The significance of the stress-induced decrease of PRL does not appear to have a major consequence on the physiology of reproduction in the rat and it is suggested that future studies be directed towards its significance in the immune system.
166 citations
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TL;DR: In this paper, the involvement of PRL in maternal behavior using nonhypophysectomized ovariectomized rats treated concurrently (type I) or sequentially (type II) withprogesterone (P) and estradiol (E2) and administered either bromocriptine (to suppress endogenous PRL secretion) or bromociriptine plus ovine PRL.
Abstract: Recent findings indicate that PRL helps stimulate the onset of maternal behavior in inexperienced hypophysectomized steroid-treated female rats. In a series of five experiments we have further examined the involvement of PRL in maternal behavior using nonhypophysectomized ovariectomized rats treated concurrently (type I) or sequentially (type II) withprogesterone (P) and estradiol (E2) and administered either bromocriptine (to suppress endogenous PRL secretion) or bromocriptine plus ovine PRL. In Exp 1 plasma PRL concentrations were measured in ovariectomized rats treated for 2 weeks with a combination of E2 and P Silastic implants. Type I steroidtreated (2mm E2, days 1–24; three 30 mm P, days 3–13) rats exhibited elevated plasma PRL levels throughout the sampling period compared with nonsteroid-treated controls. In contrast, PRL concentrations in type II steroid-treated (P, days 3–13; E2, days 13–24) females were low (similar to controls) from days 3–13 when the type II steroid-treated females were expos...
165 citations
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TL;DR: The effects of age and gender on central nervous system (CNS) serotonergic responsivity were assessed with a neuroendocrine challenge test in 30 normal adults and the finding of greater prolactin release in women than in men probably reflects the effects of nonserotonergic modulatory influences at the level of the lactotroph.
163 citations
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TL;DR: Data show that long term restricted feeding affects anterior pituitary function in adult ewes, presumably reflecting alterations in the secretion of hypothalamic releasing and inhibiting factors.
Abstract: The effects of long term restricted feeding on the synthesis, storage, and release of GH, LH, FSH, and PRL were examined in adult ovariectomized ewes. Two groups of six ewes were fed a diet of either 1000 g/day (normal feeding) or 400–600 g/day (restricted feeding) hay for 20 weeks. Restricted feeding increased mean plasma GH concentrations and the amplitude of GH pulses, but did not affect GH pulse frequency. In contrast, mean plasma LH and FSH concentrations and LH pulse frequency were decreased by restricted feeding. Mean plasma PRL concentrations were unaffected by treatment. The levels of mRNA for GH in pituitary cytosol were increased by restricted feeding, but no changes were seen in mRNA levels of α-subunit, LHβ, FSHβ, or PRL. The pituitary contents of hormones measured did not change with the level of feeding. In conclusion, these data show that long term restricted feeding affects anterior pituitary function in adult ewes, presumably reflecting alterations in the secretion of hypothalamic releas...
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TL;DR: A role for neuropeptides of the posterior lobe in the control of lactotroph function is suggested and ET-3 in log doses did not alter significantly the release of luteinizing hormone, growth hormone or thyroid stimulating hormone.
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TL;DR: Results demonstrate that GH cells have both Ca2(+)-sensitive and -insensitive PKCs and PDBu-Rs and that both populations are regulated by agonists that control prolactin synthesis and secretion by these cells.
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TL;DR: The results showed that, in premenopausal women, a high intake of saturated fats was associated with a high prolactin concentration, which supports the concept that parity, menstrual status, and saturated fat consumption influence a woman's exposure to Prolactin and therefore the risk of developing breast cancer.
