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1
Meeran, Dawud, Henryk F. Urbanski, Susan J. Gregory, Julie Townsend, and Domingo J. Tortonese. "Developmental Changes in the Hormonal Identity of Gonadotroph Cells in the Rhesus Monkey Pituitary Gland." Journal of Clinical Endocrinology & Metabolism 88, no. 6 (June 1, 2003): 2934–42. http://dx.doi.org/10.1210/jc.2002-021001.
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To help elucidate the regulatory mechanism responsible for divergent gonadotrophin secretion during sexual maturation, we examined the gonadotroph population and hormonal identity of gonadotroph subtypes in pituitary glands of juvenile (age, 1.7 ± 0.2 yr) and adult (age, 12.3 ± 0.8 yr) male rhesus monkeys (Macacca mulatta). Serum LH and testosterone concentrations were, respectively, 3 and 7 times lower in juveniles than in adults, thus confirming the different stages of development. Immunohistochemistry revealed that the proportion of LH gonadotrophs in relation to the total pituitary cell population in the juvenile animals was significantly smaller than in the adults. In a subsequent study, double immunofluorescent labeling identified three distinct gonadotroph subtypes in both age groups: ones expressing either LH or FSH and another one expressing a combination of both gonadotrophins. Whereas the number of monohormonal LH cells per unit area was greater in the adults than in the juveniles, the number of monohormonal FSH gonadotrophs was remarkably lower. However, the proportion of FSH cells (whether mono- or bihormonal) within the gonadotroph population was similar between groups. Interestingly, the proportion and number of bihormonal gonadotrophs as well as the LH/FSH gonadotroph ratio were significantly greater in the adults than in the juveniles. Taken together, these data reveal that during the juvenile-adult transition period, not only does the pituitary gonadotroph population increase, but a large number of monohormonal FSH gonadotrophs are likely to become bihormonal. Because this morphological switch occurs when marked changes in plasma gonadotrophins are known to occur, it may represent an intrapituitary mechanism that differentially regulates gonadotrophin secretion during sexual development.
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Tortonese, Domingo J., Susan J. Gregory, Rebecca C. Eagle, Carolyne L. Sneddon, Claire L. Young, and Julie Townsend. "The equine hypophysis: a gland for all seasons." Reproduction, Fertility and Development 13, no. 8 (2001): 591. http://dx.doi.org/10.1071/rd01066.
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The intrahypophysial mechanisms involved in the control of gonadotrophin secretion remain unclear. In the horse, a divergent pattern of gonadotrophins is observed at different stages of the reproductive cycle in response to a single secretagogue (gonadotrophin-releasing hormone), and dramatic changes in fertility take place throughout the year in response to photoperiod. This species thus provides a useful model to investigate the regulation of fertility directly at the level of the hypophysis. A series of studies were undertaken to examine the cytological arrangements and heterogeneity of gonadotrophin storage in the pars distalis (PD) and pars tuberalis (PT) of the hypophysis of male and female horses. Specifically, the seasonal and gonadal effects on distribution, density and hormonal identity of gonadotrophs, the existence of gonadotroph–lactotroph associations and the expression of prolactin receptors (PRL-R) as possible morphological bases for the differential control of gonadotrophin secretion were investigated. It became apparent that both isolated and clustered gonadotrophs are normally distributed around the pars intermedia and surrounding capillaries in the PD, and in the caudal ventral region of the PT. In the PD, no effects of season or of reproductive state on the density or number of gonadotrophs could be detected in either male or female animals. In contrast, a fivefold increase in gonadotroph density was observed in the PT during the sexually active stage. In males, robust gonadal effects were detected on the gonadotroph population; orchidectomy significantly reduced both the number and proportion of gonadotrophs, in relation to other hypophysial cell types, in both the PD and PT regions. Luteinizing hormone (LH) monohormonal, follicle-stimulating hormone (FSH) monohormonal and bihormonal gonadotrophs were identified in the PD and PT of male and female horses. Interestingly, in males, the relative proportions of gonadotroph subtypes and the LH/FSH monohormonal gonadotroph ratio were not affected by either season or the presence of the gonads. In contrast, a larger proportion of monohormonal gonadotrophs was clearly observed in sexually active females. Specific gonadotroph–lactotroph associations and expression of PRL-R in cells other than gonadotrophs were detected in the PD throughout the annual reproductive cycle. In addition to a stimulatory gonadal effect on lactotroph density, a substantial gonadal-independent effect of season was apparent on this variable. The findings have revealed important seasonal and gonadal effects on the cytological configuration of the equine hypophysis, which may provide the morphological basis for the intrahypophysial control of fertility.
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Kereilwe, Onalenna, Kiran Pandey, Vitaliano Borromeo, and Hiroya Kadokawa. "Anti-Müllerian hormone receptor type 2 is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion." Reproduction, Fertility and Development 30, no. 9 (2018): 1192. http://dx.doi.org/10.1071/rd17377.
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Preantral and small antral follicles may secret anti-Müllerian hormone (AMH) to control gonadotrophin secretion from ruminant gonadotrophs. The present study investigated whether the main receptor for AMH, AMH receptor type 2 (AMHR2), is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion. Expression of AMHR2 mRNA was detected in anterior pituitaries (APs) of postpubertal heifers using reverse transcription–polymerase chain reaction. An anti-AMHR2 chicken antibody was developed against the extracellular region near the N-terminus of bovine AMHR2. Western blotting using this antibody detected the expression of AMHR2 protein in APs. Immunofluorescence microscopy using the same antibody visualised colocalisation of AMHR2 with gonadotrophin-releasing hormone (GnRH) receptor on the plasma membrane of gonadotrophs. AP cells were cultured for 3.5 days and then treated with increasing concentrations (0, 1, 10, 100, or 1000 pg mL−1) of AMH. AMH (10–1000 pg mL−1) stimulated (P < 0.05) basal FSH secretion. In addition, AMH (100–1000 pg mL−1) weakly stimulated (P < 0.05) basal LH secretion. AMH (100–1000 pg mL−1) inhibited GnRH-induced FSH secretion, but not GnRH-induced LH secretion, in AP cells. In conclusion, AMHR2 is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion.
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Einspanier, A., and J. K. Hodges. "LH- and chorionic gonadotrophin-stimulated progesterone release in vitro by intact luteal tissue of the marmoset monkey (Callithrix jacchus)." Journal of Endocrinology 141, no. 3 (June 1994): 403–9. http://dx.doi.org/10.1677/joe.0.1410403.
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Abstract The application of an in vitro microdialysis system (MDS) for studies on the gonadotrophic control of luteal progesterone secretion in the marmoset monkey is described. Luteal tissue collected from a total of six animals (9 ± 1 days after ovulation) was perfused with Ringer solution (without and with lipoprotein, 0·6 μg/ml). The tissue was exposed to repeated applications of human LH (hLH) and human chorionic gonadotrophin (hCG) (1, 10 and 100 IU/ml) each of 60 min duration. Perfusate was collected in 15-min fractions and assayed for progesterone content. Results showed that addition of lipoproteins to the Ringer solution had a marked effect on progesterone secretion in terms of maintaining stable baseline levels and improving reproducibility of gonadotrophin-induced responses. Progesterone secretion was significantly stimulated by both gonadotrophins at each dose tested. Maximal elevations were obtained with 10 IU/ml and there were no apparent differences in responses to hLH and hCG in terms of either magnitude or duration. This study indicates that MDS provides a useful in vitro approach for studying the gonadotrophic control of the corpus luteum in non-human primates. The results did not demonstrate disparate actions of hLH and hCG in their ability to stimulate luteal progesterone secretion. Journal of Endocrinology (1994) 141, 403–409
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Rulli, Susana B., and Ilpo Huhtaniemi. "What have gonadotrophin overexpressing transgenic mice taught us about gonadal function?" Reproduction 130, no. 3 (September 2005): 283–91. http://dx.doi.org/10.1530/rep.1.00661.
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The two gonadotrophins, follicle-stimulating hormone and luteinising hormone, are pivotal regulators of the development and maintenance of normal fertility by maintaining testicular and ovarian endocrine function and gametogenesis. Too low gonadotrophin secretion, i.e. hypogonadotrophic hypogonadism, is a common cause of infertility. But there are also physiological and pathophysiological conditions where gonadotrophin secretion and/or action are either transiently or chronically elevated, such as pregnancy, pituitary tumours, polycystic ovarian syndrome, activating gonadotrophin receptor mutations, perimenopause and menopause. These situations can be either the primary or secondary cause of infertility and gonadal pathologies in both sexes. Also the role of gonadotrophins as tumour promoters is possible. Recently, the possibility to combine information from genetically modified mice and human phenotypes in connection with mutations of gonadotrophin or gonadotrophin receptor genes has elucidated many less well known mechanisms involved in dysregulation of gonadotrophin function. Among the genetically modified mouse models, transgenic mice with gonadotrophin hypersecretion have been developed during the last few years. In this review, we describe the key findings on transgenic mouse models overexpressing gonadotrophins and present their possible implications in related human pathologies. In addition, we provide examples of genetic mouse models with secondary effects on gonadotrophin production and, consequently, on gonadal function.
