Journal articles: 'Preovulatory luteinizing hormone surge'

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Rangel, P. L., P. J. Sharp, and C. G. Gutierrez. "Testosterone antagonist (flutamide) blocks ovulation and preovulatory surges of progesterone, luteinizing hormone and oestradiol in laying hens." Reproduction 131, no. 6 (June 2006): 1109–14. http://dx.doi.org/10.1530/rep.1.01067.

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The preovulatory release of luteinizing hormone (LH) in the domestic hen occurs after the initiation of a preovulatory surge of testosterone. The objective of this study was to determine whether this testosterone surge has functional significance in the endocrine control of ovulation. Groups of laying hens (n=10–22) were treated with the androgen receptor antagonist, flutamide, at 8 h intervals for 24 h at doses of 0, 31.25, 62.5, 125 and 250 mg. All doses reduced egg laying (P < 0.001), with the highest dose being the most effective. In a second study, laying hens (n=9) were treated with 250 mg flutamide at 8 h intervals for 24 h with a control group being given placebo (n=10). Blood samples were taken for hormone measurements at 2 h intervals for 18 h starting 4 h before the onset of darkness. The percentage of hens laying per day did not differ between groups before treatment (control, 88% vs flutamide, 86%). Ovulation was blocked in all hens treated with flutamide within 2 days while the control hens continued to lay at the pretreatment rate (80%). Preovulatory surges of plasma testosterone, progesterone, oestradiol and LH were observed in control hens but with the exception of testosterone, flutamide treatment blocked the progesterone, oestradiol and LH surges. LH concentrations declined progressively with time in the flutamide-treated hens. It is concluded that inhibition of testosterone action blocks egg laying and the preovulatory surges of progesterone, luteinizing hormone and oestradiol demonstrating a key role for the preovulatory release of testosterone in the endocrine control of ovulation in the domestic hen.

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Zheng, Cuihong, Thippeswamy Gulappa, Bindu Menon, and K. M. J. Menon. "Association between LH receptor regulation and ovarian hyperstimulation syndrome in a rodent model." Reproduction 160, no. 2 (August 2020): 239–45. http://dx.doi.org/10.1530/rep-20-0058.

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Ovarian hyperstimulation syndrome (OHSS) is a common complication of ovarian stimulation associated with the administration of human chorionic gonadotropin (hCG) during assisted reproduction. We have determined the expression of luteinizing hormone receptor (Lhcgr) mRNA, vascular endothelial growth factor (VEGF), and its transcription factor, HIF1α, during the periovulatory period in a rodent model of OHSS and compared these results with normal ovulatory periods. These results showed that the downregulation of Lhcgr mRNA in response to conditions that mimic preovulatory LH surge was significantly impaired in the OHSS group compared to the complete downregulation seen in the control group. Most importantly, the downregulation of luteinizing hormone receptor mRNA expression following hCG administration was sustained in the control group up to 48 h, whereas it remained at significantly higher levels in the OHSS group. This impairment of hCG-induced Lhcgr downregulation in the OHSS group was accompanied by significantly elevated levels of VEGF and its transcription factor, HIF1α. Furthermore, the downregulation of Lhcgr that occurs in response to a preovulatory LH surge in normal cycles was accompanied by low levels of VEGF. This study shows that, while downregulation of Lhcgr as well as low VEGF levels are seen in response to a preovulatory LH surge in normal ovarian cycle, impaired Lhcgr downregulation and elevated VEGF levels were found in the OHSS group.

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Bowen, Jennifer M., Geoffrey E. Dahl, Neil P. Evans, Lori A. Thrun, Yuedong Wang, Morton B. Brown, and Fred J. Karsch. "Importance of the Gonadotropin-Releasing Hormone (GnRH) Surge for Induction of the Preovulatory Luteinizing Hormone Surge of the Ewe: Dose-Response Relationship and Excess of GnRH*." Endocrinology 139, no. 2 (February 1, 1998): 588–95. http://dx.doi.org/10.1210/endo.139.2.5719.

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Abstract The preovulatory LH surge in the ewe is stimulated by a large sustained surge of GnRH. We have previously demonstrated that the duration of this GnRH signal exceeds that necessary to initiate and sustain the LH surge. The objective of the present study was to determine whether a similar excess exists for amplitude of the GnRH surge. Experiments were performed using an animal model in which GnRH secretion was blocked by progesterone, which in itself does not block the pituitary response to GnRH. To assess the amplitude of the GnRH surge needed to induce the LH surge, we introduced artificial GnRH surges of normal contour and duration but varying amplitudes. Twelve ewes were run through 3 successive artificial follicular phases (total of 36). Six of these artificial follicular phases were positive controls, in which progesterone was removed, the estradiol stimulus was provided, and vehicle was infused. In these control cycles, animals generated endogenous LH surges. In the remaining artificial follicular phases, progesterone was not withdrawn, the estradiol stimulus was provided, and either vehicle (negative control) or GnRH solutions of varying concentrations (experimental) were infused. The circulating GnRH concentrations achieved by infusion were monitored. No LH surges were observed in negative controls, whereas LH surges were induced in experimental cycles provided a sufficient dose of GnRH was infused. A highly significant dose-response relationship was observed between the amplitude of the GnRH surge and both the amplitude of the LH surge and the area under the curve describing the LH response, but no such relationship existed between the amplitude of the GnRH surge and the duration of the LH response. In numerous cases, LH surges similar to those in the positive control animals resulted from infusion of amounts of GnRH estimated to be considerably less than those delivered to the pituitary during the endogenously generated GnRH/LH surge. These findings indicate that, in the ewe, increased GnRH secretion drives the preovulatory LH surge in a dose-dependent fashion, and they provide evidence that the amplitude of the GnRH surge may exceed that needed to generate the LH surge.

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Choi, Yuri, Okto Lee, Kiyoung Ryu, and Jaesook Roh. "Luteinizing Hormone Surge-Induced Krüppel-like Factor 4 Inhibits Cyp17A1 Expression in Preovulatory Granulosa Cells." Biomedicines 12, no. 1 (December 27, 2023): 71. http://dx.doi.org/10.3390/biomedicines12010071.

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Previous in vivo and in vitro studies have demonstrated a dramatic up-regulation of Krüppel-like factor 4 (Klf4) in rat preovulatory granulosa cells (GCs) after LH/hCG treatment and its role in regulating Cyp19A1 expression during the luteal shift in steroidogenesis. In this study, we examined whether Klf4 also mediates the LH-induced repression of Cyp17A1 expression in primary rat preovulatory GCs. In response to LH treatment of GCs in vitro, Cyp17A1 expression declined to less than half of its initial value by 1 h, remaining low for 24 h of culture. Overexpression of Klf4 decreased basal and Sf1-induced Cyp17A1 expressions and increased progesterone secretion. Reduction of endogenous Klf4 by siRNA elevated basal Cyp17A1 expression but did not affect LH-stimulated progesterone production. Overexpression of Klf4 also significantly attenuated Sf1-induced Cyp17A1 promoter activity. On the other hand, mutation of the conserved Sp1/Klf binding motif in the promoter revealed that this motif is not required for Klf4-mediated repression. Taken together, these data indicate that the Cyp17A1 gene may be one of the downstream targets of Klf4, which is induced by LH in preovulatory GCs. This information may help in identifying potential targets for preventing the molecular changes occurring in hyperandrogenic disorders.

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Matsuwaki, T., M. Suzuki, K. Yamanouchi, and M. Nishihara. "Glucocorticoid counteracts the suppressive effect of tumor necrosis factor-alpha on the surge of luteinizing hormone secretion in rats." Journal of Endocrinology 181, no. 3 (June 1, 2004): 509–13. http://dx.doi.org/10.1677/joe.0.1810509.

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We have previously reported that tumor necrosis factor-alpha (TNF-alpha) suppressed pulsatile secretion of luteinizing hormone (LH) in adrenalectomized (ADX) rats, which was restored by replacement of glucocorticoid. In the present study, we examined the role of glucocorticoid in inducing the preovulatory LH surge under conditions of infectious stress. Intravenous injection of TNF-alpha (1 microg) into the proestrous rats at 1300 h attenuated the LH surge and decreased the number of oocytes ovulated. The inhibitory effect of TNF-alpha on the LH surge was blocked by pretreatment with indomethacin, suggesting that the effects of TNF-alpha were mediated by prostaglandins (PGs). On the other hand, ADX markedly enhanced the inhibitory effect of TNF-alpha on the LH surge and subsequent ovulation, which was almost completely restored by pretreatment with a subcutaneous injection of corticosterone (10 mg). These results suggest that glucocorticoid counteracts the inhibitory effect of the cytokines on the preovulatory LH surge by suppressing PG synthesis, and thereby helps to maintain reproductive function under infectious stress conditions.