Abstract: A study of 424 women was undertaken to determine whether there was an association between serum prolactin levels and breast cancer; whether prolactin levels would reflect degrees of risk of developing breast cancer; and whether associations between known risk factors for breast cancer and serum prolactin concentrations could be demonstrated. Prolactin levels higher than the median value in control subjects were found to be associated with a more than two-fold increase in the risk of breast cancer (relative risk, 2.1; confidence interval [CI], 1.0-4.5). Moreover, a relative risk of 1.7 (CI, 0.9-3.3) for a group of women with benign epithelial hyperplasia (high risk of developing breast cancer), and a relative risk of 1.0 (CI, 0.6-1.8) for a group with benign fibrocystic disease (low risk of developing breast cancer), provided supportive evidence that prolactin plays a role in the development of breast cancer. A considerable fall in the concentration of prolactin at menopause was noted, so those women who have an early menopause have a reduced period of exposure to high concentrations of prolactin. Similarly, there was a considerable reduction in prolactin concentration after the first pregnancy. Finally, our results showed that, in premenopausal women, a high intake of saturated fats was associated with a high prolactin concentration. Our study supports the concept that parity, menstrual status, and saturated fat consumption influence a woman's exposure to prolactin and therefore the risk of developing breast cancer.
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TL;DR: The data suggest that oxytocin acts directly on the CNS to alter behavior toward pups and that prolactin may not play a role in the maternal behavior of the house mouse.
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TL;DR: It is suggested that IL-1 induced the release of IL-6 from rat pituitary, and that the released IL- 6 stimulated the secretions of FSH, LH and PRL.
Abstract: The abilities of recombinant human interleukin 1 (IL-1) and IL-6 to induce release of FSH, LH and PRL from rat pituitary cells in vitro were examined. IL-1 and IL-6 induced significant releases of FSH, LH and PRL within 3 h. The extents of release of these compounds induced by IL-1 and IL-6 were similar to those induced by GnRH and TRH. Rat anterior pituitary cells released IL-6 spontaneously, and its release was enhanced by IL-1 beta. This effect of IL-1 beta was inhibited significantly by a rabbit anti-IL-1 beta antiserum. These findings suggest that IL-1 induced the release of IL-6 from rat pituitary, and that the released IL-6 stimulated the secretions of FSH, LH and PRL.
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TL;DR: Basal as well as stimulated oxytocin levels obtained 4 days and 3‐4 months post partum correlated significantly, indicating that each woman has an individual, characteristic level of this hormone.
Abstract: The aim of the present study was to examine suckling-related plasma levels of oxytocin and prolactin in early and established lactation and to correlate hormone profiles to success of lactation performance. Fifty-five primiparous women participated in the study. From each, 18 blood samples were drawn in connection with breast-feeding on day 4 post partum and after 3-4 months. Oxytocin and prolactin levels were determined with radio-immunoassay. Basal levels of both hormones were significantly higher 4 days post partum than 3-4 months later and after weaning. Basal prolactin levels fell significantly within 24 h of weaning. Oxytocin and prolactin levels rose in response to breast-feeding--an effect which persisted during the lactation period. The suckling-induced release of prolactin--but not that of oxytocin--was related to basal hormone levels. Basal as well as stimulated oxytocin levels obtained 4 days and 3-4 months post partum correlated significantly, indicating that each woman has an individual, characteristic level of this hormone. Milk yield did not correlate with oxytocin or prolactin levels, but prolactin levels recorded 3-4 months post partum did correlate with the remaining period of breast-feeding. In addition, mothers who breast-fed exclusively 3-4 months post partum had significantly higher oxytocin and prolactin levels than those who gave supplementary feed. There was a significant correlation between oxytocin levels at 4 days and birth weight of the infant.
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TL;DR: Results identify IFN-gamma as one of the inflammatory cytokines that, like IL-1, TNF-alpha, and IL-6, have the potential to regulate pituitary function.
Abstract: Preincubation of rat anterior pituitary (AP) cells with homologous interferon-γ (IFN-γ) caused a dose-dependent inhibition of ACTH secretion stimulated by CRF. The effect was seen in both monolayer and aggregate AP cell cultures and was not due to cytotoxicity. In monolayer cultures IFN-γ also inhibited PRL and GH release stimulated by various hypothalamic releasing factors. IFN-γ did not affect the time kinetics of the ACTH response to CRF. The dose needed for half-maximal inhibition amounted to approximately 1 (antiviral) U/ml. The effect of IFN-γ was abrogated by an IFN-γ-neutralizing monoclonal antibody. Furthermore, ACTH secretion by the AP cells was not affected by the anti-IFN-γ antibody added alone, indicating that in the culture system no endogenous IFN-γ is operational in regulating the ACTH response studied. Of the other cytokines tested [interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-α/β (IFN-α/β)] only TNF-α and IL-6 were found to inhibit CRF-stimu...
