• Animal cells and systems
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• v.13 no.4
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• pp.429-437
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• 2009

The control mechanism of gonadotropin-releasing hormone (GnRH) on gonadotropin (GTH) release was studied using cultured pituitary cell or cultured whole pituitary obtained from Testosterone (T) treated and control immature rainbow trout. The release of FSH was not changed by salmon type GnRH (sGnRH), chiken-II type (cGnRH-II), GnRH analogue ([des-$Gly^{10}D-Ala^6$] GnRH ethylamide) and GnRH antagonist ([Ac-3, 4-dehydro-$Pro^1$, D-p-F-$Phe^2$, D-$Trp^{3,6}$] GnRH) in cultured pituitary cells of T-treated and control fish. Indeed, FSH release was not also altered by sGnRH in cultured whole pituitary. All tested drugs had no effect on the release of LH in both culture systems of control fish. The levels of LH, in contrast, such as the pituitary content, basal release and responsiveness to GnRH were increased by T administration in both culture systems. In addition, the release of LH in response to sGnRH or cGnRH-II induced in a dose-dependent manner from cultured pituitary cells of T-treated fish, but which is not significantly different between in both GnRH at the concentration examined. Indeed, LH release was also increased by sGnRH in cultured whole pituitary of T-treated fish. GnRH antagonist suppressed the release of LH by sGnRH ($10^{-8}\;M$) and GnRH analogue ($10^{-8}\;M$) stimulation in a dose-dependent manner from cultured pituitary cells of T-treated fish, and which were totally inhibited by $10^{-7}\;M$ GnRH antagonist. These results indicate that the sensitivity of pituitary cells to GnRH is elevated probably through the T treatment, and that GnRH is involved in the regulation of LH release. GnRH-stimulated LH release is inhibited by GnRH antagonist in a dose-dependent manner. The effects of gonadal steroids on FSH levels are less clear.

• 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.

• Animal cells and systems
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• v.3 no.1
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• pp.1-7
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• 1999

Gonadotropin-releasing hormone (GnRH) was originally isolated as a hypothalamic peptide that regulates reproduction by stimulating the release of gonadotropins. Using comparative animal models has led to the discovery that GnRH has a more ancient evolutionary origin. Durinq evolution GnRH peptide underwent gene duplication and structural changes to give rise to multiple molecular forms of GnRHs. Mammalian GnRH initially considered to be the sole molecular form, is now grouped as a family of peptides along with GnRH variants determined from representatives in all classes of vertebrates. Vertebrate species including primates and humanshave more than one GnRH variant in individual brains; a unique GnRH form in the forebrain and chicken IIGnRH in the midbrain. Furthermore, several species of bony fish have three molecular variants of GnRH: salmon GnRH sea-bream GnRH and chicken II GnRH. Also, it has been shown that in addition to the olfactory placodes and the midbrain, there is a third embryonic source of GnRH neurons from the basal diencephalon in birds and fish, which might be true for other vertebrates. Therefore, comparative animal models like fish with discrete sites of expression of three molecular variants of GnRH in individual brains, could provide insight into novel functions of GnRH variants, conservation of gene regulation, and mechanisms governing reproduction in vertebrates.

• Korean Journal of Veterinary Research
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• v.39 no.2
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• pp.276-286
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• 1999

In the present study, to understand how gonadotropin-releasing hormone (GnRH) affects ovarian functions in superovulated rats, we examined the effects of GnRH agonist on the ovulatory response, the morphological normality and nuclear maturation of ovulated oocytes, the ovarian weight, the ovarian histology, and the circulating steroid hormone ($17{\beta}$-estradiol, progesterone and testosterone) levels in immature rats pretreated with 30IU pregnant mare serum gonadotropin (PMSG) and supplemented with 10IU human chorionic gonadotropin(hCG). GnRH agonist was intravenously injected via jugular vein catheter every 20min for 4hrs in early follicular phase (from 6hr after PMSG) of superovulated rats. In addition, GnRH antagonist, Antide, was intravenously injected in combination with GnRH agonist to verify the effects of GnRH agonist on ovarian functions. All animals were sacrificed at 72hr after PMSG administration. The administration with GnRH agonist in early follicular phase of superovulated rats caused inhibition of ovulatory response, increased the proportion of abnormal appearing oocytes(especially, in the rats of the group treated with 500ng GnRH agonist), decreased ovarian weight and promote follicular atresia, compared to those from the rats of control regimen that were not treated with GnRH agonist. In addition, the treatment with GnRH agonist in the superovulated rat distinctly decreased serum steroid hormone ($17{\beta}$-estradiol, progesterone and testosterone) levels in preovulatory phase. On the other hand, the inhibitory effects of GnRH agonist treatment in superovulation-pretreated rats on ovarian functions were totally reversed by the combination with GnRH antagonist, Antide. The nuclear maturation of oocytes recovered from the oviducts in immature rats treated with GnRH agonist and/or GnRH antagonist was characterized by prematurity and asynchronization in early follicular phase, which was similar to control group. The overall results of this study indicate that GnRH agonist disturbs directly ovarian function in early follicular phase of superovulated immature rats in terms of ovulatory response and morphological normality of ovulated oocytes. This concept has been further evidenced by the findings of a great decrease in ovarian weight, a marked increase in follicular and a distinct decrease circulating steroid hormone ($17{\beta}$-estradiol, progesterone and testosterone) levels in GnRH agonist treatment regimen in early follicular phase.