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Morello, H., L. Caligaris, B. Haymal, and S. Taleisnik. "Daily variations in the sensitivity of proestrous LH surge in the inhibitory effect of intraventricular injection of 5-HT or GABA in rats." Canadian Journal of Physiology and Pharmacology 70, no. 4 (April 1, 1992): 447–51. http://dx.doi.org/10.1139/y92-057.

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Intraventricular injection of 5-hydroxytryptamine (5-HT) into female rats at 11:00 h on the day of proestrus inhibited the preovulatory surge of luteinizing hormone (LH) and ovulation. A similar response was observed after the activation of the serotonergic system by stimulation of the median raphe nucleus. A diurnal rhythm of these responses was observed. In rats acclimated to a 14-h:10-h light: dark cycle the potency of 5-HT to inhibit the LH surge and ovulation was 2.06 and 2.3 times greater, respectively, when injected at 11:00 h than at 13:00 h. Also stimulation of the median raphe nucleus at 11:00 h was significantly more effective in inhibiting these parameters than stimulation at 13:00 h. Similarly, the ability of γ-aminobutyric acid (GABA) to inhibit the preovulatory LH surge and ovulation was greater in rats injected in the morning than in the afternoon. The results of this study indicate that during proestrus the sensitivity of 5-HT and GABA to induce inhibition of preovulatory LH release and ovulation shows daily variations with maximal effect before the critical period.Key words: serotonin, GABA, proestrous LH surge, ovulation, median raphe nucleus, daily rhythms.

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da Silva Bitecourt, Frederico, Carina Oliveira Dumont Horta, Karen Santos Lima, Bruno Bastos Godoi, Fernanda Luiza Menezes Bello, Cíntia Maria Rodrigues, Luana Pereira Leite Schetino, and Kinulpe Honorato-Sampaio. "Morphological study of apoptosis in granulosa cells and ovulation in a model of atresia in rat preovulatory follicles." Zygote 26, no. 4 (August 2018): 336–41. http://dx.doi.org/10.1017/s0967199418000291.

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SummaryPrevious studies have established a model of atresia in preovulatory follicles after stimulation of immature rats with equine chorionic gonadotropin (eCG). This gonadotropin recruits a follicular pool and the deprivation of preovulatory luteinizing hormone (LH) surge induces the atresia in preovulatory follicles. The present study investigated the occurrence of ovulation and provided some morphological features of granulosa cell (GC) apoptosis of atretic follicles at 0, 48, 72 and 120 h after eCG stimulation. Histological sections of ovaries from untreated animals (0 h) showed primordial, primary, secondary and early antral follicles. After 48 h ovaries showed large antral follicles. Preovulatory follicles were observed at 72 h, and two out of five rats displayed cumulus–oocyte complexes (COCs) in the oviducts. All animals exhibited corpora lutea after 120 h. We observed increased estradiol (E2) levels 48 h after eCG treatment that might trigger an endogenous preovulatory gonadotropin surge. Higher progesterone (P4) level, which is the hallmark of a functional corpus luteum, was observed at 120 h. Atresia in secondary and antral follicles was observed by pyknotic granulosa cell nuclei in histology and positive immunolabelling for cleaved caspase 3. We also observed macrophages in secondary and antral follicles in atresia. Transmission electron microscopy revealed GCs with compacted chromatin against the nuclear envelope, nuclear fragmentation, cell shrinkage and fragmentation. No preovulatory follicles showed apoptosis of GCs. In conclusion, our results suggested the occurrence of an endogenous gonadotropin surge, promoting ovulation and preventing atresia of preovulatory follicles.

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Roozendaal, Marjolijn M., Hans JM Swarts, Victor M. Wiegant, and John AM Mattheij. "Effect of restraint stress on the preovulatory luteinizing hormone profile and ovulation in the rat." European Journal of Endocrinology 133, no. 3 (September 1995): 347–53. http://dx.doi.org/10.1530/eje.0.1330347.

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Roozendaal MM, Swarts HJM, Wiegant VM, Mattheij JAM. Effect of restraint stress on the preovulatory luteinizing hormone profile and ovulation in the rat. Eur J Endocrinol 1995;133:347–53. ISSN 0804–4643 Plasma profiles of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured during restraint stress on the day of pro-oestrus; these profiles were considered in relation to ovulation rate on the next day. Rats bearing a permanent jugular vein cannula were subjected to restraint, which was started 0, 1 or 2 h before the presumed onset of the LH surge and ended just before the beginning of the dark period. Exposure to restraint resulted in a suppression of the secretion of both gonadotrophins on the day of pro-oestrus. Suppression of the LH surge was virtually complete (plasma LH ≤ 0.2 ng/ml) in 15 out of 32 stressed rats, and the ovaries of these rats contained graafian follicles with oocytes in germinal vesicle stage. In these rats, the LH surge did not occur 24 h later. In the remaining 17 rats, restraint resulted in a considerable suppression of the LH surge. Of these rats, five had an ovulation rate of 100% and four ovulated partially. In unruptured follicles of the latter, the oocyte had not resumed meiosis and the follicle wall was not luteinized. In the remaining eight rats with a reduced LH surge, ovulations had not occurred and graafian follicles were unaffected. The results of this study indicate that during pro-oestrus restraint stress suppresses and does not delay the release of preovulatory gonadotrophins. Partial suppression of LH by restraint does not result in induction of meiotic resumption without subsequent ovulation or in luteinized unruptured follicles. JAM Mattheij, Department of Human and Animal Physiology, Agricultural University, Haarweg 10, 6709 PJ, Wageningen, The Netherlands

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Chu, Adrienne, Lei Zhu, Ian D. Blum, Oliver Mai, Alexei Leliavski, Jan Fahrenkrug, Henrik Oster, Ulrich Boehm, and Kai-Florian Storch. "Global But Not Gonadotrope-Specific Disruption of Bmal1 Abolishes the Luteinizing Hormone Surge Without Affecting Ovulation." Endocrinology 154, no. 8 (August 1, 2013): 2924–35. http://dx.doi.org/10.1210/en.2013-1080.

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Abstract Although there is evidence for a circadian regulation of the preovulatory LH surge, the contributions of individual tissue clocks to this process remain unclear. We studied female mice deficient in the Bmal1 gene (Bmal1−/−), which is essential for circadian clock function, and found that they lack the proestrous LH surge. However, spontaneous ovulation on the day of estrus was unaffected in these animals. Bmal1−/− females were also deficient in the proestrous FSH surge, which, like the LH surge, is GnRH-dependent. In the absence of circadian or external timing cues, Bmal1−/− females continued to cycle in constant darkness albeit with increased cycle length and time spent in estrus. Because pituitary gonadotropes are the source of circulating LH and FSH, we assessed hypophyseal circadian clock function and found that female pituitaries rhythmically express clock components throughout all cycle stages. To determine the role of the gonadotrope clock in the preovulatory LH and FSH surge process, we generated mice that specifically lack BMAL1 in gonadotropes (GBmal1KO). GBmal1KO females exhibited a modest elevation in both proestrous and baseline LH levels across all estrous stages. BMAL1 elimination from gonadotropes also led to increased variability in estrous cycle length, yet GBmal1KO animals were otherwise reproductively normal. Together our data suggest that the intrinsic clock in gonadotropes is dispensable for LH surge regulation but contributes to estrous cycle robustness. Thus, clocks in the suprachiasmatic nucleus or elsewhere must be involved in the generation of the LH surge, which, surprisingly, is not required for spontaneous ovulation.

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Hatanaka, Fumiko, and Masaru Wada. "Mechanism controlling photostimulated luteinizing hormone secretion is different from preovulatory luteinizing hormone surge in Japanese quail (Coturnix coturnix japonica)." General and Comparative Endocrinology 70, no. 1 (April 1988): 101–8. http://dx.doi.org/10.1016/0016-6480(88)90098-6.

