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New Gatekeepers of Reproduction: GPR54 and Its Cognate Ligand, KiSS-1

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This article is published in Endocrinology.The article was published on 2005-04-01 and is currently open access. It has received 60 citations till now.

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Journal ArticleDOI

Postnatal remodeling of dendritic structure and spine density in gonadotropin-releasing hormone neurons.

TL;DR: Unpredictable dendritic tree remodeling in the GnRH neurons is demonstrated and evidence for an increase in direct excitatory inputs to Gn RH neurons across the time of puberty is provided.
Journal ArticleDOI

The neuroanatomy of the kisspeptin system in the mammalian brain.

TL;DR: The available data suggest that kisspeptins are synthesized in neurons in the anteroventral periventricular nucleus and the arcuate nucleus, and both populations are considered to be involved in control of gonadotropes.
Journal ArticleDOI

Development of GABA and glutamate signaling at the GnRH neuron in relation to puberty.

TL;DR: Observations suggest that developing GnRH neurons exhibit a sequence of GABA-->glutamate signaling similar to that of other neuronal networks but that it is significantly elongated so as to only be complete by the time of puberty onset.
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Effects of Single or Repeated Intravenous Administration of Kisspeptin upon Dynamic LH Secretion in Conscious Male Rats

TL;DR: The ability of kisspeptin-10 to stimulate LH release was fully preserved, and even doubled, after short-term fasting despite suppression of prevailing LH levels, and in this setting, in vivo LH responses to a terminal injection of GnRH were preserved, whereas basal and depolarization-induced GnRH release ex vivo was significantly enhanced.
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Journal ArticleDOI

The GPR54 gene as a regulator of puberty

TL;DR: Puberty is initiated when gonadotropin-releasing hormone begins to be secreted by the hypothalamus, and complementary genetic approaches in humans and mice identified genetic factors that determine the onset of puberty.
Journal ArticleDOI

Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54

TL;DR: The present study shows that loss of function of GPR54 is a cause of IHH, and it identifies GPR 54 and possibly KiSS1 protein-derived peptide as playing a major and previously unsuspected role in the physiology of the gonadotropic axis.
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The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54.

TL;DR: Stimulation of oxytocin secretion after kisspeptin administration to rats confirmed this hypothesis that human GPR54 was highly expressed in placenta, pituitary, pancreas, and spinal cord, suggesting a role in the regulation of endocrine function.
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Metastasis suppressor gene KiSS-1 encodes peptide ligand of a G-protein-coupled receptor.

TL;DR: It is shown that KiSS-1 encodes a carboxy-terminally amidated peptide with 54 amino-acid residues, which is isolated from human placenta as the endogenous ligand of an orphan G-protein-coupled receptor (hOT7T175) and named ‘metastin’.
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A Role for Kisspeptins in the Regulation of Gonadotropin Secretion in the Mouse

TL;DR: Kisspeptins are products of the KiSS-1 gene, which bind to a G protein-coupled receptor known as GPR54, and it is concluded that kisspeptin-GPR54 signaling may be part of the hypothalamus circuitry that governs the hypothalamic secretion of GnRH.
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