• Clinical and Experimental Reproductive Medicine
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• v.44 no.2
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• pp.57-62
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• 2017

The purpose of this paper is to assimilate all data pertaining to the use of gonadotropin-releasing hormone (GnRH) antagonists in in vitro fertilization cycles after ovulation trigger to reduce the symptoms of ovarian hyperstimulation syndrome (OHSS). A systematic review of the literature was performed to identify all studies performed on the use of a GnRH antagonist in IVF cycle post-ovulation trigger with patients at high risk for OHSS. Ten studies were identified and reviewed. Descriptions of the studies and their individual results are presented in the following manuscript. Due to significant heterogeneity among the studies, it was not possible to perform a group analysis. The use of GnRH antagonists post-ovulation trigger for treatment of OHSS has been considered for almost 20 years, though research into its use is sparse. Definitive conclusions and recommendations cannot be made at this time, though preliminary data from these trials demonstrate the potential for GnRH antagonists to play a role in the treatment of OHSS in certain patient populations.

• Journal of Embryo Transfer
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• v.12 no.1
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• pp.117-122
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• 1997

The objective of this study was to enhance the pregnancy rate of repeat-breeder Hanwoo with gonadotropin-releasing hormone(Gn-RH) at the time, dose and site of administration.The results obtained were summaried as fallows:1.Ovulation time and pregnancy rate following GnRH administration time was 46.0, 27.4, 42.0 and 43.2hr and 33.3, 57.1, 37.5 and 40.0% at non-treatment, estus, 1st A' and 2nd Al treatment, respectively.2. Ovulation in repeat-breeder was induced 100% within 24hr with GnRH administration at the time of estrus.3. Ovulation time and pregnancy rate following GnRH adminstration dose and site was 25.2, 32.6, 17.6 and 27.6hr, and 28.6, 42.9, 75.0 and 66.7% at 50$\mu$g+IU, 50$\mu$g+IM, 100$\mu$g+IU and 100$\mu$g+IM treatments, respectively. It is concluded that GnRH administration for repeat-breeder was enhanced the pregnancy rate when treated with 100$\mu$g intrauterine at the time of estrus.

• Korean Journal of Veterinary Research
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• v.21 no.1
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• pp.59-64
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• 1981

Holstein-Friesian cows(n=284) were given $100{\mu}g$ of gonadotropin-releasing hormone(GnRH) or saline solution by intramuscular injection at 10 to 22 days after parturition, and were investigated their reproductive performance and frequency of ovarian cysts. Among them 28 cystic cows were injected with $150{\mu}g$ of GnRH intramuscularly and examined the recovery rate. The results obtained in this study were summarized as follows: 1. The interval from calving to 1st ovulation was reduced from 28.2 days in controls to 16.5 days for cows given GnRH (p<0.01). 2. The intervals from calving to 1st estrus and from calving to conception were extended significantly in control group (p<0.05). 3. Inseminations per conception and conception rate at 1st insemination did not reveal difference between two groups. 4. Frequency of ovarian cysts was reduced from 14.0% in control to 4.20% for cows given GnRH (p<0.05). 5. Of the 28 cystic cows receiving $150{\mu}g$ of GnRH, 23(82.1%) responded to 1st treatment and returned to estrus $24.2{\pm}4.3$ days after treatment. 6. These data provide evidence for reduction in infertility and reproductive disorders in early postpartum dairy cows given GnRH as a prophylactic.

• Journal of Ginseng Research
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• v.36 no.1
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• pp.47-54
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• 2012

Korean red ginseng (KRG) has been used worldwide as a traditional medicine for the treatment of various reproductive diseases. Gonadotropin releasing hormone (GnRH) neurons are the fundamental regulators of pulsatile release of gonadotropin required for fertility. In this study, an extract of KRG (KRGE) was applied to GnRH neurons to identify the receptors activated by KRGE. The brain slice patch clamp technique in whole cell and perforated patch was used to clarify the effect of KRGE on the membrane currents and membrane potentials of GnRH neurons. Application of KRGE (3 ${\mu}g$/${\mu}L$) under whole cell patch induced remarkable inward currents (56.17${\pm}$7.45 pA, n=25) and depolarization (12.91${\pm}$3.80 mV, n=4) in GnRH neurons under high $Cl^-$ pipette solution condition. These inward currents were not only reproducible, but also concentration dependent. In addition, inward currents and depolarization induced by KRGE persisted in the presence of the voltage gated $Na^+$ channel blocker tetrodotoxin (TTX), suggesting that the responses by KRGE were postsynaptic events. Application of KRGE under the gramicidin perforated patch induced depolarization in the presence of TTX suggesting its physiological significance on GnRH response. Further, the KRGE-induced inward currents were partially blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; non-NMDA glutamate receptor antagonist, 10 ${\mu}M$) or picrotoxin (PIC; $GABA_A$ receptor antagonist, 50 ${\mu}M$), and almost blocked by PIC and CNQX mixture. Taken together, these results suggest that KRGE contains ingredients with possible GABA and non-NMDA glutamate receptor mimetic activity, and may play an important role in the endocrine function of reproductive physiology, via activation of $GABA_A$ and non-NMDA glutamate receptors in GnRH neurons.