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Gibson, Erin M., Stephanie A. Humber, Sachi Jain, Wilbur P. Williams, Sheng Zhao, George E. Bentley, Kazuyoshi Tsutsui, and Lance J. Kriegsfeld. "Alterations in RFamide-Related Peptide Expression Are Coordinated with the Preovulatory Luteinizing Hormone Surge." Endocrinology 149, no. 10 (June 19, 2008): 4958–69. http://dx.doi.org/10.1210/en.2008-0316.

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The preovulatory LH surge is triggered when the circadian pacemaker, the bilateral suprachiasmatic nucleus (SCN), stimulates the GnRH system in the presence of high estrogen concentrations (positive feedback). Importantly, during the remainder of the estrous cycle, estradiol inhibits LH release via negative feedback. We have recently documented the presence of a novel mammalian RFamide-related peptide (RFRP), a putative gonadotropin-inhibitory hormone (GnIH), that presumably acts upstream of GnRH to modulate the negative feedback effects of estrogen. The present series of studies used female Syrian hamsters to examine the possibility that, in addition to driving the LH surge positively, the SCN concomitantly coordinates the removal of steroid-mediated RFRP inhibition of the gonadotropic axis to permit the surge. We found that the SCN forms close appositions with RFRP cells, suggesting the possibility for direct temporal control of RFRP activity. During the time of the LH surge, immediate-early gene expression is reduced in RFRP cells, and this temporal regulation is estrogen dependent. To determine whether projections from the SCN regulate the timed reduction in activation of the RFRP system, we exploited the phenomenon of splitting. In split animals in which the SCN are active in antiphase, activation of the RFRP system is asymmetrical. Importantly, this asymmetry is opposite to the state of the GnRH system. Together, these findings point to novel circadian control of the RFRP system and potential participation in the circuitry controlling ovulatory function.

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Cahill, David J., Peter G. Wardle, Christopher R. Harlow, and M. G. R. Hull. "Onset of the preovulatory luteinizing hormone surge: diurnal timing and critical follicular prerequisites." Fertility and Sterility 70, no. 1 (July 1998): 56–59. http://dx.doi.org/10.1016/s0015-0282(98)00113-7.

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HASHIMOTO, Inoru, Tsuyoshi OKUDAIRA, Atushi KANAYAMA, Kenichiro MUTOH, and Mitsumori KAWAMINAMI. "Preprogramming of luteal progestational function by preovulatory luteinizing hormone surge in cycling rats." Japanese journal of animal reproduction 36, no. 1 (1990): 41–53. http://dx.doi.org/10.1262/jrd1977.36.41.

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Williams, Wilbur P., Stephan G. Jarjisian, Jens D. Mikkelsen, and Lance J. Kriegsfeld. "Circadian Control of Kisspeptin and a Gated GnRH Response Mediate the Preovulatory Luteinizing Hormone Surge." Endocrinology 152, no. 2 (December 29, 2010): 595–606. http://dx.doi.org/10.1210/en.2010-0943.

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Abstract In spontaneously ovulating rodents, the preovulatory LH surge is initiated on the day of proestrus by a timed, stimulatory signal originating from the circadian clock in the suprachiasmatic nucleus (SCN). The present studies explored whether kisspeptin is part of the essential neural circuit linking the SCN to the GnRH system to stimulate ovulation in Syrian hamsters (Mesocricetus auratus). Kisspeptin neurons exhibit an estrogen-dependent, daily pattern of cellular activity consistent with a role in the circadian control of the LH surge. The SCN targets kisspeptin neurons via vasopressinergic (AVP), but not vasoactive intestinal polypeptide-ergic, projections. Because AVP administration can only stimulate the LH surge during a restricted time of day, we examined the possibility that the response to AVP is gated at the level of kisspeptin and/or GnRH neurons. Kisspeptin and GnRH activation were assessed after the administration of AVP during the morning (when AVP is incapable of initiating the LH surge) and the afternoon (when AVP injections stimulate the LH surge). Kisspeptin, but not GnRH, cellular activity was up-regulated after morning injections of AVP, suggesting that time-dependent sensitivity to SCN signaling is gated within GnRH but not kisspeptin neurons. In support of this possibility, we found that the GnRH system exhibits pronounced daily changes in sensitivity to kisspeptin stimulation, with maximal sensitivity in the afternoon. Together these studies reveal a novel mechanism of ovulatory control with interactions among the circadian system, kisspeptin signaling, and a GnRH gating mechanism of control.

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Peter, A. T., W. T. K. Bosu, and R. J. DeDecker. "Suppression of preovulatory luteinizing hormone surges in heifers after intrauterine infusions of Escherichia coli endotoxin." American Journal of Veterinary Research 50, no. 3 (March 1, 1989): 368–73. https://doi.org/10.2460/ajvr.1989.50.03.368.

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SUMMARY A study was conducted to test the hypothesis that high cortisol concentrations associated with products of infections (endotoxin) cause derangement in the neuroendocrine mechanism controlling ovulation in heifers. Eight Holstein heifers were given 2 injections of prostaglandin (pg), 11 days apart, to synchronize estrus. Starting from 25 hours after the second injection of pg (pg-2), the uterus of each heifer was infused with 5 ml of pyrogen-free water (control, n = 3) or Escherichia coli endotoxin (5 μg/kg of body weight) in 5 ml of pyrogen-free water (treated, n = 5), once every 6 hours for 10 treatments. Blood samples were obtained every 15 minutes via indwelling jugular catheter for an hour before and 2 hours after each infusion, then hourly until an hour before the next infusion. Ultrasonography of the ovaries was performed every 12 hours, starting 24 hours after pg-2 injection until 96 hours after pg-2 injection. Serum concentrations of luteinizing hormone and cortisol were determined by validated radioimmunoassays. Changes in cortisol concentrations were not detected in control heifers with preovulatory luteinizing hormone surges at 60 to 66 hours after pg-2 injection, followed by ovulations 72 to 96 hours after pg-2 was injected. None of the treated heifers ovulated, and the resulting follicular cysts (14 to 18 mm diameter) persisted for 7 to 21 days. In all treated heifers, serum cortisol concentrations increased (4- to 10-fold) during the first 2 hours after each infusion and then decreased gradually until the next infusion. Luteinizing hormone concentrations remained at baseline values throughout the treatment period in all treated heifers. These findings suggested that endotoxin-induced increases in cortisol concentrations during the preovulatory period of the estrous cycle prevented ovulations by blunting the preovulatory luteinizing hormone surges.

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Volk, Katrina M., Veronika V. Pogrebna, Jackson A. Roberts, Jennifer E. Zachry, Sarah N. Blythe, and Natalia Toporikova. "High-Fat, High-Sugar Diet Disrupts the Preovulatory Hormone Surge and Induces Cystic Ovaries in Cycling Female Rats." Journal of the Endocrine Society 1, no. 12 (November 2, 2017): 1488–505. http://dx.doi.org/10.1210/js.2017-00305.

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Abstract Diet-induced obesity has been associated with various metabolic and reproductive disorders, including polycystic ovary syndrome. However, the mechanisms by which obesity influences the reproductive system are still not fully known. Studies have suggested that impairments in hormone signaling are associated with the development of symptoms such as acyclicity and ovarian cysts. However, these studies have often failed to address how these hormonal changes arise and how they might contribute to the progression of reproductive diseases. In the present study, we used a high-fat, high-sugar (HFHS) diet to induce obesity in a female rodent model to determine the changes in critical reproductive hormones that might contribute to the development of irregular estrous cycling and reproductive cycle termination. The HFHS animals exhibited impaired estradiol, progesterone (P4), and luteinizing hormone (LH) surges before ovulation. The HFHS diet also resulted in altered basal levels of testosterone (T) and LH. Furthermore, alterations in the basal P4/T ratio correlated strongly with ovarian cyst formation in HFHS rats. Thus, this model provides a method to assess the underlying etiology of obesity-related reproductive dysfunction and to examine an acyclic reproductive phenotype as it develops.

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Kishi, Hisashi, Toshiyuki Okada, Satoko Kawazu, Mariko Otsuka, Kazuyoshi Taya, Gen Watanabe, and Shuji Sasamoto. "Effects of passive immunization against oestradiol-17β and inhibin on the secretion of gonadotrophin in the cyclic golden hamster (Mesocricetus auratus)." Reproduction, Fertility and Development 9, no. 4 (1997): 447. http://dx.doi.org/10.1071/r96076.