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Matson, Christine, and B. T. Donovan. "Acute effects of GnRF-induced gonadotrophin secretion upon ovarian steroid secretion in the ferret." Acta Endocrinologica 111, no. 3 (March 1986): 373–77. http://dx.doi.org/10.1530/acta.0.1110373.
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Abstract. The effects of an increase in endogenous gonadotrophin secretion on the production of oestradiol, progesterone, androstenedione and testosterone by the ovaries of anaesthetized anoestrous and oestrous ferrets were followed. Gonadotrophin secretion was enhanced by the injection of gonadotrophin releasing factor (GnRF), and serial blood samples were collected over 9 h for hormone assay. Thyrotrophic hormone releasing factor (TRF) or acetic acid were injected for control purposes. The plasma content of oestradiol in oestrous females was significantly higher than during anoestrus, but secretion of this steroid was not increased by any means. The plasma concentration of progesterone in anoestrous females was significantly higher than during oestrus. It was increased by GnRF in anoestrous ferrets and less markedly in oestrous females. The plasma concentration of androstenedione was raised by GnRF to a greater extent during anoestrus than during oestrus. Testosterone was present in higher concentration in the plasma during anoestrus than during oestrus, and the level was increased by GnRF administration. These findings indicate that the ovaries of the anoestrous ferret secrete significant quantities of steroid hormones, and that they respond readily to gonadotrophic hormone.
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Daniels, M., P. Newland, J. Dunn, P. Kendall-Taylor, and M. C. White. "Long-term effects of a gonadotrophin-releasing hormone agonist ([d-Ser(But)6]GnRH(1–9)nonapeptide-ethylamide) on gonadotrophin secretion from human pituitary gonadotroph cell adenomas in vitro." Journal of Endocrinology 118, no. 3 (September 1988): 491–96. http://dx.doi.org/10.1677/joe.0.1180491.
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ABSTRACT We have studied the effects of TRH and native gonadotrophin-releasing hormone (GnRH), and of a GnRH agonist (Buserelin; [d-Ser(But)6]GnRH(1–9) nonapeptide-ethylamide), on LH, FSH, α subunit and LH-β subunit secretion from three human gonadotrophin-secreting pituitary adenomas in dispersed cell culture. During a 24 h study, treatment with 276 nmol TRH/1 resulted in a significant (P < 0·05) stimulated release of FSH and α subunit from all three adenomas, and LH from the two adenomas secreting detectable concentrations of this glycoprotein; treatment with 85 nmol GnRH/l significantly (P < 0·05) stimulated the release of α subunit from all three, but FSH from only two and LH from only one adenoma. During a long-term 28-day study, basal FSH and α subunit concentrations were maintained, but secretion of LH, and LH-β (detectable from one tumour only), declined with time from two of the three adenomas. Addition of Buserelin to the cultures resulted in the continuous (P < 0·05) stimulation of α subunit secretion from all three adenomas, and of LH and FSH from two, whilst a transient stimulatory effect on LH and FSH secretion was seen from a third adenoma, with subsequent secretion rates declining towards control values. These data show that human gonadotrophin-secreting adenomas demonstrate variable stimulatory responses to hypothalamic TRH and GnRH, and that during chronic treatment with a GnRH agonist the anticipated desensitizing effect of the drug was not observed in two out of three adenomas studied. The mechanism for this is not clear, but such drugs are unlikely to be of therapeutic value in the management of gonadotrophin-secreting tumours. The data also suggest that GnRH and GnRH agonists have a differential effect on the in-vitro release of intact gonadotrophins and the common α subunit. J. Endocr. (1988) 118, 491–496
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Hanson, P. L., S. J. B. Aylwin, J. P. Monson, and J. M. Burrin. "FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas." European Journal of Endocrinology 152, no. 3 (March 2005): 363–70. http://dx.doi.org/10.1530/eje.1.01854.
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Objective: Non-functioning pituitary adenomas (NFPAs) are characterised by the lack of symptoms of hormone hypersecretory syndromes but in vitro studies have demonstrated that tumour cells may stain for gonadotrophins and/or their α- or β-subunits. In this study, we aimed to examine the pattern of secretion of LH and FSH from a series of pituitary adenomas cultured in vitro and where data were available to relate the results to pre-operative serum gonadotrophin levels. Methods: The in vitro secretion of LH and FSH was measured from 46 cultured NFPAs and compared with pre-operative serum gonadotrophin levels in 38 patients. Peritumorous ‘normal’ pituitary cell cultures from 20 additional pituitary tumour patients were used for comparison with the NFPA group. Results: A median pre-operative LH:FSH ratio of 0.33:1 was found in 38 patients with NFPAs. Preferential secretion of FSH was also documented from media of 46 NFPAs cultured in vitro with a median LH:FSH ratio of 0.32:1. A significant correlation (r = 0.43, P < 0.01) was observed between serum and media levels of FSH but not LH. Peritumorous ‘normal’ pituitary cells released LH and FSH in a reversed ratio (median LH:FSH ratio = 3.6:1, P < 0.01 compared with NFPAs). Conclusions: This study has evaluated pre-operative serum gonadotrophin levels and in vitro release of hormones in cultures of surgically removed tissue from patients with NFPAs. The data suggest preferential secretion of FSH occurs both in vitro and in vivo. By demonstrating that NFPAs cultured in vitro reflect the in vivo situation of preferential secretion of FSH, it may be possible in future to perform functional studies using this system to elucidate the cellular and molecular mechanisms involved in the development of an imbalance in gonadotroph cells preferentially overproducing FSH in NFPAs.
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Thomas, G. B., A. S. McNeilly, F. Gibson, and A. N. Brooks. "Effects of pituitary-gonadal suppression with a gonadotrophin-releasing hormone agonist on fetal gonadotrophin secretion, fetal gonadal development and maternal steroid secretion in the sheep." Journal of Endocrinology 141, no. 2 (May 1994): 317–24. http://dx.doi.org/10.1677/joe.0.1410317.
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Abstract In order to investigate the regulation of the hypothalamo-pituitary-gonadal axis during fetal development, sheep fetuses at day 70 of gestation were implanted subcutaneously with a biodegradable implant containing the longacting gonadotrophin-releasing hormone (GnRH) agonist, buserelin. The treatment of fetuses with a GnRH agonist throughout the last half of gestation (term=145 days) abolished the increase in plasma LH concentrations that was seen in 2-day-old control lambs in response to an injection of GnRH. This attenuated response was associated with corresponding reductions in the pituitary content of LH and FSH. Immunolocalization studies revealed that pituitary glands from newborn lambs implanted with a GnRH agonist during fetal development were devoid of immunopositive LH- and FSH-containing cells. At birth the testicular weights of GnRH agonist-treated ram lambs were significantly decreased by 40% when compared with controls. This was associated with a 45% reduction in the total number of Sertoli cells per testis. In newborn ewe lambs GnRH agonist treatment had no effect on ovarian weight or on the morphological appearance of the ovaries. GnRH agonist treatment had no effect on the plasma concentrations of progesterone and oestrone in the maternal circulation or on the length of gestation. These results show (1) that GnRH positively regulates the synthesis and secretion of gonadotrophins in the fetus, (2) that reduced fetal gonadotrophic support during the last half of gestation results in a reduction in testicular growth, and (3) that fetal gonadotrophins do not affect maternal steroid secretion. Journal of Endocrinology (1994) 141, 317–324
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Antonio, Leen, Maarten Albersen, Jaak Billen, Geert Maleux, Anne-Sophie Van Rompuy, Peter Coremans, Philippe Marcq, Niels Jørgensen, and Dirk Vanderschueren. "Testicular Vein Sampling Can Reveal Gonadotropin-Independent Unilateral Steroidogenesis Supporting Spermatogenesis." Journal of the Endocrine Society 3, no. 10 (July 30, 2019): 1881–86. http://dx.doi.org/10.1210/js.2019-00180.
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Abstract Suppressed gonadotropins combined with high-normal serum testosterone concentrations in oligozoospermic men suggest either use of exogenous testosterone or presence of a testosterone-producing tumor. We describe the case of a 31-year-old man referred for primary infertility. Gonadotropins were undetectably low, but testosterone and estradiol were in the high-normal range. Semen analysis showed oligoasthenospermia. He denied using exogenous testosterone. Scrotal ultrasound showed microlithiasis and millimetric hypolucent lesions in the left testis but no intratesticular mass. Human chorionic gonadotropin was low. To investigate unilateral hormone secretion, selective testicular venous sampling was performed. Testosterone and estradiol were clearly higher on the left side than on the right (130 vs 26 nmol/L and 1388 vs 62 pmol/L, respectively), with a left spermatic vein–to-periphery gradient of 4.3 for testosterone and 13 for estradiol; there were no similar gradients on the right side. This finding confirms that all sex steroid secretion came from the left testis. The patient was therefore referred for left orchidectomy. Histopathology revealed multifocal seminoma, germ cell neoplasia in situ, and Leydig cell hyperplasia but no choriocarcinoma. However, gonadotrophin levels increased after orchidectomy, indicating that the source of gonadotropin-independent sex steroid secretion was removed. Testosterone and estradiol decreased to the mid-normal range. Sperm concentration improved. This report thus shows that endogenous testosterone secretion in one testicle supports spermatogenesis without measurable levels of gonadotropins. Selective testicular venous sampling is useful to identify the site of unilateral secretion when the clinical picture is inconclusive. However, histopathology could not reveal the factor that stimulated Leydig cell steroidogenesis.