• 대한생식의학회:학술대회논문집
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• 1996.06a
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• pp.40-57
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• 1996

• 대한생식의학회:학술대회논문집
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• 2007.06a
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• pp.95-102
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• 2007

• Fisheries and Aquatic Sciences
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• v.14 no.4
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• pp.379-388
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• 2011

The mechanism by which gonadotropin-releasing hormone (GnRH) and dopamine (DA) control gonadotropin (GTH) release was studied in male and female rainbow trout using cultured pituitary cells obtained at different reproductive stages. The mechanisms of follicle-stimulating hormone (FSH) release by GnRH and DA could not be determined yet. However, basal and salmon-type GnRH (sGnRH)- or chicken-II-type GnRH (cGnRH-II)- induced luteinizing hormone (LH) release increased with gonadal maturation in both sexes. LH release activity was higher after sGnRH stimulation than cGnRH-II stimulation at maturing stages in both sexes. The GnRH antagonist ([Ac-3, 4-dehydro-$Pro^1$, D-p-F-$Phe^2$, D-$Trp^{3,6}$] GnRH) suppressed LH release by sGnRH stimulation in a dose-dependent manner, although the effect was weak in maturing fish. The role of DA as a GTH-release inhibitory factor differs during the reproductive cycle: the inhibition of sGnRH-stimulated LH release by DA was stronger in immature fish than in maturing, ovulating, or spermiated fish. DA did not completely inhibit sGnRH-stimulated LH release, and DA alone did not alter basal LH release. Relatively high doses ($10^{-6}$ or $10^{-5}M$) of domperidone (DOM, a DA D2 antagonist) increased LH release, which did not change with reproductive stage in either sex. The potency of DOM to enhance sGnRH-stimulated LH release was higher in maturing and ovulated fish than in immature fish. These data suggest that LH release from the pituitary gland is controlled by dual neuroendocrine mechanisms by GnRH and DA in rainbow trout, as has been reported in other teleosts. The mechanism of control of FSH release, however, remains unknown.

• Animal cells and systems
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• v.5 no.3
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• pp.217-224
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• 2001

The present study examines the expression and regulation of gonadotropin-releasing hormone (GnRH) and its receptor (GnRH-R) mRNA levels during mouse ovarian development. A fully processed, mature GnRH mRNA together with intron-containing primary transcripts was expressed in the immature mouse ovary as determined by Northern blot analysis and reverse transcription-polymerase chain reaction (RT-PCR). The size of ovarian GnRH mRNA was similar to that of hypothalamus, but its amount was much lower than that in the hypothalamus. Quantitative RT-PCR procedure also revealed the expression of GnRH-R mRNA in the ovary, but the estimated amount was a thousand-fold lower than that in the pituitary gland. We also examined the regulation of ovarian GnRH and GnRH-R mRNA levels during the follicular development induced by pregnant mare's serum gonadotropin (PMSG) and/or human chorionic gonadotropin (hCG). Ovarian luteinizing hormone receptor (LH-R) mRNA was abruptly increased st 48 h after the PMSG administration and rapidly decreased to the basal level thereafter. Ovarian GnRH mRNA level was slightly decreased at 48 h after the PMSG administration, and then returned to the basal value. GnRH-R mRNA level began to increase at 24 h after the PMSG treatment, decreased below the uninduced basal level at 48 h, and gradually increased thereafter. HCG administration did not alter ovarian GnRH mRNA level, while it blocked the PMSG-induced increase in GnRH mRNA level. Taken together, the present study demonstrates that the expression of GnRH and GnRH-R mRNA are regulated by gonadotropin during follicular development, suggesting possible intragonadal paracrine roles of GnRH and GnRH-R in the mouse ovarian development.

• Animal cells and systems
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• v.11 no.2
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• pp.93-98
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• 2007

Gonadotropin-releasing hormone (GnRH), synthesized in the hypothalamus, plays a pivotal role in the regulation of vertebrate reproduction. Since molecular isoforms of GnRH and their receptors (GnRHR) have been isolated in a broad range of vertebrate species, GnRH and GnRHR provide an excellent model for understanding the molecular co-evolution of a peptide ligand-receptor pair. Vertebrate species possess multiple forms of GnRH, which have been created through evolutionary mechanisms such as gene/chromosome duplication, gene deletion and modification. Similar to GnRHs, GnRH receptors (GnRHR) have also been diversified evolutionarily. Comparative ligand-receptor interaction studies for non-mammalian and mammalian GnRHRs combined with mutational mapping studies of GnRHRs have aided the identification of domains or motifs responsible for ligand binding and receptor activation. Here we discuss the molecular basis of GnRH-GnRHR co-evolution, particularly the structure-function relationship regarding ligand selectivity and signal transduction of mammalian and non-mammalian GnRHRs.

• Clinical and Experimental Pediatrics
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• v.55 no.1
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• pp.6-10
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• 2012

Human puberty is a complex, coordinated biological process with multiple levels of regulations. The timing of puberty varies greatly in children and is influenced by both environmental and genetic factors. The key genes of pubertal onset, $KISS1$, $GPR54$, $GNRH1$ and $GNRHR$, may be major causal factors underlying gonadotropin-releasing hormone-dependent precocious puberty (GDPP). Two gain-of-function mutations in $KISS1$ and $GPR54$ have been identified recently as genetic causes of GDPP. $GNRH1$ and $GNRHR$ are also gene candidates for GDPP; however no mutations have been identified in these genes. Presently potential genetic causes like $LIN28B$ continues to appear; many areas of research await exploration in this context. In this review, I focus primarily on the genetic causes of GDPP.