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TL;DR: Prolactin may regulate Nb2 T cell-proliferative responses by modulating the transcriptional induction of various growth-related genes through transcriptional response to prolactin in cultured T cells.
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TL;DR: Data from animal studies suggest that the ability of azapirones to decrease body temperature and increase corticotropin and corticosterone is mediated by stimulation of presynaptic and postsynaptic serotonin (5‐hydroxytryptamine, 5‐HT) type1A subtype receptors, respectively.
Abstract: In healthy volunteers, the azapirones--buspirone, ipsapirone, and gepirone--increase plasma cortisol and decrease body temperature; buspirone and gepirone also increase plasma prolactin and growth hormone. Data from animal studies suggest that the ability of azapirones to decrease body temperature and increase corticotropin and corticosterone is mediated by stimulation of presynaptic and postsynaptic serotonin (5-hydroxytryptamine, 5-HT) type 1A subtype receptors, respectively. The mechanism of altered growth hormone and prolactin secretion is less clear. While animal studies implicate changes in dopamine function, current human investigations suggest that 5-HT1A receptors also may be involved in these endocrine responses. Further investigations, using more selective 5-HT receptor antagonists, will be required to resolve this issue.
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TL;DR: The abnormal baseline findings are consistent with increased central noradrenergic activity in depression and indicate the necessity of accounting for these baseline effects when investigating hormonal responses to the putative serotonergic challenges.
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TL;DR: Four kinds of cultured clonal cell line were established from estrogen-induced mammotropic pituitary tumor and among these newly established cell lines, MtT/Se was the smallest in size and showed estrogen-dependent proliferation and the many small secretory-like granules present in the cytoplasm of MtT-Se cells showed no immunocytochemically positive reaction for anterior pituitarian hormone.
Abstract: Four kinds of cultured clonal cell line were established from estrogen-induced mammotropic pituitary tumor. These clones showed differences of hormone secretion, morphology, and response to estrogen. One clone tentatively designated MtT/E, consisted of spindle-shaped epithelial cells and showed the strongest adhesion to the culture dish, but did not secrete any pituitary hormone. The second cell line, designated MtT/S, secreted only GH, showed very weak contact with the culture dish, and proliferated almost anchorage independently. The MtT/S cells were mainly spherical and formed floating or weakly adherent clusters. Some of them had very long dendriteor neurite-like cell processes. Electron microscopic examination of the MtT/S cells showed a normal somatotrope-like appearance, i.e. the presence in the cytoplasm of many GH-containing secretory granules, well developed rough endoplasmic reticulum, and Golgi apparatus. Furthermore, these cells secreted GH in response to stimulation with GRF. The third cell ...
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TL;DR: It is concluded that prolactin is the main luteotrophic factor in the cyclic dog during the second half of the luteal period.
Abstract: The role of prolactin and LH in the control of the function of the corpus luteum in the dog was studied. Experiments were performed to interfere with the secretion of a) prolactin by administering a dopamine agonist and b) LH by desensitisation with a long-acting LHRH and by stimulation. Treatments with prolactin-lowering dosages of bromocriptine, (20 micrograms/kg body weight twice a day, orally; n = 8) which started between day 1-5 (n = 4) and day 20-24 (n = 4) of the luteal period resulted in a similar pattern of progesterone, concentration in peripheral blood in both groups. The progesterone release in the second half of the luteal period (13.1 +/- 1.8% (sem) of the progesterone release of the total luteal period) was significantly lower than in control dogs (24.7 +/- 2.2%). Treatment at about day 30 of the luteal period with LHRH CR (1.34 mg, intramuscularly; n = 3), which significantly suppressed the LH level, did not reduce the progesterone release in the second half of the luteal period, 21.3 +/- 4.7% compared to 24.7 +/- 2.2% in the control dogs. The endogenous LH peak resulting from treatment with LHRH had no effect on the progesterone concentration in the blood. It is concluded that prolactin is the main luteotrophic factor in the cyclic dog during the second half of the luteal period.
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TL;DR: The results are consistent with the hypothesis of dopaminergic overactivity in schizophrenia, which might be caused by altered amino acid precursor availability and could be related to the decrease in melatonin and reduction in thyroid hormone levels.