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Kereilwe, Onalenna, and Hiroya Kadokawa. "Bovine gonadotrophs express anti-Müllerian hormone (AMH): comparison of AMH mRNA and protein expression levels between old Holsteins and young and old Japanese Black females." Reproduction, Fertility and Development 31, no. 4 (2019): 810. http://dx.doi.org/10.1071/rd18341.
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Anti-Müllerian hormone (AMH) is secreted from ovaries and stimulates gonadotrophin secretion from bovine gonadotroph cells. Other important hormones for endocrinological gonadotroph regulation (e.g. gonadotrophin-releasing hormone, inhibin and activin) have paracrine and autocrine roles. Therefore, in this study, AMH expression in bovine gonadotroph cells and the relationships between AMH expression in the bovine anterior pituitary (AP) and oestrous stage, age and breed were evaluated. AMH mRNA expression was detected in APs of postpubertal heifers (26 months old) by reverse transcription-polymerase chain reaction. Based on western blotting using an antibody to mature C-terminal AMH, AMH protein expression was detected in APs. Immunofluorescence microscopy utilising the same antibody indicated that AMH is expressed in gonadotrophs. The expression of AMH mRNA and protein in APs did not differ between oestrous phases (P>0.1). We compared expression levels between old Holsteins (79.2±10.3 months old) and young (25.9±0.6 months old) and old Japanese Black females (89.7±20.3 months old). The APs of old Holsteins exhibited lower AMH mRNA levels (P<0.05) but higher AMH protein levels than those of young Japanese Black females (P<0.05). In conclusion, bovine gonadotrophs express AMH and this AMH expression may be breed-dependent.
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Miller, D. W., and A. N. Brooks. "Placental steroids are involved in the late-gestation decrease in gonadotrophin secretion in the ovine fetus." Proceedings of the British Society of Animal Science 1999 (1999): 66. http://dx.doi.org/10.1017/s1752756200002210.
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The mid-gestation peak in activity of the fetal gonadotrophic axis is thought to be crucial for normal reproductive development. It is clear that the increase to mid-gestation is a result of the concomitant rise in gonadotrophs (Thomas et al., 1993). The mechanisms responsible for the decrease after mid-gestation are unclear, but may involve feedback from the placental steroids (Challis et al., 1981; Gluckman et al., 1983). The aim was to determine the roles of the placental steroids, progesterone and oestradiol, in the late-gestation decline in fetal gonadotrophins using the oestradiol antagonist ICI 182,780 and the progesterone antagonist RU486.
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Johnson, M. S., R. Mitchell, and G. Fink. "The role of protein kinase C in LHRH-induced LH and FSH release and LHRH self-priming in rat anterior pituitary glands in vitro." Journal of Endocrinology 116, no. 2 (February 1988): 231–39. http://dx.doi.org/10.1677/joe.0.1160231.
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ABSTRACT We have investigated the role of protein kinase C (PKC) in LHRH-induced LH and FSH secretion and LHRH priming. Hemipituitary glands from pro-oestrous rats were incubated with agents known to affect PKC and with or without LHRH, during which time the secretion of gonadotrophins was measured. Phorbol esters and phospholipase C, activators of PKC, released LH and FSH in a concentration-dependent manner and potentiated the LHRH-induced secretion of gonadotrophins in parallel with their ability to release these hormones alone. Inhibitors of PKC had either no effect on LH release (1-(5-isoquinolinesulphonyl)-2-methylpiperazine hydrochloride) or they augmented LHRH-induced gonadotrophin release (polymyxin B and 8-(N,N-diethylamino) octyl-3,4,5-trimethoxybenzoate). Neither the activators nor the inhibitors of PKC, when present with LHRH, caused any change in LHRH priming, even though the activators alone produced a release of gonadotrophins that showed a temporal pattern similar to that produced by LHRH priming. The profiles of effects on LH and FSH secretion were always qualitatively similar. These results show that PKC may be involved in general regulation of gonadotrophin release but that it is not important in acute responses to LHRH nor in LHRH self-priming. J. Endocr. (1988) 116, 231–239
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Nangalama, A. W., and G. P. Moberg. "Interaction between cortisol and arachidonic acid on the secretion of LH from ovine pituitary tissue." Journal of Endocrinology 131, no. 1 (October 1991): 87–94. http://dx.doi.org/10.1677/joe.0.1310087.
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ABSTRACT In several species, glucocorticoids act directly on the pituitary gonadotroph to suppress the gonadotrophin-releasing hormone (GnRH)-induced secretion of the gonadotrophins, especially LH. A mechanism for this action of these adrenal steroids has not been established, but it appears that the glucocorticoids influence LH release by acting on one or more post-receptor sites. This study investigated whether glucocorticoids disrupt GnRH-induced LH release by altering the liberation of arachidonic acid from plasma membrane phospholipids, a component of GnRH-induced LH release. Using perifused ovine pituitary tissue, it was established that exposure of gonadotrophs to 1–1000 nmol cortisol/l for 4 h or longer significantly reduced GnRH-stimulated LH release with the maximal inhibitory effect being observed after 6 h of exposure to cortisol. This suppressive effect of cortisol could be reversed by administration of arachidonic acid, which in its own right could stimulate LH release from ovine pituitary tissue. Furthermore, the inhibitory effect of cortisol on GnRH-stimulated LH release could be directly correlated with decreased pituitary responsiveness to GnRH-stimulated arachidonic acid liberation, consistent with our hypothesis that glucocorticoids can suppress GnRH-induced secretion of LH by reducing the amount of arachidonic acid available for the exocytotic response of GnRH. Journal of Endocrinology (1991) 131, 87–94
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Ludwig, K. "Molecular mechanisms of gonadotrophin releasing hormone-stimulated gonadotrophin secretion." Human Reproduction 8, suppl 2 (November 1, 1993): 23–28. http://dx.doi.org/10.1093/humrep/8.suppl_2.23.
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Anderson, L. "Intracellular mechanisms triggering gonadotrophin secretion." Reviews of Reproduction 1, no. 3 (September 1, 1996): 193–202. http://dx.doi.org/10.1530/revreprod/1.3.193.
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Anderson, L. "Intracellular mechanisms triggering gonadotrophin secretion." Reviews of Reproduction 1, no. 3 (September 1, 1996): 193–202. http://dx.doi.org/10.1530/ror.0.0010193.
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Tsatsoulla, A., S. M. Shalet, and W. R. Robertson. "Bioactive gonadotrophin secretion in man." Clinical Endocrinology 35, no. 3 (September 1991): 193–206. http://dx.doi.org/10.1111/j.1365-2265.1991.tb03522.x.
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Khurshid, S., G. F. Weinbauer, and E. Nieschlag. "Effects of administration of testosterone and gonadotrophin-releasing hormone (GnRH) antagonist on basal and GnRH-stimulated gonadotrophin secretion in orchidectomized monkeys." Journal of Endocrinology 129, no. 3 (June 1991): 363–70. http://dx.doi.org/10.1677/joe.0.1290363.
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ABSTRACT The aim of the present investigation was to investigate the effects of testosterone on basal and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin secretion in the presence and absence of a GnRH antagonist in a non-human primate model (Macaca fascicularis). Orchidectomized animals were used in order to avoid interference by testicular products other than testosterone involved in gonadotrophin feedback. Concomitant and delayed administration of testosterone at doses that provided serum levels either within the intact range (study 1) or markedly above that range (study 2) did not influence the suppression of basal gonadotrophin release induced by the GnRH antagonist during a 15-day period. To assess the possible effects of testosterone treatment at the pituitary level (study 3) GnRH stimulation tests (500 μg) were performed before and on days 8 and 15 of treatment with high-dose testosterone and GnRH antagonist alone or in combination. Testosterone alone abolished the gonadotrophin responses to exogenous GnRH observed under pretreatment conditions. With GnRH antagonist alone, an increased responsiveness (P <0·05) to GnRH was seen on day 8 and a similar response compared with pretreatment on day 15. Following combined treatment with GnRH antagonist and testosterone, GnRH-induced gonadotrophin secretion was consistently lower compared with that after GnRH antagonist alone (P <0·05), but was increased compared with that after testosterone alone (P<0·05). Thus, in the presence of a GnRH antagonist the feedback action of testosterone on LH and FSH was diminished. The present work in GnRH antagonist-treated orchidectomized monkeys demonstrates that (I) unlike in rats, testosterone fails to stimulate FSH secretion selectively, (II) the negative feedback action of testosterone on GnRH-stimulated LH and FSH secretion is altered in the presence of a GnRH antagonist and (III) GnRH antagonists induce a transient period of increased responsiveness of gonadotrophic hormone release to exogenous GnRH. The observation that a GnRH antagonist reduced the feedback effects of testosterone suggests that testosterone action on pituitary gonadotrophin release, at least in part, is mediated via hypothalamic GnRH. Journal of Endocrinology (1991) 129, 363–370
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Lapcik, O., A. Perheentupa, M. Bicikova, I. Huhtaniemi, R. Hampl, and L. Starka. "The effect of epitestosterone on gonadotrophin synthesis and secretion." Journal of Endocrinology 143, no. 2 (November 1994): 353–58. http://dx.doi.org/10.1677/joe.0.1430353.
