• 한국양식학회지
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• 제9권1호
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• pp.3-10
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• 1996

인간의 태반성 성선자극호르몬(HCG) 또는 성선자극호르몬-방출호르몬 유도체(GnRH-A)와 pimozide를 이용하여 산란시기의 암컷황복에서 인공 산란을 유도하였다. 호르몬 또는 호르몬유도체의 효과는 배란 후 인공수정시켜 수정율과 배체형성율 및 면역방사측정법으로 혈액의 plasma 내 성선자극호르몬(GTH) 양을 측정하여 결정하였다. 수정율과 배체형성율이 가장 좋은 HCG 농도는 어체중 kg 당 1,000 IU이었다. 또한 GnRH-A ($10\;{\mu}g/kg$)와 pimozide를 동시에 처리했을 때 수정율과 배체형성율이 좋은 pimozide의 농도는 5 mg/kg이었다. Pimozide(1, 5 mg/kg)를 단독으로 처리한 어류에서는 plasma 내 GTH양에 영향을 줄 수 없었지만, GnRH-A와 동시에 처리했을 때 GTH양은 현저히 증가되었다. GnRH-A와 pimozide 및 dopamine을 동시에 처리했을 때 혈액의 plasma 내 GTH양은 크게 감소되었다. 이상의 결과는 산란시기 또는 이시기이외에 황복의 뇌로부터 여러 가지 성선자극호르몬과 성선자극억제호르몬을 분비됨을 시사해 준다.

• Journal of Ginseng Research
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• 제36권1호
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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.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 한국생물과학협회 학술발표대회
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• pp.189.1-189
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• 2000

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 2003년도 한국생물과학협회 학술발표대회
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• pp.161.1-161
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• 2003

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 2001년도 한국생물과학협회 학술발표대회
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• pp.191.1-191
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• 2001

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 한국생물과학협회 학술발표대회
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• pp.188.1-188
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• 2000

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 한국생물과학협회 학술발표대회
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• pp.188.2-188
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• 2000

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 2001년도 공동 춘계학술대회
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• pp.69.2-69
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• 2001

No Abstract, See Full Text

• Animal cells and systems
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• 제11권2호
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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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• 제55권1호
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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.