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To investigate the physiological importance of oestradiol-17b and inhibin in the regulation of gonadotrophin secretion in the cyclic golden hamster, females were passively immunized against two hormones. When 200 µL antiserum against oestradiol-17β (oestradiol-AS) was given on Day 3 (Day 1 = day of ovulation), the preovulatory gonadotrophin surge was completely blocked for 24 h and the length of the oestrous cycle was also prolonged for one day. In the group given 200µL oestradiol-AS on Day 3, basal levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) increased slightly and superovulation (19·6 ± 0·8, mean ± s.e.m.) occurred. When 200 µL antiserum against inhibin (inhibin-AS) was given at 1100 hours on Day 3, a dramatic increase in plasma FSH and a slight increase in LH were noted, resulting in superovulation (38·2 ± 2·6) on the expected Day 1. The present study indicates clearly that inhibin plays a major role in regulating the specific ovulation rate in the hamster through the control of FSH secretion. Present results also indicate that oestradiol-17β suppresses basal LH secretion. Oestradiol-17β may act as an indicator of the follicular maturation, and the high plasma concentration of oestradiol-17β noted from Day 3 to Day 4 may play an important role in determining the timing of initiation of the preovulatory gonadotrophin surge.

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Ziecik, A., J. E. Tilton, F. Espana, and R. Weigl. "Effect of Human Chorionic Gonadotropin on Preovulatory Luteinizing Hormone Surge and Ovarian Hormone Secretion in Gilts2." Journal of Animal Science 64, no. 4 (April 1, 1987): 1134–43. http://dx.doi.org/10.2527/jas1987.6441134x.

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Hall, J. E., A. E. Taylor, K. A. Martin, J. Rivier, D. A. Schoenfeld, and W. F. Crowley. "Decreased release of gonadotropin-releasing hormone during the preovulatory midcycle luteinizing hormone surge in normal women." Proceedings of the National Academy of Sciences 91, no. 15 (July 19, 1994): 6894–98. http://dx.doi.org/10.1073/pnas.91.15.6894.

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Fraser, Hamish M., and Philippe Bouchard. "Control of the preovulatory luteinizing hormone surge by gonadotropin-releasing hormone antagonists Prospects for clinical application." Trends in Endocrinology & Metabolism 5, no. 2 (March 1994): 87–93. http://dx.doi.org/10.1016/1043-2760(94)90007-8.

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Robertson, Jessica L., Donald K. Clifton, Horacio O. de la Iglesia, Robert A. Steiner, and Alexander S. Kauffman. "Circadian Regulation of Kiss1 Neurons: Implications for Timing the Preovulatory Gonadotropin-Releasing Hormone/Luteinizing Hormone Surge." Endocrinology 150, no. 8 (May 14, 2009): 3664–71. http://dx.doi.org/10.1210/en.2009-0247.

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Wallace, J. M., A. S. McNeilly, and D. T. Baird. "Induction of ovulation during anoestrus in two breeds of sheep with multiple injections of LH alone or in combination with FSH." Journal of Endocrinology 111, no. 1 (October 1986): 181–90. http://dx.doi.org/10.1677/joe.0.1110181.

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ABSTRACT The gonadotrophic requirements for the induction of ovulation and formation of a viable corpus luteum in two breeds of seasonally anoestrous sheep of differing fecundity was investigated. Welsh Mountain (n = 20) and Damline ewes (n = 19) were given LH or FSH either alone or in combination. Luteinizing hormone was injected i.v. at an increasing frequency for 72 h (one injection every 3 h for 24 h, one every 2 h for 24 h, and one every hour for 24 h) and FSH was injected in an identical manner for the first 36 h of treatment. Exogenous LH alone and in combination with FSH induced a preovulatory LH surge in all 19 ewes and ovulation in 18 out of 19 ewes of both breeds. However exogenous FSH alone was ineffective. The incidence of normal corpus luteum function in ewes induced to ovulate was low and not related to treatment, timing or magnitude of the LH/FSH surge. It is concluded that in both breeds studied (a) it is the infrequency of LH pulses which limits the development of preovulatory follicles during seasonal anoestrus, (b) that the requirement for FSH remains unknown, and (c) that the induction of inadequate corpora lutea during seasonal anoestrus reflects either defects in hormonal priming of the preovulatory follicle and/or inappropriate luteotrophic support after ovulation. J. Endocr. (1986) 111, 181–190

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Neal-Perry, Genevieve, Diane Lebesgue, Matthew Lederman, Jun Shu, Gail D. Zeevalk, and Anne M. Etgen. "The Excitatory Peptide Kisspeptin Restores the Luteinizing Hormone Surge and Modulates Amino Acid Neurotransmission in the Medial Preoptic Area of Middle-Aged Rats." Endocrinology 150, no. 8 (May 7, 2009): 3699–708. http://dx.doi.org/10.1210/en.2008-1667.

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Reproductive success depends on a robust and appropriately timed preovulatory LH surge. The LH surge, in turn, requires ovarian steroid modulation of GnRH neuron activation by the neuropeptide kisspeptin and glutamate and γ-aminobutyric acid (GABA) neurotransmission in the medial preoptic area (mPOA). Middle-aged females exhibit reduced excitation of GnRH neurons and attenuated LH surges under estrogen-positive feedback conditions, in part, due to increased GABA and decreased glutamate neurotransmission in the mPOA. This study tested the hypothesis that altered kisspeptin regulation by ovarian steroids plays a role in age-related LH surge dysfunction. We demonstrate that middle-aged rats exhibiting delayed and attenuated LH surges have reduced levels of Kiss1 mRNA in the anterior hypothalamus under estrogen-positive feedback conditions. Kisspeptin application directly into the mPOA rescues total LH release and the LH surge amplitude in middle-aged rats and increases glutamate and decreases GABA release to levels seen in the mPOA of young females. Moreover, the N-methyl-d-aspartate receptor antagonist MK801 blocks kisspeptin reinstatement of the LH surge. These observations suggest that age-related LH surge dysfunction results, in part, from reduced kisspeptin drive under estrogen-positive feedback conditions and that kisspeptin regulates GnRH/LH release, in part, through modulation of mPOA glutamate and GABA release.

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24

Cox, N. M., J. L. Ramirez, I. A. Matamoros, and W. A. Bennett. "Estrogen Induces Estrus Unaccompanied by a Preovulatory Surge in Luteinizing Hormone in Suckled Sows1." Biology of Reproduction 38, no. 3 (April 1, 1988): 592–96. http://dx.doi.org/10.1095/biolreprod38.3.592.

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Polkowska, Jolanta, and Franciszek Przekop. "The effect of corticotropin-releasing factor (CRF) on the gonadotropin hormone releasing hormone (GnRH) hypothalamic neuronal system during preovulatory period in the ewe." Acta Neurobiologiae Experimentalis 57, no. 2 (June 30, 1997): 91–99. http://dx.doi.org/10.55782/ane-1997-1216.

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Effects of infusions of corticotropin releasing factor (CRF) into the 3rd ventricle of the brain of ewes during the proestrus on the immunoreactive (ir) gonadotropin hormone releasing hormone (GnRH) neuronal system, pituitary luteinizing hormone(LH) producing cells and LH concentrations in the blood plasma were studied. None of the CRF-treated sheep displayed the estrous activity nor ovulated on the day of estrus (17th day of the cycle), and two days later when they were slaughtered. The GnRH center of CRF treated ewes situated in the preoptico-septal area was well organized, but irGnRH stores in the median eminence were low in comparison to the controls (sheep from the late follicular phase of the estrous cycle). The feature and the number of LH-cells in CRF-treated ewes were typical for the preovulatory phase of the cycle but the plasma concentrations of LH did not exceed basal levels. These results suggest that CRF induced decrease of irGnRH stores in the nerve terminals of the ME can be responsible for the blockade of the preovulatory surge of GnRH/LH in the sheep.

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26

Hoeger, Kathleen M., Lisa A. Kolp, Frank J. Strobl, and Johannes D. Veldhuis. "Evaluation of LH secretory dynamics during the rat proestrous LH surge." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 1 (January 1, 1999): R219—R225. http://dx.doi.org/10.1152/ajpregu.1999.276.1.r219.