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Abstract The effects of 3-week treatment with increasing doses of epitestosterone (ET) on gonadotrophin gene expression and secretion, on testosterone and 5α-dihydrotestosterone (DHT) levels, and on the weight of testes and prostates, were studied in intact adult male rats. The hormones were delivered by means of silastic capsules of different lengths filled with the steroid. One group of rats received testosterone (T) instead of ET, to compare the results with previous studies concerning the testosterone effect. The controls were given capsules with glucose only. Treatment with ET, as well as with T, significantly reduced the weights of prostates. When the data from ET-treated rats and controls were combined, a significant negative correlation (P<0·001) was found between the weight of prostates and serum ET. T, in contrast to ET, also decreased significantly the weights of testes. ET treatment caused a significant reduction of serum T levels but only an insignificant decline of DHT levels, independent of the dose. Serum and pituitary (p) luteinizing hormone (LH) levels in the ET-treated rats did not change. Pituitary mRNA contents for the βLH subunit (βLH-mRNA) showed a dose-dependent significant increase, up to 170% (P<0·01), with ET treatment. pFSH decreased with the lowest ET (2 cm) dose (P<0·05), but no change was observed with the other doses. The mRNA for the common α-subunit also increased with the ET load. In conclusion, ET acts at several sites in the regulation of gonadotrophin formation and release. It enhances the steady-state mRNA levels of both gonadotrophins in the pituitary. At the same time, ET may act directly in the pituitary by inhibition of post-transcriptional events in LH synthesis. A direct inhibitory effect of ET at the hypothalamic level is also possible. The circulating levels of both gonadotrophins are thus the result of these composite effects. Journal of Endocrinology (1994) 143, 353–358
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Pinilla, L., P. Garnelo, M. Tena-Sempere, F. Gaytan, and E. Aguilar. "Mechanisms of reproductive deficiency in male rats treated neonatally with a gonadotrophin-releasing hormone antagonist." Journal of Endocrinology 142, no. 3 (September 1994): 517–25. http://dx.doi.org/10.1677/joe.0.1420517.
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Abstract It is well known that males injected neonatally with oestradiol or antiserum or antagonists (ANT) against gonadotrophin-releasing hormone (GnRH) show multiple reproductive disorders. In the present work, in males treated neonatally with GnRH-ANT, we have analysed: (1) whether the impairment of reproductive function can be blocked by simultaneous treatment with gonadotrophins, (2) the possible differences in the effects of GnRH-ANT injected before or after the proliferation of Sertoli cells which takes place between days 1 and 15 of age, and (3) the mechanism(s) for the increased FSH secretion observed in adulthood. Experimental designs included: administration of GnRH-ANT between days 1 and 16 or 15 and 30 of age, simultaneous administration of gonadotrophins and GnRH-ANT to neonatal males, and measurement of FSH secretion after orchidectomy or specific destruction of Leydig cells with ethylene dimethane sulphonate (EDS) in adult males treated neonatally with GnRH-ANT. The principal new data presented in our studies are the following: (1) delayed puberty was observed not only in males injected neonatally with GnRH-ANT, but also in those injected with gonadotrophins or with GnRH-ANT and gonadotrophins, (2) the decreased fertility and increased FSH secretion observed in adult males treated neonatally with GnRH-ANT were normalized by simultaneous administration of GnRH-ANT and gonadotrophins, and (3) the increased FSH secretion in adult males treated neonatally with GnRH-ANT remained after EDS or orchidectomy, suggesting that mechanisms other than decreased inhibin secretion were involved in the increased secretion of FSH. Journal of Endocrinology (1994) 142, 517–525
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Miller, D. W., D. Blache, and G. B. Martin. "The role of intracerebral insulin in the effect of nutrition on gonadotrophin secretion in mature male sheep." Journal of Endocrinology 147, no. 2 (November 1995): 321–29. http://dx.doi.org/10.1677/joe.0.1470321.
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Abstract The effect of nutrition on gonadotrophin secretion may be exerted through a central metabolic signal that reflects nutritional status. We have previously found that glucose and insulin concentrations are elevated in the cerebrospinal fluid (CSF) of rams in which the secretion of gonadotrophins has been stimulated by a nutritional supplement of lupin grain (Lupinus angustifolius). In the present study, we tested the hypothesis that insulin and/or glucose is a metabolic modulator of GnRH secretion and mediates the effects of nutrition on gonadotrophin secretion. Six mature rams were fed a diet that maintained live weight and then given a series of infusions, each for 12 h/day for 4 days, in a cross-over design. The treatments were: artificial CSF (aCSF), glucose (50 μmol/h) in aCSF, insulin (0·6 ng/h) in aCSF, and glucose (50 μmol/h) plus insulin (0·6 ng/h) in aCSF; all infused at a rate of 5 μl/min. At the same time as the infusion treatments, two other groups of four rams without cerebral cannulae were fed either the maintenance diet or the same diet supplemented with 750 g lupin grain per head per day for 4 days, again in a cross-over design. Rams fed the lupin supplement showed an increase in both LH pulse frequency and mean FSH on day 4 (P<0·05). Infusion of aCSF or glucose did not affect gonadotrophin secretion. Rams infused with insulin or insulin plus glucose showed an increase (P<0·05) in LH pulse frequency but no increase in FSH concentrations on day 4 of infusion. The magnitude of the LH response to insulin was similar to the nutritional response of feeding lupin supplements. There was no effect of any of the infusion treatments on plasma prolactin or insulin secretion. These data show that changes in insulin concentrations in the CSF lead to changes in LH secretion and support the hypothesis that insulin is a metabolic modulator of GnRH secretion and mediates the effects of nutrition on gonadotrophin secretion. Journal of Endocrinology (1995) 147, 321–329
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Nagahara, Yasuhito, Akira Miyake, Keiichi Tasaka, Yasuhiro Kawamura, Toshihiro Aono, and Osamu Tanizawa. "Possible site of negative and positive feedback action of oestrogen on gonadotrophin secretion in normal women." Acta Endocrinologica 108, no. 4 (April 1985): 440–44. http://dx.doi.org/10.1530/acta.0.1080440.
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Abstract. For determination of the site of action of oestrogen (E) during the negative and positive feedback phases of gonadotrophin secretions, studies were made on the pituitary response to a small amount of LRH and the pulsatility of gonadotrophins after E administration in normal cycling women in the mid-follicular phase. The pituitary responses to an iv bolus of 2.5 μg of synthetic LRH were evaluated by measuring serum LH and FSH 2 h before and 8 h after administration of 20 mg of conjugated E (Premarin). In the next cycle, the pituitary responses to a same dose of LRH were also observed 2 h before and 56 h after E injection. The mean levels of serum LH and FSH and the peak responses to LRH were significantly (P < 0.05) decreased 8 h after E injection, but were significantly (P < 0.05) increased 56 h after E administration. In the third cycle, the pulsatility of gonadotrophins was evaluated by measuring serum LH and FSH every 15 min for 180 min before and 8 h and 56 h after E injection. The pulse frequencies of gonadotrophins were not significantly different before and 8 h and 56 h after E injection. The amplitudes of pulses 56 h after Premarin injection were significantly higher than those before the injection. These findings suggest that the negative and positive feedback effects of E on gonadotrophin secretion may be caused, in part, by its direct action on the pituitary response to LRH.
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Bergendahl, M., and I. Huhtaniemi. "The time since castration influences the effects of short-term starvation on gonadotrophin secretion in male rats." Journal of Endocrinology 143, no. 2 (November 1994): 209–19. http://dx.doi.org/10.1677/joe.0.1430209.
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Abstract Short-term starvation suppresses the pituitary-testicular function in rats, evidently through inhibition of gonadotrophin-releasing hormone (GnRH) release. However, when gonadotrophin secretion is strongly enhanced, e.g. after castration, starvation does not suppress gonadotrophins. To test whether the time since castration affects the pituitary response to starvation, adult male rats were totally deprived of food for five days (only water allowed) immediately (acute castration) or two weeks after castration (chronic castration). The pituitary contents of GnRH receptors were decreased by starvation in sham-operated animals, unaffected in acutely castrated rats, but increased in chronically castrated animals, in comparison with appropriate controls (P<0·01). Castration per se increased steady-state mRNA levels of the common α-chain and the LH and FSH β-chains in all groups studied. The only consistent effect of starvation on these parameters was the 1·7 to 2-fold increase in the pituitary content of LH β-subunit mRNA in acutely and chronically castrated rats (P<0·01). Starvation alone suppressed LH secretion, acute castration eliminated this effect, but in chronically castrated rats, the starvation effect was stimulatory. Starvation did not affect FSH secretion in sham-operated and acutely castrated rats, but after chronic castration, the effect was stimulatory. In conclusion, the overall effect of starvation on gonadotrophins shifts gradually after castration from suppression, in sham-operated rats, to stimulation, in chronically castrated animals. Parallel changes in pituitary GnRH receptors suggest similar changes in GnRH secretion. Hence, starvation has both negative and positive effects on the GnRH-gonadotrophin-axis. The negative effect is evidently androgen-dependent and dominates in testes-intact animals. After chronic castration, only the positive, non-androgen dependent, stimulatory effect remains. Journal of Endocrinology (1994) 143, 209–219
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Clayton, R. N., A. Detta, S. I. Naik, L. S. Young, and H. M. Charlton. "Gonadotrophin releasing hormone receptor regulation in relationship to gonadotrophin secretion." Journal of Steroid Biochemistry 23, no. 5 (November 1985): 691–702. http://dx.doi.org/10.1016/s0022-4731(85)80004-2.
