• Journal of Aquaculture
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• v.11 no.4
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• pp.513-519
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• 1998

Ovulation of maturing femal mandarin fish, Siniperca scherzeri was induced using single injection of human chorionic gonadotropin (HCG) or gonadotropin releasing hormone-analogue (GnRH-a), GnRH-a plus prostaglandin F2 (PG$F_2$) or GnRH-a plus pimozide. The response was evaluated by fertilization, embryo-formation and hatching rate after insemination. Those rates were generally higher in GnRH-a group than in HCG group. The higher hatching rat of above 89% was achived using a dosage of 5,000 IU/kg HCG plus 10 ${\mu}$g/kg GnRH-a, 10${\mu}$g/kg GnRH-a plus 500 ng/kg PGF2, and 10 ug/kg GnRH-a plus 1-5 mg/kg pimozide. Ovulation was induced in all female injected with sex-maturation hormones and stimulator, but blocked in female injected with HCG plus GnRH-a plus dopamine combination, and GnRH-a plus PGF2 plus indometacin combination. These results show that the mandarin fish in spawning period secrete a sex-mutruation assosiated hormones and gonadotropin-releasing -inhibiting factor(GRIF).

• 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.

• Development and Reproduction
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• v.5 no.1
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• pp.81-88
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• 2001

Gonadotropin-releasing hormone (GnRH) has been known to play a role in the regulation of hCG secretion by human placenta. Recently, a gene encoding the second f개m of GnRH (GnRH-II) was identified in human. Herein, we demonstrate that GnRH-II is expressed in human placenta and assess GnRH-II expression by nested RT-PCR and immunohistochemistry in human placenta during the first trimester. We found that two altematively spliced transcripts of GnW-II mRNA were expressed in human placental tissues of first trimester and the shorter variant had a 21-bp deletion in GnRH-associated peptide (GAP). Immunoreactive GnRH-II was localized in both cytotrophoblastic and syncytiotrophoblastic cytoplasm. The immunostaining intensity was stronger in cytotrophoblast. Villous stromal cells also showed GnRH-II immunoreactiyiry. The results of our study report that the second isoform of GnRH (GnRH-II) is expressed in the first trimester human placenta and we suggest that GnRH-II may also play a regulatory role in maintenance of early pregnancy and hCG secretion in human placenta.

• 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.

• The Korean Journal of Zoology
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• v.33 no.4
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• pp.435-445
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• 1990

Gonadotropin releasing horrnone (GnRH) is known to be extrahypothalamically localized with a broad range including gonad. It remains, however, unknown whether GnRH is locally synthesized in the gonad. The present srudy aims to identity expression and cellular localization of GnRH-Iike mRNA and immunoreactive GnRH in the rat gonad. GnRH radioimmunoassay and chromatographic extracts on G-50 sephadex column showed that rat gonadal extracts contained a substantial amount of immunoreactive GnRH similar to the hypothalamic and synthetic GnRH. Although a wide distribution of immunostainable GnRH-like molecule with different cell types in the rat ovary was observed, the major cell population hybridized with GnRH probe appears to be granulosa. theca cells and corpus luteum. Immunoreactive GnRH-Iike peptides were distributed m various regions of testis, including spermatogenic cells, Sertoli cells and Leydig cells. In situ hybridization revealed that positive signals of GnRH-Iike mRNA were predominandy present in Sertoli cells within some seminiferous tubules, but absent in the outside of seminiferous tubules in the testis. This study clearly demonstrated that GnRH-Iike molecule present in the rat gonad may be resulted from the local synthetic machinery of GnRH supporting the notion that this peptide may act as autocrine and/or paracrine role in intra-gonadal communication.

• Development and Reproduction
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• v.22 no.2
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• pp.119-132
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• 2018

GnRH (gonadotropin-releasing hormone) is a supreme hormone regulating reproductive activity in most animals. The sequences of amino acid and nucleic acid of GnRH reported up to now are examined from the evolutionary framework of Chordata. All identified GnRH are classified into GnRH1, GnRH2, or GnRH3. In all three forms of GnRH both N-terminal and C-terminal are conserved, which allows for effective binding to their receptors. The three amino acids in the middle of GnRH1 sequence have altered diversely from the primitive Chordata, which is indicative of the adaptation process to the ambient environment. GnRH2 and GnRH3 sequences are well conserved. There are more diverse modifications in the nucleic acids than in amino acid sequence of GnRH1. These variations can result from meiosis, mutation, or epigenetics and indicate that GnRH is the product of natural selection.

• 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.

• Korean Journal of Animal Reproduction
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• v.27 no.3
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• pp.207-213
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• 2003

This objective of this experiment were to evaluate the effect of various estrus synchronization programs on estrus detection rate and pregnancy rate in Hanwoo. After Postpartum 60 Days, a total of 150 cows divided into 2 groups. Cows Group 1 were treated with one luteolytic dosage of PGF$_2$$\alpha$(25 mg, im; lutalyse. USA) on Day 0, and with a second dosage 14 d later; cows in Group 2 were treated with GnRH(l00 $\mu\textrm{g}$, im; Conceral. Korea) on Day 0, PGF$_2$$\alpha$ 7 d later, GnRH 2 d later, and then time-inseminated approximately 16 h after this second treatment with GnRH. Ovarian morphology was monitored cows by trans-rectal ultrasonography from 24 hr to 32 hrs after second GnRH injection. The result obtained summarized as follows: 1. Cows synchronization of estrus with GnRH+PGF$_2$$\alpha$+GnRH(Ov-synch) and PGF$_2$$\alpha$ were 91.3 and 40.0%, respectively. 2. Induced ovulation were 24 to 32hr after the second GnRH injection, but high induced ovulation was 28hr. 3. High conception rate were 24hr insemination after the second GnRH injection. 4. Conception rate with PGF$_2$$\alpha$, CIDR and GnRH treatment were 50.0, 36.0 and 76.9%, respectively.

• 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.

• 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.