• Fisheries and Aquatic Sciences
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• v.3 no.1
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• pp.37-43
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• 2000

We used a mammalian GnRH antagonist, $[Ac-3,4-dehydro-Pro^1,\;D-p-F-Phe^2,\;D-Trp^{3.6}]$-GnRH, to examine the details of the salmon type gonadotropin-releasing hormone (sGnRH) and GnRH agonist analog $(Des-Gly^{10}$[d-Ala^6]-ethylamide GnRH; GnRHa) functions in the control of maturational gonadotropin (GTH II) secretion, in precocious male rainbow trout, in both in vivo and in vitro experiments. In the in vivo study, plasma GTH II levels increased by sGnRH or GnRHa treatment, but the response was more rapid and stronger in the GnRHa treatment group. The increase in GTH II was significantly suppressed by the GnRH antagonist, while the antagonist had no effect on basal GTH II levels in both groups. The GnRH antagonist showed stronger suppression of GTH II levels in the sGnRH treatment fish than in the GnRHa treatment fish. In addition, plasma androgenic steroid hormones (testosterone and 11-ketotestosterone) increased by the sGnRH or GnRHa treatment. The GnRH antagonist significantly inhibited the increases in plasma androgenic steroid hormone levels stimulated by the sGnRH or GnRHa, while the antagonist had no effect on basal androgenic steroid hormone levels in both groups. In the in vitro study, treatment with sGnRH or GnRHa increased GTH II release from the cultured dispersed pituitary cells, but the response was stronger in the GnRHa treatment group. The increase in GTH II release by GnRH was suppressed by adding the GnRH antagonist, dose­dependently. On the other hand, basal release of GTH II did not decrease by the GnRH antagonist treatment in both groups. These results suggest that the GnRH antagonist, $[Ac-3,4-dehydro-Pro^1,\;D-p-F-Phe^2,\;D-Trp^{3.6}]-GnRH$, used in this study is effective in blocking the action of GnRH-induced GTH II release from the pituitary gland both in vivo and in vitro.

• The Korean Journal of Zoology
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• v.34 no.4
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• pp.491-499
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• 1991

The present experiment was carried out 1) to study the developmental topography of GnRH neuronal system and 2) to characterize the cellular localization of GnRH neurons in the prenatal brain development of the rat. At embryonic day (I) 14.5, immunoreactive cell bodies of GnRH were first seen in the nasal septum and in the ganglion terminate located in the ventral protion of the caudal olfactory bulb. Two days later (E 16.5), GnRH-containing neurons were observed at the level of olfactory tubercle and diagonal band of Broca, which is the first appearance in the intracerebral region. From 118.5, the topographic pattern of immunoreactive GnRH perikarya was similar to that of adult rats. The present data suggest that GnRH neurons were originated from the nasal septum and gradually extended to the hvpothalamic regions with increasing fetal age.

• 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 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.

• Korean Journal of Veterinary Research
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• v.57 no.3
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• pp.155-158
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• 2017

Surgical castration performed to reduce male-associated problems results in pain and microbial infections in male animals. Therefore, immunocontraception, which is mediated by the animal's own antibodies against reproductive hormones, has been recommended as an alternative to surgical castration when considering the animal's welfare. In this study, a new immunocontraceptive vaccine composed of six tandem copies of gonadotropin-releasing hormone (GnRH) fused to rat granulocyte-macrophage colony-stimulating factor (GM-CSF) was developed, and its efficacy was evaluated in male rats. Three different doses (10, 50, and $100{\mu}g$) of recombinant GM-CSF-GnRH protein were injected three times at intervals of two weeks into male rats. The rats vaccinated with three doses of GM-CSF-GnRH produced a significantly higher level of antibodies against GnRH than that in the negative control rats. Severe atrophy of gonads was observed in rats vaccinated with three doses of GM-CSF-GnRH but not in the negative control rats. The results reveal that the new GnRH vaccine conjugated with rat GM-CSF induces efficient immunocontraception in male rats. This formulation of the immunocontraceptive vaccine would be applicable to both domestic and pet male animals.

• Korean Journal of Veterinary Research
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• v.57 no.1
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• pp.23-29
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• 2017

This study investigated the effects of gonadotropin-releasing hormone (GnRH) vaccine on pig growth, carcass quality, and sensory perceptions of pork meat by Thai consumers. Male crossbred pigs (n = 30) were separated into three groups of 10 pigs each: boars, immunocastrated pigs, and surgically castrated pigs. The immunocastrated group was immunized at 13 and 19 weeks of age with GnRH vaccine ($400{\mu}g/dose$). All pigs were slaughtered at 24 weeks of age. Blood samples were collected and testes size determined. Testes weight and back fat thickness were recorded at the time of slaughter, and meat samples were collected for sensory assessment by Thai consumers. Testosterone and progesterone concentration levels decreased significantly two weeks after the second dose of GnRH (p < 0.05), and the GnRH antibody titer of the immunocastrated pigs was significantly high two weeks after the second dose of GnRH (p < 0.05). GnRH vaccine significantly reduced the weight and size of testes. Thai consumers reported no significant differences in odor or flavor among meat samples from the three groups. In conclusion, immunocastration improved growth performance, removed the need for castration surgery, and avoided "boar taint" in the meat. It has also no distinct trace of the boar taint same as pork that is currently produced from physically castrated pig which is making it acceptable to consumers.