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Kuhn, Jean Marc, Lise Duranteau, Max A. Rieu, Najiba Lahlou, Marc Roger, and Jean Pierre Luton. "Evidence of oestradiol-induced changes in gonadotrophin secretion in men with feminizing Leydig cell tumours." European Journal of Endocrinology 131, no. 2 (August 1994): 160–66. http://dx.doi.org/10.1530/eje.0.1310160.
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Kuhn JM, Duranteau L, Rieu MA, Lahlou N, Roger M, Luton JP. Evidence of oestradiol-induced changes in gonadotrophin secretion in men with feminizing Leydig cell tumours. Eur J Endocrinol 1994;131:160–6. ISSN 0804–4643 To study the sex steroid-gonadotrophin relationship, plasma oestradiol (E2), testosterone and gonadotrophin-releasing hormone (GnRH)-induced (100 μg iv) gonadotrophin response were measured in 42 male partners of infertile couples with normal sperm count (group I) and in 21 men with Leydig cell tumour (LCT, group II) in which a basal evaluation was repeated after tumour removal. Plasma free α-subunit (FAS), immunoreactive α-inhibin and luteinizing hormone (LH) pulse analysis were assessed in 10 LCT before and in six of them after surgery. Testosterone was significantly (p < 0.01) lower whereas E2 was significantly (p < 0.001) higher in group II than in group I. Gonadotrophin data were similar in both groups. The mean FAS was higher in group II than in group I and α-inhibin was higher than the normal range in 6/10 LCT. In group II, E2 levels were significantly (p < 0.01) and negatively correlated with testosterone, FSH, GnRH-induced gonadotrophin rise and LH pulse amplitude but not frequency. Significant (p < 0.001) changes were observed after surgery: E2 and α-inhibin fell; testosterone, LH and FSH rose; whereas FAS did not change significantly. The LH pulse amplitude but not frequency increased significantly (p < 0.05). In conclusion E2 oversecreted by LCT decreased LH and testosterone levels concomitantly. The GnRH-induced gonadotrophin level rose and the LH pulse amplitude decreased when the plasma E2 level rose, whereas the pulse frequency remained unaffected. A concomitant increase in α-inhibin and E2 is likely to be responsible for the drop in plasma FSH levels. These data support an action of excessive amounts of E2 at pituitary level, perhaps by decreasing the sensitivity of gonadotrophs to GnRH. JM Kuhn, Service d'Endocrinologie, Hôpital de Bois Guillaume, 147 avenue du Maréchal Juin, 76230 Bois Guillaume, France
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Evans, J. J., and K. J. Catt. "Gonadotrophin-releasing activity of neurohypophysial hormones: II. The pituitary oxytocin receptor mediating gonadotrophin release differs from that of corticotrophs." Journal of Endocrinology 122, no. 1 (July 1989): 107–16. http://dx.doi.org/10.1677/joe.0.1220107.
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ABSTRACT Neurohypophysial hormones stimulate gonadotrophin release from dispersed rat anterior pituitary cells in vitro, acting through receptors distinct from those which mediate the secretory response to gonadotrophin-releasing hormone (GnRH). The LH response to oxytocin was not affected by the presence of the phosphodiesterase inhibitor, methyl isobutylxanthine, but was diminished in the absence of extracellular calcium and was progressively increased as the calcium concentration in the medium was raised to normal. In addition, the calcium channel antagonist, nifedipine, suppressed oxytocin-stimulated secretion of LH. It is likely that the mechanisms of LH release induced by GnRH and neurohypophysial hormones are similar, although stimulation of gonadotrophin secretion is mediated by separate receptor systems. Oxytocin was more active than vasopressin in releasing LH, but less active in releasing ACTH. The highly selective oxytocin agonist, [Thr4,Gly7]oxytocin, elicited concentration-dependent secretion of LH but had little effect on corticotrophin secretion. The neurohypophysial hormone antagonist analogues, [d(CH2)5Tyr(Me)2]-vasopressin, [d(CH2)5Tyr(Me)2,Orn8]vasotocin and [d(CH2)5d-Tyr(Et)2Val4,Cit8]vasopressin, inhibited the LH response to both oxytocin and vasopressin. However, [d(CH2)5Tyr(Me)2]vasopressin was much less effective in inhibiting the ACTH response to the neurohypophysial hormones, and [d(CH2)5Tyr-(Me)2,Orn8]vasotocin and [d(CH2)5d-Tyr(Et)2,Val4, Cit8]vasopressin exhibited no inhibitory activity against ACTH release. Thus, agonist and antagonist analogues of neurophypophysial hormones display divergent activities with regard to LH and ACTH responses, and the neuropeptide receptor mediating gonadotroph activation is clearly different from that on the corticotroph. Whereas the corticotroph receptor is a vasopressin-type receptor an oxytocin-type receptor is responsible for gonadotrophin release by neurohypophysial hormones. Journal of Endocrinology (1989) 122, 107–116
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Beindorff, Nicola, and Almuth Einspanier. "Luteotrophic effects of relaxin, chorionic gonadotrophin and FSH in common marmoset monkeys (Callithrix jacchus)." REPRODUCTION 139, no. 5 (May 2010): 923–30. http://dx.doi.org/10.1530/rep-09-0257.
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In early pregnant primates, relaxin (RLX) is highly upregulated within the corpus luteum (CL), suggesting that RLX may have an important role in the implantation of the blastocyst. Therefore, the aim of the present study was to investigate the local effects of RLX and gonadotrophins on the maintenance of the CL using anin vitromicrodialysis system. CLs of common marmoset monkeys were collected by luteectomy during different stages of the luteal phase and early pregnancy. Each CL was perfused with either Ringer's solution alone or Ringer's solution supplemented with either porcine RLX (250, 500 and 1000 ng/ml) or gonadotrophins (50 IU/ml). Application of RLX provoked a significant luteal response of progesterone (P4) and oestradiol (E2) secretions during the mid-luteal phase (500 ng/ml: P454±42%, E224±11%; 1000 ng/ml: E216±13%), and especially during the late luteal phase (250 ng/ml: P453±10%; 500 ng/ml: P444±15%; 1000 ng/ml: P462±15%, E218±7%). The effects of RLX on steroid secretion were irrespective of the RLX dosages. While treatment with human chorionic gonadotrophin did not affect luteal steroid or RLX secretion, the application of FSH resulted in a significant increase in the secretion of both P4(20±8%) and E2(37±28%), and a prominent rise in RLX during early pregnancy. In conclusion, our results demonstrate that RLX and FSH have a luteotrophic function in the marmoset monkeys; moreover, FSH has a function beyond its traditional role just as a follicle-stimulating hormone.
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Lopata, A., and K. Oliva. "Chorionic gonadotrophin secretion by human blastocysts." Human Reproduction 8, no. 6 (June 1993): 932–38. http://dx.doi.org/10.1093/oxfordjournals.humrep.a138170.
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López-Calderón, A., M. I. Gonzaléz-Quijano, J. A. F. Tresguerres, and C. Ariznavarreta. "Role of LHRH in the gonadotrophin response to restraint stress in intact male rats." Journal of Endocrinology 124, no. 2 (February 1990): 241–46. http://dx.doi.org/10.1677/joe.0.1240241.
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ABSTRACT A hypothalamic site of action has been hypothesized for the inhibitory effect of chronic stress on gonadotrophin secretion. The aim of the present study was to examine the temporal changes in hypothalamic LHRH content and gonadotrophin secretion during restraint stress, and the pituitary responsiveness to LHRH stimulation in chronically stressed rats. Adult male rats were killed after being restrained for 0, 20, 45, 90, 180 and 360 min or for 6 h daily over 2, 3 and 4 days. After 20–45 min of stress there was an increase in plasma concentrations of LH (P<0·01) and a decrease in hypothalamic LHRH content (P<0·01), suggesting a negative correlation between plasma LH and hypothalamic LHRH concentrations. Plasma concentrations of FSH were also increased by restraint, but the FSH response was slower and less than the plasma LH response, being significant after 90 min of restraint. Plasma LH and FSH and hypothalamic LHRH concentrations were decreased in chronically stressed rats. In rats restrained for 6 h daily over 4 days, the response of plasma gonadotrophins to administration of 500 ng LHRH was enhanced 45 min after the injection. On the basis of these observations we concluded that in the intact rat, stress may acutely stimulate LHRH and gonadotrophin secretion, and the inhibitory effect of chronic stress on plasma LH and FSH seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a decrease in LHRH secretion. Journal of Endocrinology (1990) 124, 241–246
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Farnworth, P. G. "Gonadotrophin secretion revisited. How many ways can FSH leave a gonadotroph?" Journal of Endocrinology 145, no. 3 (June 1995): 387–95. http://dx.doi.org/10.1677/joe.0.1450387.