Abstract: Basal serum amino acids (including central monoamine precursors), central monoamines, and hormones were studied in schizophrenic patients (drug-naive; n = 20; drug-withdrawn for 3 or more days, n = 67; neuroleptic-treated, n = 23) and healthy subjects (n = 90) to answer the following questions: (1) Do neuroleptic-withdrawn and neuroleptic-naive patients differ on these serum measures? (2) What are the effects of neuroleptic treatment on these measures? (3) On which variables do drug-free and neuroleptic-treated patients differ? Because serum amino acid, central monoamine, and hormone levels were similar in drug-naive and drug-withdrawn patients, data from these groups ("drug-free") were combined and compared to those of healthy subjects and neuroleptic-treated patients. Asparagine, citrulline, phenylalanine, and cysteine were higher, while tyrosine, tryptophan, and the ratio of tryptophan to competing amino acids were significantly lower in drug-free schizophrenic patients than in healthy subjects. Dopamine was increased, and melatonin and thyroid hormones were decreased in drug-free schizophrenic patients compared to healthy subjects. Norepinephrine, epinephrine, and prolactin were higher in neuroleptic-treated men compared to drug-free male patients or healthy men. These results are consistent with the hypothesis of dopaminergic overactivity in schizophrenia, which might be caused by altered amino acid precursor availability and could be related to the decrease in melatonin and reduction in thyroid hormone levels.
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TL;DR: The results are consistent with the hypothesis that nicotine inactivates nicotinic cholinergic receptors in brain by an allosteric mechanism, and that prolonged inactivation of nicotinilcholine receptors leads to their increased number.
Abstract: The effects of chronic injections of nicotine on nicotine-induced prolactin release in the rat were measured and compared to the effects of this treatment on [3H]acetylcholine binding to nicotinic cholinergic sites in the hypothalamus. Treatment with nicotine for 10 days (s.c. injections twice daily) abolished prolactin release in response to an acute i.v. injection of nicotine given 2, 6 or 8 days after the last of the chronic injections of nicotine. At each of these time points, the binding of [3H]acetylcholine in the hypothalamus from rats treated chronically with nicotine was significantly higher than in the hypothalamus from control rats. By 14 days after the last chronic injection of nicotine, the prolactin response to an acute injection of nicotine was restored. Coinciding with the return of the nicotine-induced prolactin response, the binding of [3H]acetylcholine had returned to control values. These results are consistent with the hypothesis that nicotine inactivates nicotinic cholinergic receptors in brain by an allosteric mechanism, and that prolonged inactivation of nicotinic cholinergic receptors leads to their increased number.
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TL;DR: The number of drugs which suppress prolactin by acting on pituitary D2 receptors, and which are useful in the treatment of hyperprolactinemia, continues to increase and parenteral application appears to be a logical solution to the problem of the high first-pass effect.
Abstract: 1. Prolactin is a 21,500 Dalton single-chain polypeptide hormone but may occur in 50 kDa and 150 kDa molecular variants. 2. These large PRL variants may be secreted predominantly; this condition is termed "macroprolactinemia". It is characterized by high immunological and normal biological serum levels of prolactin, and lack of clinical symptoms of hyperprolactinemia. 3. The information on PRL is encoded on chromosome 6. Transcription can be enhanced and suppressed by a variety of hormonal factors. 4. PRL is secreted in a pulsatile fashion; it displays a circadian rhythm (with a maximum during sleep) and is stimulated by some amino acids. PRL also responds to mechanical stimulation of the breast. 5. PRL rises during pregnancy, and maintainance of hyperprolactinemia (and, thereby, physiological infertility) is dependent on the frequency and duration of breast feedings. 6. Hypothalamic regulation of prolactin mainly involves tonic inhibition via portal dopamine. The physiological importance of various stimulating factors present in the hypothalamus is still incompletely understood. In particular, there is still no place for TRH in PRL physiology. 7. PRL is released in response to stress; this response may be mediated by opioids. The low-estrogen, low-gonadotropin amenorrhea of endurance-training women is not mediated by prolactin, however. 8. Estrogens stimulate PRL gene transcription via at least two independent mechanisms. There are many clinical examples of this estrogen effect on prolactin serum levels, and also on the growth of prolactinomas. 9. Mild hyperprolactinemia remains an enigma which cannot satisfactorily be resolved by biochemical or radiological testing. The border between "normal" and "elevated" prolactin is ill-defined. The possibility of macroprolactinemia complicates this matter even further. 10. The number of drugs which suppress prolactin by acting on pituitary D2 receptors, and which are useful in the treatment of hyperprolactinemia, continues to increase. In the field of ergot alkaloids, parenteral application appears to be a logical solution to the problem of the high first-pass effect; in addition, this form of treatment is frequently better tolerated than the oral route. 11. Prolactinoma development is presently being studied employing molecular biological techniques; the question of whether tumorigenesis can be attributed to specific defects of gene regulation remains to be answered.