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The preovulatory luteinizing hormone (LH) surge results from the integration of complex interactions among gonadal steroids and hypothalamic and pituitary hormones. To evaluate changes in LH secretory dynamics that occur during the rat LH surge, we have 1) obtained frequently sampled serum LH concentration time series, 2) used both waveform-dependent and waveform-independent convolution analyses, and 3) independently assessed proestrous LH half-life and basal non-gonadotropin-releasing hormone (GnRH)-dependent LH secretion during the LH surge. Waveform-independent pulse analysis revealed a 24-fold increase in the maximal pulsatile LH secretory rate attained during late proestrus compared with early proestrus. A 15-fold increase was quantified for the mean LH secretory rate. In complementary analyses, we applied a measured LH half-life of 17 ± 2.7 min and a median basal LH secretion rate of 0.0046 μg ⋅ l−1 ⋅ min−1 for convolution analysis, revealing a 16-fold increase in the mass of LH released/burst and more than sixfold rise in the amplitude of the secretory peaks. Evaluation of the approximate entropy of the LH surge profiles was performed, showing an increase in the orderliness of the LH release process during the surge. We conclude that both quantitative (mass/burst) and qualitative (approximate entropy) features of LH release are regulated during the proestrous LH surge.

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Tejada, Francisco, Asunción Cremades, Manuel Avilés, Maria T. Castells, and Rafael Peñafiel. "Hypokalemia alters sex hormone and gonadotropin levels: evidence that FSH may be required for luteinization." American Journal of Physiology-Endocrinology and Metabolism 275, no. 6 (December 1, 1998): E1037—E1045. http://dx.doi.org/10.1152/ajpendo.1998.275.6.e1037.

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Hypokalemia produced different effects on steroid sex hormone concentrations in plasma and ovary in the mouse. Estradiol levels were slightly increased, whereas circulating progesterone was markedly decreased in all estrous periods. The preovulatory surge of gonadotropins and the secondary surge of follicle-stimulating hormone (FSH) at estrus were also decreased, but basal levels of both gonadotropins were unaffected. Supplementation with luteinizing hormone (LH), FSH, or gonadotropin-releasing hormone (GnRH) at proestrus rapidly normalized plasma and ovarian progesterone levels at this stage of the estrous cycle. Plasma progesterone levels at diestrus were restored only by combined treatment, at the periovulatory stage, with LH and FSH or GnRH but not by LH or FSH alone. The results demonstrate a lack of steroidogenic activity in the corpus luteum of the potassium-deficient mice and, furthermore, that FSH plays an important role in luteinization in the hypokalemic mice. We conclude that alteration of the transcellular potassium gradient may affect the regulation of the periovulatory surge of gonadotropins and progesterone secretion, probably by altering the release of GnRH from the hypothalamus. In addition, the results suggest that FSH may play a certain role as a luteotropic hormone in mice.

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28

Marshall, Lorna A., Mary C. Martin, and Robert B. Jaffe. "Effect of preovulatory estradiol concentrations on luteinizing hormone diurnal secretory patterns: A hypothesis for the timing of the luteinizing hormone surge." American Journal of Obstetrics and Gynecology 159, no. 5 (November 1988): 1123–27. http://dx.doi.org/10.1016/0002-9378(88)90427-9.

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29

Taleisnik, S., B. Haymal, and L. Caligaris. "Intraventricular injection of agents that enhance cyclic adenosine monophosphate formation leads to inhibition of proestrous luteinizing hormone surge in rats." Acta Endocrinologica 129, no. 3 (September 1993): 273–78. http://dx.doi.org/10.1530/acta.0.1290273.

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The effect of increasing hypothalamic levels of 3′,5′-cyclic adenosine monophosphate (cAMP) on the preovulatory surge of luteinizing hormone (LH) and ovulation was studied in cycling rats. Animals bearing chronically implanted guiding cannulae into the third ventricle were injected with agents known to enhance the cellular levels of cAMP. Hourly blood samples from the unanesthetized, unrestrained rats were obtained between 11.00 and 1 7.00 h through a plastic cannula inserted into the jugular vein. Intraventricular injections of serotonin (7.5 mg/ml; 2 μl) in the morning of proestrous blocked the preovulatory surge of LH and ovulation. This effect was assigned to an increased neuronal level of cAMP because it was prevented by a serum anti-cAMP. Third-ventricle injections of 2 μl of forskolin (0.5 mmol/l), guanosine 5′-0-(3-thiotriphosphate) (2 mmol/l) or dibutyryl-cAMP (1 mmol/l) at 11.00 h on the day of proestrus mimicked the inhibitory effect of serotonin on the proestrous release of LH. It is suggested that serotonin inhibits LH surge by acting directly on LH-releasing hormone neurons and/or on neurons that provide inputs to these neurons involving cAMP as a second messenger. Neurons releasing γ-aminobutyric acid (GABA) may serve as interneurons sensitive to serotonin, as well as to cAMP, inasmuch as the inhibitory effect of forskolin on the release of LH was partially blocked by the GABA antagonists, picrotoxin and bicuculline.

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Clarkson, J., X. d'Anglemont de Tassigny, A. S. Moreno, W. H. Colledge, and A. E. Herbison. "Kisspeptin-GPR54 Signaling Is Essential for Preovulatory Gonadotropin-Releasing Hormone Neuron Activation and the Luteinizing Hormone Surge." Journal of Neuroscience 28, no. 35 (August 27, 2008): 8691–97. http://dx.doi.org/10.1523/jneurosci.1775-08.2008.

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31

Legan, S. J., K. M. Franklin, X. L. Peng, and M. J. Duncan. "Novel Wheel Running Blocks the Preovulatory Luteinizing Hormone Surge and Advances the Hamster Circadian Pacemaker." Journal of Biological Rhythms 25, no. 6 (December 2010): 450–59. http://dx.doi.org/10.1177/0748730410385648.

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32

Williams, Wilbur P., Stephan G. Jarjisian, Jens D. Mikkelsen, and Lance J. Kriegsfeld. "Circadian Control of Kisspeptin and a Gated GnRH Response Mediate the Preovulatory Luteinizing Hormone Surge." Endocrine Reviews 32, no. 1 (February 1, 2011): 153. http://dx.doi.org/10.1210/edrv.32.1.zef153.

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33

Williams, Wilbur P., Stephan G. Jarjisian, Jens D. Mikkelsen, and Lance J. Kriegsfeld. "Circadian Control of Kisspeptin and a Gated GnRH Response Mediate the Preovulatory Luteinizing Hormone Surge." Journal of Clinical Endocrinology & Metabolism 96, no. 2 (February 1, 2011): 556. http://dx.doi.org/10.1210/jcem.96.2.zeg556.

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34

Smith, J. T., S. M. Popa, D. K. Clifton, G. E. Hoffman, and R. A. Steiner. "Kiss1 Neurons in the Forebrain as Central Processors for Generating the Preovulatory Luteinizing Hormone Surge." Journal of Neuroscience 26, no. 25 (June 21, 2006): 6687–94. http://dx.doi.org/10.1523/jneurosci.1618-06.2006.

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35

González-Martínez, David, Christelle De Mees, Quentin Douhard, Claude Szpirer, and Julie Bakker. "Absence of Gonadotropin-Releasing Hormone 1 and Kiss1 Activation in α-Fetoprotein Knockout Mice: Prenatal Estrogens Defeminize the Potential to Show Preovulatory Luteinizing Hormone Surges." Endocrinology 149, no. 5 (January 17, 2008): 2333–40. http://dx.doi.org/10.1210/en.2007-1422.