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Tomasi, Paolo A., Giuseppe Fanciulli, Michele Zini, Maria A. Demontis, Alessandra Dettori, and Giuseppe Delitala. "Pulsatile gonadotrophin secretion in hypothyroid women of reproductive age." European Journal of Endocrinology 136, no. 4 (April 1997): 406–9. http://dx.doi.org/10.1530/eje.0.1360406.
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Abstract Hypothyroid women may have various disturbances of the reproductive system. Although menstrual cycle disturbances and infertility have been reported in hypothyroidism, gonadotrophin levels have usually been found in the normal range. We have investigated whether female hypothyroid patients of reproductive age have any alteration in the pulsatile secretory pattern of gonadotrophin secretion. LH and FSH were assayed on days 2–5 of the menstrual cycle in blood samples taken every 10 min for 8 h from six hypothyroid women and six age-matched control subjects. Pulsatility was analysed using the Cluster and Detect programs. There was no significant difference in the number of peaks identified (3·7±0·8 vs 3·7±0·8 for LH, and 3·7±0·8 vs 4·2±0·5 for FSH), the mean duration of peaks (LH: 68·0±6·9 vs 72·±5·1 min; FSH: 81·9±8·1 vs 71·2±10·3 min), the area under the peaks (LH: 91·5±20·4 vs 148·2±55·1IU/l per min; FSH: 71·5±4·5 vs 62·7±15·0IU/l per min), and the incremental amplitude from baseline (LH: 2·2±0·4 vs 3·0±0·8 IU/l; FSH: 1·4±0·2 vs 2·1±0·5IU/l). However, the absolute pulse amplitude was greater in hypothyroid patients (LH: 14·5±1·4 vs 8·3±1·3 IU/l, FSH: 9·0±1·5 vs 5·8±1·2 IU/l, P=0·04), as were the integrated concentrations (LH: 6·6±0·7 vs 3·3±0·4OU/l per min, P<0·01; FSH: 4·3±0·4 vs 2·1±0·5IU/l per min, Oestradiol values were comparable in the two groups 42·7±0·4 vs 43·±9·7 pg/ml). These results indicate that in hypothyroid women there is an increased baseline level with a normal pulsatility of the gonadotrophin secretion. Similar oestrogen levels in both groups, and normal or nearnormal cycles in our patients suggest either a decreased biological potency of the gonadotrophins or a mild ovarian resistance. European Journal of Endocrinology 136 406–409
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Angervo, M., R. Koistinen, and M. Seppälä. "Epidermal growth factor stimulates production of insulin-like growth factor-binding protein-1 in human granulosa-luteal cells." Journal of Endocrinology 134, no. 1 (July 1992): 127–31. http://dx.doi.org/10.1677/joe.0.1340127.
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ABSTRACT Insulin-like growth factor-I (IGF-I) enhances and epidermal growth factor (EGF) inhibits gonadotrophin-induced aromatization in granulosa cells. Our previous studies have shown that human ovarian granulosa cells synthesize insulin-like growth factor-binding protein-1 (IGFBP-1) which inhibits IGF-stimulated DNA synthesis. The present study addresses the effect of EGF and gonadotrophins in the regulation of IGFBP-1 release by human granulosa cells cultured in serum-free medium. At concentrations of 1–100 μg/l EGF was found to stimulate IGFBP-1 secretion. This was not due to cell proliferation, as the viable cell count remained unaffected. Growth hormone and gonadotrophins had no effect on IGFBP-1 secretion when added alone to culture medium. These results suggest that EGF regulates IGFBP-1 secretion in human granulosa-luteal cells. Journal of Endocrinology (1992) 134, 127–131
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Evans, J. J., G. Robinson, and K. J. Catt. "Gonadotrophin-releasing activity of neurohypophysial hormones: I. Potential for modulation of pituitary hormone secretion in rats." Journal of Endocrinology 122, no. 1 (July 1989): 99–106. http://dx.doi.org/10.1677/joe.0.1220099.
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ABSTRACT Neurohypophysial hormones have been implicated in the control of anterior pituitary function, and oxytocin has been shown to stimulate gonadotrophin excretion and ovarian follicular development in certain species. To determine the role of neurohypophysial peptides in the control of gonadotrophin release, their actions on LH and FSH secretion were analysed in rats in vivo and in vitro. In adult female rats, administration of oxytocin during early pro-oestrus advanced the spontaneous LH surge and markedly increased peripheral LH levels at 15.00 h compared with control animals. In cultured pituitary cells from adult female rats, oxytocin and vasopressin elicited dose-related increases in LH and FSH release. Such responses were not affected by a potent gonadotrophin-releasing hormone (GnRH) antagonist that abolished GnRH agonist-induced release of LH and FSH. Oxytocin did not enhance GnRH agonist-stimulated gonadotrophin release to the same extent as it increased basal secretion, but at low concentrations of GnRH agonist the effects were additive. The gonadotrophin responses to oxytocin and vasopressin were inhibited by the specific neurohypophysial hormone antagonists, [d(CH2)5d-Ile2,Ile4,Arg8]vasopressin and [d(CH2)5Tyr (Me),Arg8]vasopressin. These results provide direct evidence that neurohypophysial hormones can stimulate gonadotrophin secretion through a receptor system distinct from the GnRH receptor. Such a mechanism could represent a complementary hypothalamic control system for long-term modulation of LH and FSH secretion by exerting a basal or tonic influence on gonadotrophin production. Journal of Endocrinology (1989) 122, 99–106
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Birnie, L. M., P. J. Broadbent, J. S. M. Hutchinson, R. G. Watt, and D. F. Dolman. "Effects of gonadotrophin releasing hormone agonist treatment on oestrous cycle length and superovulatory response in maiden heifers." Proceedings of the British Society of Animal Science 1995 (March 1995): 141. http://dx.doi.org/10.1017/s030822960002907x.
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Current variability in superovulatory response prevents the economical production of large numbers of high quality embryos and limits the use of embryo transfer. Pulsatile administration of GnRH (gonadotrophin releasing hormone) elicits pulsatile secretion of LH (luteinising hormone) while chronic treatment with a potent GnRH agonist reduces LH secretion. Using the latter, gonadotrophin-dependent preovulatory antral follicle development may be suppressed, resulting in a uniform cohort of small antral follicles in the absence of a dominant follicle which could then be superstimulated by exogenous gonadotrophin.
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Crawford, J. L., D. A. Heath, L. J. Haydon, B. P. Thomson, and D. C. Eckery. "Gene expression and secretion of LH and FSH in relation to gene expression of GnRH receptors in the brushtail possum (Trichosurus vulpecula) demonstrates highly conserved mechanisms." REPRODUCTION 137, no. 1 (January 2009): 129–40. http://dx.doi.org/10.1530/rep-08-0347.
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In eutherian mammals, the gonadotrophins (LH and FSH) are synthesized and stored in gonadotroph cells under the regulation of multiple mechanisms including GnRH. Very little is known about the regulation of gonadotrophin secretion and storage in pituitary glands of marsupials. This study revealed, using quantitative PCR and heterologous RIA techniques, thatLHBmRNA expression levels remained constant over the oestrous cycle, regardless of the presence of a preovulatory LH surge, which is characteristic of a hormone secreted under regulation. Our sampling regime was unable to detect pulses of LH during the follicular phase, althoughGNRHRmRNA levels had increased at this time. Pulses of LH were, however, detected in the luteal phase of cycling females, in anoestrus females and in males. There was a positive correlation between gene expression ofFSHBand plasma levels of FSH at different stages of the oestrous cycle and no pulses of FSH were detected at any time; all characteristics of a hormone secreted via the constitutive pathway. Usingin situhybridisation and immunohistochemistry methods, we determined that mRNA expression ofLHBandFSHB, and protein storage of gonadotrophins exhibited a similar pattern of localisation within the pituitary gland. Additionally, sexual dimorphism of gonadotroph populations was evident. In summary, these findings are similar to that reported in eutherians and considering that marsupial evolution diverged from eutherians over 100 million years ago suggests that the regulation of gonadotrophins is highly conserved indeed.
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Dalkin, A. C., S. J. Paul, D. J. Haisenleder, G. A. Ortolano, M. Yasin, and J. C. Marshall. "Gonadal steroids effect similar regulation of gonadotrophin subunit mRNA expression in both male and female rats." Journal of Endocrinology 132, no. 1 (January 1992): 39–45. http://dx.doi.org/10.1677/joe.0.1320039.