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TL;DR: A rapidly expanding body of evidence indicates that cytokines do indeed regulate pituitary hormone secretion, and the dominant route of this modulation appears to be via the brain and hypothalamus, although a role for direct effects on the pituitsary has not been excluded.
Abstract: A rapidly expanding body of evidence indicates that cytokines do indeed regulate pituitary hormone secretion. Recent studies with cytokines in vivo and in vitro support the idea that cytokines are the principal mediators of the neuroendocrine responses previously observed in infectious and inflammatory states. The dominant route of this modulation appears to be via the brain and hypothalamus, although a role for direct effects on the pituitary has not been excluded. These effects may be mediated by circulating cytokines, endogenously produced cytokines, or both. A number of receptor systems and second messengers may be involved, and a role for arachidonate metabolite pathways appears particularly likely. A final question: Of what use to the organism is the ability of immune activation to control pituitary hormone secretion? For some pituitary secretions there is a reasonable basis for speculation. Glucocorticoids serve to limit the severity of immune responses and recent studies argue that defects in this pathway permit the expression of autoimmune disease. Inhibition of thyroid function may limit the catabolic side effects of infectious illness. Stimulation of growth hormone could have the same effect, and growth hormone and prolactin may serve to enhance some immune responses.
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TL;DR: The roles of OT, VIP, and 5-HT in controlling the N and D surges of PRL in ovariectomized (OVX) rats receiving a physiological dopamine-lowering stimulus, copulomimetic stimulation are investigated.
Abstract: In female rats the mating stimulus induces a bimodal pattern of PRL secretion. A surge of PRL occurs at approximately 0300 h, called the nocturnal surge (N). Another surge occurs at 1700 h on the same day, called the diurnal surge (D). By lowering dopaminergic tone pharmacologically, we have recently demonstrated the existence of an endogenous rhythm stimulatory to PRL secretion in female rats. The periods of this stimulatory influence coincide with the periods of the N and D surges of PRL that occur in mated rats. In addition, we have shown that the 0300 h component of this endogenous rhythm is regulated by oxytocin (OT) and vasoactive intestinal peptide (VIP), and the 1700 h component is regulated by OT and serotonin (5-HT). In this study, we investigated the roles of OT, VIP, and 5-HT in controlling the N and D surges of PRL in ovariectomized (OVX) rats receiving a physiological dopaminelowering stimulus, copulomimetic stimulation. Blood samples were obtained the day before the experiments between 1700...
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TL;DR: The data suggest that enhanced noradrenergic activity of the locus coeruleus stimulates alpha and/or beta adrenergic receptors in depressed patients during SD and this mechanism could well be involved in the antidepressant effect of this therapy.
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TL;DR: What is known about the molecular heterogeneity of the pituitary hormones prolactin and growth hormone is summarized and the implications for clinical biochemists are discussed.
Abstract: The pituitary hormones prolactin and growth hormone are related single-chain polypeptides. Both hormones exist in the circulation in several molecular forms, and this heterogeneity may account for some of the complex and sometimes contradictory actions, in vivo and in vitro, of both hormones. It may also lead to problems with quantitation by immunoassays and discrepancies between the results given by assays using different antibodies. Modified forms of the hormones may have markedly different activity in bioassays from that of the parent hormone, but the clinical significance of this is unclear. In this review we summarize what is known about the molecular heterogeneity of the hormones and briefly discuss the implications for clinical biochemists.