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Sex differences in gonadal function are driven by either cyclical (females) or tonic (males) hypothalamic GnRH1 release and, subsequently, gonadotrophin (LH and FSH) secretion from the pituitary. This sex difference seems to depend on the perinatal actions of gonadal hormones on the hypothalamus. We used α-fetoprotein (AFP) knockout mice (Afp−/−) to study the mechanisms by which estrogens affect the sexual differentiation of the GnRH1 system. Afp−/− mice lack the protective actions of AFP against estrogens circulating during embryonic development, leading to infertility probably due to a hypothalamic dysfunction. Therefore, we first determined whether Afp−/− females are capable of showing a steroid-induced preovulatory LH surge by FOS/GnRH1 immunohistochemistry and RIA of plasma LH levels. Because the KISS1/GPR54 system is a key upstream regulator of the GnRH1 system as well as being sexually dimorphic, we also analyzed whether Kisspeptin-10 neurons were activated in Afp−/− mice after treatment with estradiol and progesterone. We found that the GnRH1 and Kisspeptin-10 neuronal systems are defeminized in Afp−/− females because they did not show either steroid-induced LH surges or significant FOS/GnRH1 double labeling. Furthermore, Kisspeptin-10 immunoreactivity and neural activation, measured by the number of double-labeled FOS/Kisspeptin-10 cells, were lower in Afp−/− females, suggesting a down-regulation of GnRH1 function. Thus, the sex difference in the ability to show preovulatory LH surges depends on the prenatal actions of estrogens in the male hypothalamus and, thus, is lost in Afp−/− females because they lack AFP to protect them against the defeminizing effects of estrogens during prenatal development.

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36

Porkka-Heiskanen, T., JH Urban, FW Turek, and JE Levine. "Gene expression in a subpopulation of luteinizing hormone-releasing hormone (LHRH) neurons prior to the preovulatory gonadotropin surge." Journal of Neuroscience 14, no. 9 (September 1, 1994): 5548–58. http://dx.doi.org/10.1523/jneurosci.14-09-05548.1994.

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37

Bittman, Eric L. "Circadian Function in Multiple Cell Types Is Necessary for Proper Timing of the Preovulatory LH Surge." Journal of Biological Rhythms 34, no. 6 (September 17, 2019): 622–33. http://dx.doi.org/10.1177/0748730419873511.

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The timing of the preovulatory surge of luteinizing hormone (LH), which occurs on the evening of proestrus in female mice, is determined by the circadian system. The identity of cells that control the phase of the LH surge is unclear: evidence supports a role of arginine vasopressin (AVP) cells of the suprachiasmatic nucleus (SCN), but it is not known whether vasopressinergic neurons are necessary or sufficient to account for circadian control of ovulation. Among other cell types, evidence also suggests important roles of circadian function of kisspeptin cells of the anteroventral periventricular nucleus (AvPV) and gonadotropin-releasing hormone (GnRH) neurons of the preoptic area (POA), whose discharge is immediately responsible for the discharge of LH from the anterior pituitary. The present studies used an ovariectomized, estradiol-treated preparation to determine critical cell types whose clock function is critical to the timing of LH secretion. As expected, the LH surge occurred at or shortly after ZT12 in control mice. In further confirmation of circadian control, the surge was advanced by 2 h in tau mutant animals. The timing of the surge was altered to varying degrees by conditional deletion of Bmal1 in AVPCre, KissCreBAC, and GnRHCreBAC mice. Excision of the mutant Cnsk1e (tau) allele in AVP neurons resulted in a reversion of the surge to the ZT12. Conditional deletion of Bmal1 in Kiss1 or GnRH neurons had no noticeable effect on locomotor rhythms, but targeting of AVP neurons produced variable effects on circadian period that did not always correspond to changes in the phase of LH secretion. The results indicate that circadian function in multiple cell types is necessary for proper timing of the LH surge.

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RAWLINGS, N. C., I. A. JEFFCOATE, W. D. CURRIE, and S. J. COOK. "CONTROL OF THE SURGE RELEASE OF LH AND FSH IN ESTRADIOL- AND PROGESTERONE-TREATED OVARIECTOMIZED EWES." Canadian Journal of Animal Science 68, no. 4 (December 1, 1988): 1089–96. http://dx.doi.org/10.4141/cjas88-124.

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Ovariectomized ewes were treated with silastic rubber implants releasing constant amounts of estradiol. During this time the ewes were treated with progesterone-releasing implants for 8–12 d, followed by a 5-d rest period and a second period of progesterone exposure of approximately 12 d duration. Following the first exposure to progesterone all ewes experienced a transient, but large release of LH and FSH from the pituitary, resembling that seen in intact ewes prior to ovulation (the so called preovulatory LH and FSH surges), but with amplitudes in the lower end of the range for the preovulatory surges in intact ewes. Following the second exposure to progesterone, the amplitudes of LH and FSH surges were reduced in most ewes. Altering mean progesterone levels between 0.9 ± 0.43 ng mL−1 and 2.2 ± 0.26 ng mL−1 in the second exposure did not affect the amplitude of LH or FSH surges, neither did altering estradiol levels from physiological to 4 × physiological. However, altering the temporal pattern of progesterone in both exposures from a sharp increase and decrease at either end of the period, to a more gradual increase and decrease, resembling the normal luteal phase of intact ewes, resulted in an increased amplitude of LH and FSH surges following the second exposure to progesterone. Key words: Ovariectomized ewe, luteinizing hormone, follicle-stimulating hormone, progesterone, estradiol

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39

Chandrasekhar, Yallampalli, and David T. Armstrong. "Effects of the antiandrogen hydroxyflutamide on progesterone secretion by preovulatory rat follicles in vivo and in vitro." Canadian Journal of Physiology and Pharmacology 69, no. 9 (September 1, 1991): 1288–93. http://dx.doi.org/10.1139/y91-189.

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Serum and ovarian progesterone levels and in vitro production of progesterone by preovulatory follicles were measured on proestrus in pregnant mare's serum gonadotropin (PMSG) primed immature rats in which the luteinizing hormone (LH) surge and ovulation were blocked by administration of the antiandrogen hydroxyflutamide. Serum progesterone levels observed at 12:00 on proestrus were significantly elevated, twofold above those observed in vehicle-treated controls, by in vivo administration of 5 mg hydroxyflutamide 4 h earlier. In control rats, proestrous progesterone did not increase until 16:00, in parallel with rising LH levels of the LH surge. No LH surge occurred in the hydroxyflutamide-treated rats, ovulation was blocked, and serum progesterone declined throughout the afternoon of proestrus, from the elevated levels present at 12:00. Administration of human chorionic gonadotropin (hCG) at 11:00 advanced the elevation of serum progesterone by 2 h in vehicle-treated controls and prevented the decline in progesterone levels in hydroxyfiutamide-treated rats. The patterns of change in ovarian tissue concentrations with time and treatment were essentially similar to those observed for serum progesterone. In in vitro experiments, progesterone secretion during 24 h culture of preovulatory follicles obtained on PMSG-induced proestrus was significantly increased, sixfold, by addition to the culture media of 370 μM but not of 37 μM hydroxyflutamide. Testosterone (50 nM) and hCG (20 mIU/mL) caused 26- and 14-fold increases, respectively, in progesterone secretion by cultured follicles. Hydroxyflutamide significantly reduced the stimulatory effect of testosterone but not of hCG on progesterone secretion in vitro. These results suggest that the antiandrogen hydroxyflutamide stimulates progesterone secretion, both in vivo and in vitro, through an initial androgen-agonistic action, before its antagonistic action is expressed. Its androgen-antagonistic action is responsible for its ability to inhibit testosterone-induced progesterone secretion in vitro. Its failure to reduce hCG-stimulated progesterone secretion in vivo and in vitro indicates that the latter stimulation is exerted independently of, and not as a consequence of, androgen action. The decrease in serum progesterone levels on the afternoon of proestrus therefore appears to be a consequence rather than a cause of the absence of an LH surge in the hydroxyflutamide-treated rats. It is concluded that the inhibitory effect of hydroxyflutamide on the preovulatory LH surge and ovulation is due not to inhibition of progesterone secretion at the ovarian level but most likely to neuroendocrine site(s) of action of the inhibitor.Key words: antiandrogen, hydroxyflutamide, progesterone, luteinizing hormone, ovulation, human chorionic gonadotropin.

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Choi, Hyeonhae, and Jaesook Roh. "Role of Klf4 in the Regulation of Apoptosis and Cell Cycle in Rat Granulosa Cells during the Periovulatory Period." International Journal of Molecular Sciences 20, no. 1 (December 26, 2018): 87. http://dx.doi.org/10.3390/ijms20010087.