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ABSTRACT Gonadal steroids can act both indirectly via gonadotrophin-releasing hormone (GnRH) and directly on the pituitary to regulate gonadotrophin subunit gene expression. Recent studies to assess a possible direct action at the pituitary have shown that testosterone, when given to males in the absence of endogenous GnRH action, selectively increases FSH-β mRNA concentrations. Conversely, in females, oestradiol appears to regulate gonadotrophin subunit mRNAs primarily via GnRH. The present study was designed to determine whether these differing results reflect specific actions of the gonadal steroids themselves or different responses of the pituitary gonadotroph cells in males and females. Rats which had been castrated 7 days earlier were given silicone elastomer implants (s.c.) containing oestradiol (plasma oestradiol 68 ± 4 ng/l) in males or testosterone (plasma testosterone 3·5 ± 0·3 μg/l) in females in the absence or presence of a GnRH antagonist. Seven days later pituitaries were removed and steady-state mRNA concentrations measured by dotblot hybridization. In males, oestradiol reduced LH-β and FSH-β but not α mRNA. The antagonist reduced levels of all three subunit mRNAs in males and the addition of oestradiol had no further effect, suggesting that oestradiol regulates gonadotrophin subunit gene expression in males by suppressing GnRH secretion. In females, testosterone reduced all three subunit mRNAs though FSH-β remained threefold higher than in intact animals. The GnRH antagonist was as effective as testosterone alone and reduced α and LH-β to levels found in intact animals. FSH-β mRNA was partially reduced by antagonist alone in ovariectomized females but the addition of testosterone increased FSH-β twofold versus antagonist alone (as has been observed in males). These findings, together with earlier data, suggest that testosterone increased FSH-β twofold versus antagonist alone (as has been observed in males). These findings, together with earlier data, suggest that testosterone reduces gonadotrophin subunit mRNAs by inhibiting GnRH secretion and also acts directly on the gonadotroph to increase steady-state FSH-β mRNA concentrations in both males and females. Journal of Endocrinology (1992) 132, 39–45
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Dada, M. O., and C. A. Blake. "Monosodium l-glutamate administration: effects on gonadotrophin secretion, gonadotrophs and mammotrophs in prepubertal female rats." Journal of Endocrinology 104, no. 2 (February 1985): 185—NP. http://dx.doi.org/10.1677/joe.0.1040185.
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ABSTRACT We have studied gonadotrophin secretion and immunocytochemically stained gonadotrophs and mammotrophs in 35-day-old female rats which had been treated with monosodium glutamate (MSG) as neonates. We also compared our morphometric data in the saline-treated controls with those we have previously obtained in normal adult female rats. The size of the anterior pituitary glands was reduced but the serum levels, the pituitary gland concentrations and contents, and the in-vitro basal release rates of LH and FSH were not significantly altered by MSG treatment. The size of the LH and FSH cells was reduced by MSG administration, but the volume and numerical densities of LH and FSH cells, and the percentage of LH and FSH cells in the pars distalis were not affected. The results suggest that in spite of the smaller size of LH and FSH cells and of the anterior pituitary glands in the MSG-treated rats, the cells contain normal amounts of hormone and the basal LH and FSH secretion rates of the glands are not significantly depressed, contributing to the maintenance of normal serum gonadotrophin concentrations. The volume density of prolactin cells was not increased by MSG treatment. The volume density of gonadotrophs and the percentage of cells which are gonadotrophs in anterior pituitary glands of prepubertal female rats were greater than those in adult female rats, but the reverse was true for the volume density of prolactin cells, suggesting a reciprocal relationship between the relative numbers of gonadotrophs and mammotrophs in prepubertal and adult female rats. J. Endocr. (1985) 104, 185–192
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Evans, A. C. O., and N. C. Rawlings. "Effects of a long-acting gonadotrophin-releasing hormone agonist (Leuprolide) on ovarian follicular development in prepubertal heifer calves." Canadian Journal of Animal Science 74, no. 4 (December 1, 1994): 649–56. http://dx.doi.org/10.4141/cjas94-094.
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We studied the effects of reducing gonadotrophin secretion on ovarian follicular development in young prepubertal heifer calves. Calves received a GnRH agonist (n = 5, 15 mg of Leuprolide acetate, i.m.) or carrier (n = 5) at 8 and 12 w of age. Starting at 8 and 34 w of age, ovarian follicles were monitored daily for 17 d, and at 10, 15, 25 and 35 w of age, blood samples were collected every 15 min for 12 h for measurement of serum concentration of LH and FSH. GnRH agonist treatment did not affect the age and body weight at puberty (P > 0.05). Agonist treatment suppressed follicle numbers and in two heifers follicle emergence (growth above 4–5 mm) was blocked immediately. In three agonist-treated heifers, follicle emergence was blocked after one extended wave of follicular growth. At 34 w of age the pattern of ovarian follicular growth did not differ between groups but oestradiol secretion was lower in agonist-treated heifers. During agonist treatment basal and mean concentrations of FSH, and LH and FSH pulse amplitude were decreased but basal LH concentrations increased (P < 0.05). At 25 and 35 w of age some rebound in gonadotrophin secretion was seen.We concluded that disrupting gonadotrophin secretion in young prepubertal heifer calves by GnRH agonist treatment, suppressed ovarian follicular growth but that a rebound in gonadotrophin secretion prevented long term-effects on sexual development. Key words: Follicle stimulating hormone, gonadotrophin-releasing hormone, heifer calves, luteinising hormone ovarian follicles
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Nicol, L., M.-O. Faure, J. R. McNeilly, J. Fontaine, C. Taragnat, and A. S. McNeilly. "Bone morphogenetic protein-4 interacts with activin and GnRH to modulate gonadotrophin secretion in LβT2 gonadotrophs." Journal of Endocrinology 196, no. 3 (January 4, 2008): 497–507. http://dx.doi.org/10.1677/joe-07-0542.
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We have shown previously that, in sheep primary pituitary cells, bone morphogenetic proteins (BMP)-4 inhibits FSHβ mRNA expression and FSH release. In contrast, in mouse LβT2 gonadotrophs, others have shown a stimulatory effect of BMPs on basal or activin-stimulated FSHβ promoter-driven transcription. As a species comparison with our previous results, we used LβT2 cells to investigate the effects of BMP-4 on gonadotrophin mRNA and secretion modulated by activin and GnRH. BMP-4 alone had no effect on FSH production, but enhanced the activin+GnRH-induced stimulation of FSHβ mRNA and FSH secretion, without any effect on follistatin mRNA. BMP-4 reduced LHβ mRNA up-regulation in response to GnRH (±activin) and decreased GnRH receptor expression, which would favour FSH, rather than LH, synthesis and secretion. In contrast to sheep pituitary gonadotrophs, which express only BMP receptor types IA (BMPRIA) and II (BMPRII), LβT2 cells also express BMPRIB. Smad1/5 phosphorylation induced by BMP-4, indicating activation of BMP signalling, was the same whether BMP-4 was used alone or combined with activin±GnRH. We hypothesized that activin and/or GnRH pathways may be modulated by BMP-4, but neither the activin-stimulated phosphorylation of Smad2/3 nor the GnRH-induced ERK1/2 or cAMP response element-binding phosphorylation were modified. However, the GnRH-induced activation of p38 MAPK was decreased by BMP-4. This was associated with increased FSHβ mRNA levels and FSH secretion, but decreased LHβ mRNA levels. These results confirm 1. BMPs as important modulators of activin and/or GnRH-stimulated gonadotrophin synthesis and release and 2. important species differences in these effects, which could relate to differences in BMP receptor expression in gonadotrophs.
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Irvine, C. H. G., and S. L. Alexander. "Secretion rates and short-term patterns of gonadotrophin-releasing hormone, FSH and LH in the normal stallion in the breeding season." Journal of Endocrinology 117, no. 2 (May 1988): 197–206. http://dx.doi.org/10.1677/joe.0.1170197.
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ABSTRACT Pituitary venous blood was collected by a painless non-surgical cannulation method from five ambulatory stallions at 5-min intervals for 5–6 h during the breeding season. In four adult stallions, statistical analysis showed that pulses of gonadotrophin-releasing hormone (GnRH) and LH were coincident (P <0·01), as were pulses of FSH and LH (P <0·05). Furthermore, the patterns of changes in concentration of FSH and LH were highly correlated in each of the four stallions. However, seemingly ineffective pulses of GnRH were also observed, with 28% of GnRH pulses failing to induce a significant gonadotrophin pulse. In the four adult stallions the amplitude of pituitary venous gonadotrophin pulses varied markedly but no correlation with GnRH pulse amplitude was observed. Peak secretion of FSH, but not LH, during pulses was correlated with the length of the interpulse interval. Consequently, the ratio of FSH to LH during peaks was least (P <0·02) when the interpulse interval was 30 min or less. Thus, differential FSH and LH secretion was achieved within a constant steroid milieu. Two stallions had regular contact with oestrous mares, and in these horses the secretion of GnRH and gonadotrophins occurred almost continuously with rapid, rhythmic pulses superimposed upon a tonic background. Mean (± s.d.) interval between GnRH pulses was 31·4 ± 9·8 min and 27·7 ± 10·1 min. This secretory pattern was not observed in the two stallions which had infrequent contact with oestrous mares, although the small numbers precluded statistical testing of this apparent difference. No GnRH pulses were observed in one of these stallions, while in the other mean (± s.d.) GnRH pulse interval was 45·0 ± 48·7 min, the large variance being partly due to rapid pulses during a period in which the stallion teased mares. The fifth stallion was pubertal, and GnRH and LH secretion occurred in 15 and 0% of samples respectively, while low levels of FSH secretion were observed in 37% of samples and jugular testosterone levels were immeasurably low. We conclude that there is a statistically significant synchrony between pulses of GnRH, LH and FSH in the pituitary venous blood of stallions. Furthermore, decreasing intervals between gonadotrophin pulses result in a significant reduction in secretion of FSH but not LH. J. Endocr. (1988) 117, 197–206
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McNeilly, A. S. "Prolactin and the control of gonadotrophin secretion." Journal of Endocrinology 115, no. 1 (October 1987): 1–5. http://dx.doi.org/10.1677/joe.0.1150001.
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WAAL, H. A. DELEMARRE-VAN, J. M. B. WENNINK, and R. J. H. ODINK. "Gonadotrophin and Growth Hormone Secretion Throughout Puberty." Acta Paediatrica 80, s372 (January 1991): 26–31. http://dx.doi.org/10.1111/j.1651-2227.1991.tb17964.x.
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Dedes, Ioannis. "Kisspeptins and the control of gonadotrophin secretion." Systems Biology in Reproductive Medicine 58, no. 3 (February 29, 2012): 121–28. http://dx.doi.org/10.3109/19396368.2011.651555.
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Genazzani, A. R., A. D. Genazzani, C. Volpogni, F. Pianazzi, G. A. Li, N. Surico, and F. Petraglia. "Opioid control of gonadotrophin secretion in humans." Human Reproduction 8, suppl 2 (November 1, 1993): 151–53. http://dx.doi.org/10.1093/humrep/8.suppl_2.151.
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Fingscheidt, U., GF Weinbauer, HL Fehm, and E. Nieschlag. "Regulation of gonadotrophin secretion by inhibin, testosterone and gonadotrophin-releasing hormone in pituitary cell cultures of male monkeys." Journal of Endocrinology 159, no. 1 (October 1, 1998): 103–10. http://dx.doi.org/10.1677/joe.0.1590103.
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The effects of bovine inhibin, testosterone and GnRH on gonadotrophin secretion by primate pituitary cells were characterized in vitro using pituitaries from six male rhesus monkeys and one male cynomolgus monkey. The effect of inhibin on basal secretion of FSH and LH was investigated. Dose-response curves in monkeys and rats were compared. GnRH dose-response curves in the presence and absence of testosterone were also examined in monkeys. In monkey pituitary cells, testosterone at a concentration of 10(-7) M had no effect on LH or FSH secretion. Inhibin suppressed FSH secretion to 50.8% of that of controls with no effect on LH. In rats, FSH secretion was suppressed to 45.0% of that of controls with a median effective dose (ED50, 95% range) of 1.298 (1.064-1.584) U/ml, compared with 1.024 (0.7204-1.455) U/ml in monkeys. In monkey pituitary cells, LH release was stimulated 9.9-fold and FSH 3.3-fold by GnRH. Testosterone had no effect on basal or GnRH-stimulated gonadotrophin release. These results support the view that the pituitary is not the target organ for the negative feedback action of testosterone in the male. In vitro, inhibin is the major regulator of FSH secretion at the pituitary level.
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Naik, S. I., G. Saade, A. Detta, and R. N. Clayton. "Homologous ligand regulation of gonadotrophin-releasing hormone receptors in vivo: relationship to gonadotrophin secretion and gonadal steroids." Journal of Endocrinology 107, no. 1 (October 1985): 41–47. http://dx.doi.org/10.1677/joe.0.1070041.
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ABSTRACT A single injection of gonadotrophin-releasing hormone (GnRH) (60 ng s.c., 42·9 nmol) induced biphasic GnRH receptor regulation in normal intact adult female mice. A transient 22% receptor decrease occurred 30–60 min after injection of GnRH when peak serum decapeptide concentrations were reached (137 ± 41 (s.e.m.) ng/l). This GnRH receptor decrease occurred shortly after the peak serum LH values at 15–30 min. The subsequent rapid (within 1 h) return of GnRH receptor levels to normal suggested transient receptor occupancy by GnRH rather than true receptor loss. At 8 h after injection of GnRH a significant 35% increase in GnRH receptors was consistently observed, when serum GnRH levels were undetectable and serum LH had returned to basal levels. This receptor increase was not due to increased receptor affinity, and was prevented by a non-specific protein synthesis inhibitor. Ovariectomy, which caused a 50% fall in GnRH receptors (59·4 ± 4·9 fmol/pituitary gland in intact controls; 26·9 ± 2·6 in ovariectomized mice) abolished the induction by GnRH of its own receptors, although the initial transient decrease occurred over the period of the acute serum LH and FSH rise. Despite a 50% reduction in GnRH receptors in ovariectomized mice, increased serum gonadotrophin levels and responsiveness to GnRH were maintained, indicating dissociation between receptor changes and gonadotrophin levels. No GnRH receptor up-regulation was observed 8 h after a single GnRH injection (60 ng s.c.) in either intact or orchidectomized normal male mice. However, the same treatment doubled GnRH receptors in GnRH-deficient (hpg) female mice. While GnRH appears to up-regulate its own receptors by a direct action on pituitary gonadotrophs in the GnRH-deficient mouse its action in the normal female mouse pituitary appears secondary to stimulation of a gonadal product, presumably oestrogens. J. Endocr. (1985) 107, 41–47
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Hearn, J. P., J. K. Hodges, and S. Gems. "Early secretion of chorionic gonadotrophin by marmoset embryos in vivo and in vitro." Journal of Endocrinology 119, no. 2 (November 1988): 249–55. http://dx.doi.org/10.1677/joe.0.1190249.
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ABSTRACT The control mechanisms of early pregnancy in primates differ from those in non-primate species in the early secretion of chorionic gonadotrophin (CG) by the embryo and in the support of the corpus luteum. This study describes the initiation of secretion of CG by the embryo of the marmoset monkey examined in vivo and in vitro. A bioassay for gonadotrophin, which did not distinguish between CG and LH, was adapted and validated for the marmoset. A system of embryo culture was developed whereby embryos were grown from morula/blastocyst stages until at least the differentiation of the trophoblast and yolk sac, facilitated by the embryo attaching to a monolayer of marmoset fibroblast cells. Gonadotrophin concentrations were measured in the peripheral circulation of marmosets during precisely timed stages during the first 84 days of the 144-day gestation period, providing a profile of secretion that was maintained at high levels for longer than the profile seen in Old World primates, including man. A clear increase above baseline levels was seen by day 17 after ovulation, implantation commencing in the marmoset on days 11–13. Gonadotrophin was secreted by embryos in culture from the time of attachment in vitro, but there was no clear evidence of secretion before attachment. Levels of gonadotrophin secreted by embryos in vitro increased rapidly, reaching a maximum mean production rate of 90 mIU/24 h within 4 days after attachment. The experimental systems developed here will allow the examination of the local function of CG at the implantation site, intra-embryonic control of its secretion and its possible involvement in embryonic development. J. Endocr. (1988) 119, 249–255
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Knight, P. G., and R. J. Castillo. "Effects of bovine follicular fluid on gonadotrophin secretion in intact and chronically ovariectomized ewes before and after desensitization of pituitary gonadotrophs to gonadotrophin-releasing hormone." Journal of Endocrinology 117, no. 3 (June 1988): 431–39. http://dx.doi.org/10.1677/joe.0.1170431.
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ABSTRACT Intact and chronically ovariectomized ewes were treated for 4 days with charcoal-treated bovine follicular fluid (FF) or charcoal-treated bovine serum during the late-anoestrous period, and the effects on basal and gonadotrophin-releasing hormone (GnRH)-induced secretion of LH and FSH observed. Subsequently, ewes received s.c. implants containing a sustained-release formulation of a potent GnRH agonist d-Ser(But)6-Azgly10-LHRH (ICI 118630) to desensitize pituitary gonadotrophs to hypothalamic stimulation, and the effects of bovine FF and bovine serum were re-assessed 2 weeks later. Chronic exposure (for 2–3 weeks) to ICI 118630 significantly reduced basal levels of LH and FSH in both intact and ovariectomized ewes and completely abolished both spontaneous LH pulses as well as exogenous GnRH-induced acute increases in plasma LH and FSH levels. Treatment with bovine FF significantly reduced plasma FSH levels, but not LH levels, in both intact and ovariectomized ewes before and after chronic exposure to ICI 118630. In intact ewes before exposure to ICI 118630, treatment with bovine FF actually enhanced pulsatile LH secretion and raised mean plasma LH levels by 240% (P <0·05). No such stimulatory effect of bovine FF on LH secretion was observed in intact ewes exposed to ICI 118630 or in ovariectomized ewes before or after exposure to ICI 118630, suggesting that the effect probably involved an alteration in ovarian steroid feedback affecting hypothalamic GnRH output. Treatment with bovine FF did not significantly affect the magnitude of GnRH-induced surges of LH or of FSH observed in either intact or ovariectomized ewes before exposure to ICI 118630. These observations indicate that charcoal-treated bovine FF, a rich source of inhibin, can directly suppress pituitary FSH secretion in vivo, irrespective of whether a functionally intact hypothalamo-pituitary-ovarian axis is present. J. Endocr. (1988) 117, 431–439
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SAUDER, S. E., M. S. FRAGER, G. D. CASE, R. P. KELCH, and J. C. MARSHALL. "EFFECTS OF CHANGING GONADOTROPHIN-RELEASING HORMONE PULSE FREQUENCY ON GONADOTROPHIN SECRETION IN MEN." Clinical Endocrinology 28, no. 6 (June 1988): 647–56. http://dx.doi.org/10.1111/j.1365-2265.1988.tb03857.x.
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