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In the ovary, the luteinizing hormone (LH) surge suppresses the proliferation and induces the luteinization of preovulatory granulosa cells (GCs), which is crucial for the survival of terminally-differentiated GCs. Krüppel-like factor 4 (Klf4) has been shown to play a role in regulating the cell cycle and apoptosis in various cell types. The rapid induction of Klf4 expressions by LH was observed in preovulatory GCs. To evaluate whether Klf4 affects GC proliferation and survival, primary rat GCs were isolated from pregnant mare serum gonadotropin-primed Sprague–Dawley rat ovaries and transfected with a Klf4 expression vector or Klf4-specific siRNA, followed by determination of the transcript levels of apoptosis-related and cell cycle-related genes. Cell proliferation, viability, and apoptosis were analyzed by BrdU incorporation, a Cell Counting Kit-8 assay, a bioluminescence caspase 3/7 assay, and flow cytometry. LH treatment increased Klf4 mRNA expression in preovulatory GCs. Transcripts of B-cell lymphoma 2 (Bcl-2) and cell cycle promoters (Cyclin D1 and Cyclin D2) decreased, whereas those of the cell cycle inhibitor, p21, increased. Altering the expression of Klf4 by overexpression or knockdown consistently affected the expression of Bcl-2 and Cyclin D1. In agreement with this, Klf4 overexpression reduced cell viability, increased the fraction of apoptotic cells, and arrested cell cycle progression in G1 phase. We conclude that Klf4 increases the susceptibility of preovulatory GCs to apoptosis by down-regulating Bcl-2, and promotes LH-induced cell cycle exit. It appears to be a key regulator induced by the LH surge that determines the fate of GCs in preovulatory follicles during the luteal transition.

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Arai, Koji Y., Hisashi Kishi, Satoshi Onodera, Wanzhu Jin, Gen Watanabe, Akira K. Suzuki, Shinji Takahashi, Toshihiko Kamada, Toshio Nishiyama, and Kazuyoshi Taya. "Cyclic changes in messenger RNAs encoding inhibin/activin subunits in the ovary of the golden hamster (Mesocricetus auratus)." Journal of Endocrinology 185, no. 3 (June 2005): 561–75. http://dx.doi.org/10.1677/joe.1.06140.

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To elucidate changing patterns of inhibin/activin subunit mRNAs in the ovary of the golden hamster (Mesocricetus auratus) during the oestrous cycle, inhibin/activin subunit cDNAs of this species were cloned and ribonuclease protection assay and in situ hybridization were carried out. Inhibin α-subunit mRNA was localized in granulosa cells of primary, secondary, tertiary and atretic follicles throughout the 4-day oestrous cycle. It was also expressed in luteal cells on days 1 (oestrus), 2 (metoestrus) and 3 (dioestrus). βA-subunit mRNA was localized in granulosa cells of large secondary (>200 μm) and tertiary follicles throughout the oestrous cycle. βB-subunit mRNA was confined to granulosa cells of large secondary and tertiary follicles. Both α- and βA-subunit mRNAs were also found in ovarian interstitial cells and theca interna cells of tertiary and atretic follicles in the evening of day 4 (pro-oestrus). A striking increase in βA-subunit mRNA levels was also observed during the preovulatory period. The expression pattern of βA-subunit mRNA during the preovulatory period is unique and not found in other species. An i.v. injection of anti-luteinizing hormone-releasing hormone (LHRH) serum before the LH surge abolished the expression of α- and βA-subunit mRNAs in ovarian interstitial cells and theca interna cells. The treatment also abolished the preovulatory increase in βA-subunit mRNA. Furthermore, administration of human chorionic gonadotrophin (hCG), which followed the injection of anti-LHRH serum, restored the expression patterns of α- and βA-subunit mRNAs. The present study revealed that the golden hamster showed a unique expression pattern of βA-subunit mRNA in response to the LH surge.

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Kulvinder, Kochar Kaur. "A Posit that Luteinizing Hormone Independent Escalation of Progesterone Might be the Physiological Trigger for the Gonadotrophins Surge in Case of Human Menstrual Cycle." Open Access Journal of Gynecology 6, no. 3 (August 6, 2021): 1–11. http://dx.doi.org/10.23880/oajg-16000220.

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The present ovarian cycle model posits that ovulation gets triggered by a crucially maintained escalation of estradiol. Nevertheless, a deep probing of the published literature besides the work of team of Dozortev, Diamond along with Pellicer, more specifically Dozortev DI demonstrated significant doubt about the relative parts of progesterone as well as estradiol in the event of ovulation. Here proof provided by Dozortev DI’s work is presented that gives so much proof regarding the part played by estradiol has been misrepresented till the day, whereas the actual ovulation trigger is the Luteinizing hormone independent preovulatory progesterone surge in the circulation to about 0.5mg/ml. Moreover the recent work accommodates with the present work on the capacity of progesterone for ovulation trigger with its clearly proven capacity of blocking ovulation at the time of pregnancy, or when delivered in the kinds of synthetic progestins in the form of Oral contraceptive pills in addition to the experimental results with regards to estradiol benzoate stimulates ovulation in the lack of progesterone.

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Akema, Tatsuo, and Fukuko Kimura. "The mode of GABAB receptor-mediated inhibition of the preovulatory luteinizing hormone surge in female rats." Brain Research 562, no. 1 (October 1991): 169–72. http://dx.doi.org/10.1016/0006-8993(91)91203-d.

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Griesgraber, Max J., Kayla M. Onslow, Sydney Shuping, Elizabeth Bowdridge, Steven Hardy, Eliana Aerts, Lique Coolen, et al. "25 Role of Kndy and Arcuate Kiss1r-Containing Neurons in the Preovulatory Luteinizing Hormone Surge and Puberty Onset of Female sheep." Journal of Animal Science 101, Supplement_3 (November 6, 2023): 235–36. http://dx.doi.org/10.1093/jas/skad281.284.

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Abstract Neurons within the arcuate nucleus (ARC) of the hypothalamus containing kisspeptin, neurokinin B (NKB), and dynorphin (KNDy neurons) have an important role in regulating the pulsatile secretion of gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH). In sheep, kisspeptin neurons also contribute to the LH surge, as kisspeptin receptor (Kiss1r) antagonist administration reduces surge amplitude by 50% and KNDy neurons are likely involved, based on increased Fos expression at the time of the surge. However, the extent to which kisspeptin acts within the ARC regulate the GnRH/LH surge remains unclear. Thus, herein we tested the hypothesis that deletion of KNDy or ARC Kiss1r-containing neurons would impair the LH surge. Adult female sheep received bilateral injections targeting the ARC of NKB-saporin (NKB-SAP, n = 8), kisspeptin-saporin (Kiss-SAP, n = 10), or blank-saporin (Blank-SAP, n = 7) as a control. In other work, NKB-SAP lesioned over 90% of ovine KNDy neurons, while Kiss-SAP lesioned 67% of Kiss1r-containing cells without affecting KNDy or GnRH cell number. Ewes were also ovariectomized and a subcutaneous silastic estradiol (E2) implant was inserted at the time of neurosurgery. Two artificial luteal phases were simulated with progesterone-containing CIDRs, immediately followed by E2 treatment via implants to induce an LH surge. Blood samples were collected every two to four hours over two days and analyzed for LH via radioimmunoassay. LH surge amplitude in six of eight NKB-SAP ewes (49.5 ± 11.7 ng/mL) was significantly reduced compared with Blank-SAP control ewes (156.7 ± 20.2 ng/mL, p = 0.0001), a reduction similar to that produced by treatment with a Kiss1r antagonist. Nine of ten Kiss-SAP treated ewes displayed little to no increase of LH at the time of the expected surge (16.6 ± 5.3 ng/mL, p < 0.0001). Lesion effectiveness is currently being assessed by RNAscope, however all Kiss-SAP animals examined to date have significantly reduced ARC Kiss1r cell numbers except a single ewe which exhibited a normal LH surge. Based on these data, we propose that in ewes, KNDy neurons contribute to, but are not required for, the LH surge. In contrast, ARC Kiss1r-containing cells are essential for a functional LH surge. Given these results, we are currently assessing the role of ARC Kiss1r neurons in ovine puberty using a similar approach. Our data to date shows that time to puberty onset is similar for Kiss-SAP, Blank-SAP, and non-surgical control animals as measured by an increase in progesterone (p = 0.35). Blood samples to detect LH pulses and the LH surge are currently being analyzed, as are ARC Kiss1r cell numbers.

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Cassina, M. P., and J. D. Neill. "Gonadotropin-releasing hormone-induced desensitization may account for the decrease in pituitary responsiveness after the preovulatory luteinizing hormone surge." Endocrinology 137, no. 3 (March 1996): 1057–62. http://dx.doi.org/10.1210/endo.137.3.8603574.

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Leon, Silvia, and Víctor M. Navarro. "Novel Biology of Tachykinins in Gonadotropin-Releasing Hormone Secretion." Seminars in Reproductive Medicine 37, no. 03 (May 2019): 109–18. http://dx.doi.org/10.1055/s-0039-3400252.

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AbstractThe tachykinin family of peptides, composed of the neurokinins A and B (NKA, NKB) and substance P are involved in the central control of gonadotropin-releasing hormone (GnRH) release through a variety of neuronal circuitries that mediate the activation of Kiss1 neurons and the synchronization of their activity within the arcuate nucleus. The major outcome of this role is the precise regulation of the pulsatile pattern of GnRH release. In addition, tachykinins are involved in the maturation of the reproductive axis by determining the optimal timing of puberty onset, as well as in the timing of the preovulatory luteinizing hormone surge in females. Therefore, the action of tachykinins in reproduction appears to extend to all the critical aspects required for the successful attainment and maintenance of fertility. In this review, we summarize the latest advances in our understanding of the biology of tachykinins in the control of GnRH release, addressing the existing controversies, open questions, and future perspectives.

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Legan, Sandra J., Kathleen M. Donoghue, Kathleen M. Franklin, and Marilyn J. Duncan. "Phenobarbital blockade of the preovulatory luteinizing hormone surge: association with phase-advanced circadian clock and altered suprachiasmatic nucleus Period1 gene expression." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 5 (May 2009): R1620—R1630. http://dx.doi.org/10.1152/ajpregu.90914.2008.

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The suprachiasmatic nucleus (SCN) controls the timing of the preovulatory luteinizing hormone (LH) surge in laboratory rodents. Barbiturate administration during a critical period on proestrus delays the surge and prolongs the estrous cycle 1 day. Because a nonphotic timing signal (zeitgeber) during the critical period that phase advances activity rhythms can also induce the latter effect, we hypothesized that barbiturates delay the LH surge by phase-advancing its circadian timing signal beyond the critical period. In experiment 1, locomotor rhythms and estrous cycles were monitored in hamsters for 2–3 wk preinjection and postinjection of vehicle or phenobarbital and after transfer to darkness at zeitgeber time (ZT) 6 on proestrus. Phenobarbital delayed estrous cycles in five of seven hamsters, which exhibited phase shifts that averaged twofold greater than those exhibited by vehicle controls or phenobarbital-injected hamsters with normal cycles. Experiment 2 used a similar protocol, but injections were at ZT 5, and blood samples for LH determination were collected from 1200 to 1800 on proestrus and the next day via jugular cannulae inserted the day before proestrus. Phenobarbital delayed the LH surge 1 day in all six hamsters, but it occurred at an earlier circadian time, supporting the above hypothesis. Experiment 3 investigated whether phenobarbital, like other nonphotic zeitgebers, suppresses SCN Period1 and Period2 transcription. Two hours postinjection, phenobarbital decreased SCN expression of only Period1 mRNA, as determined by in situ hybridization. These results suggest that phenobarbital advances the SCN pacemaker, governing activity rhythms and hormone release in part by decreasing its Period1 gene expression.

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Tonellotto dos Santos, Joabel, Rogério Ferreira, Bernardo Garziera Gasperin, Lucas Carvalho Siqueira, João Francisco de Oliveira, Robson AS Santos, Adelina M. Reis, and Paulo Bayard Gonçalves. "Molecular characterization and regulation of the angiotensin-converting enzyme type 2/Angiotensin-(1-7)/MAS receptor axis during the ovulation process in cattle." Journal of the Renin-Angiotensin-Aldosterone System 13, no. 1 (August 8, 2011): 91–98. http://dx.doi.org/10.1177/1470320311417273.

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The objective of this study was to characterize the profiles of Ang-(1-7), MAS receptor, ACE2, NEP and PEP during the ovulatory process in cattle. For this study, 40 synchronized cows with follicular diameter ≥ 12 mm were ovariectomized at different time-points (0, 3, 6, 12 and 24 h) after i.m. application of gonadotropin-releasing hormone (GnRH) to induce a luteinizing hormone surge. Follicular fluid was collected for measuring Ang-(1-7) by radioimmunoassay. Theca and granulosa cells were isolated from the preovulatory follicles to evaluate the gene expression of MAS receptor, ACE2, NEP and PEP by qRT-PCR assay. Cross-contamination between theca and granulosa cells was tested by RT-PCR to detect cytochrome P450 aromatase (CYP19A1) and 17α-hydroxylase (CYP17A1) mRNA. Ang-(1-7) levels were constant until 12 h and then increased ( p < 0.05) at 24 h after GnRH. Messenger RNA expression of MAS, ACE2, NEP and PEP was detected in theca and granulosa cells at all time-points after GnRH. In granulosa cells, ACE2, NEP and PEP were differentially expressed after GnRH treatment ( p < 0.05). In conclusion, the Ang-(1-7), MAS receptor, ACE2, NEP and PEP profiles in preovulatory follicles indicate that Ang-(1-7) plays a role in the regulation of the ovulatory process in cattle.

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Cheng, Xiaobing B., Mark Jimenez, Reena Desai, Linda J. Middleton, Shai R. Joseph, Guang Ning, Charles M. Allan, Jeremy T. Smith, David J. Handelsman, and Kirsty A. Walters. "Characterizing the neuroendocrine and ovarian defects of androgen receptor-knockout female mice." American Journal of Physiology-Endocrinology and Metabolism 305, no. 6 (September 15, 2013): E717—E726. http://dx.doi.org/10.1152/ajpendo.00263.2013.

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Homozygous androgen receptor (AR)-knockout (ARKO) female mice are subfertile due to both intra- and extraovarian (neuroendocrine) defects as defined by ovary transplantation. Using ARKO mice, this study set out to reveal the precise AR-regulated pathways required for optimal androgen-regulated ovulation and fertility. ARKO females exhibit deficient neuroendocrine negative feedback, with a reduced serum luteinizing hormone (LH) response to ovariectomy (OVX) ( P < 0.01). Positive feedback is also altered as intact ARKO females, at late proestrus, exhibit an often mistimed endogenous ovulatory LH surge. Furthermore, at late proestrus, intact ARKO females display diminished preovulatory serum estradiol (E2; P < 0.01) and LH ( P < 0.05) surge levels and reduced Kiss1 mRNA expression in the anteroventral periventricular nucleus ( P < 0.01) compared with controls. However, this reduced ovulatory LH response in intact ARKO females can be rescued by OVX and E2 priming or treatment with endogenous GnRH. These findings reveal that AR regulates the negative feedback response to E2, E2-positive feedback is compromised in ARKO mice, and AR-regulated negative and positive steroidal feedback pathways impact on intrahypothalamic control of the kisspeptin/GnRH/LH cascade. In addition, intraovarian AR-regulated pathways controlling antral to preovulatory follicle dynamics are disrupted because adult ARKO ovaries collected at proestrus have small antral follicles with reduced oocyte/follicle diameter ratios ( P < 0.01) and increased proportions of unhealthy large antral follicles ( P < 0.05) compared with controls. As a consequence of aberrant follicular growth patterns, proestrus ARKO ovaries also exhibit fewer preovulatory follicle ( P < 0.05) and corpora lutea numbers ( P < 0.01). However, embryo development to the blastocyst stage is unchanged in ARKO females, and hence, the subfertility is a consequence of reduced ovulations and not altered embryo quality. These findings reveal that the AR has a functional role in neuroendocrine regulation and timing of the ovulatory LH surge as well as antral/preovulatory follicle development.

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Park, Ok-Kyong, and Kelly E. Mayo. "Transient Expression of Progesterone Receptor Messenger RNA in Ovarian Granuiosa Cells after the Preovulatory Luteinizing Hormone Surge." Molecular Endocrinology 5, no. 7 (July 1991): 967–78. http://dx.doi.org/10.1210/mend-5-7-967.

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Journal articles on the topic 'Preovulatory luteinizing hormone surge'

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