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Open AccessJournal ArticleDOI

A Role for Kisspeptins in the Regulation of Gonadotropin Secretion in the Mouse

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TLDR
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.
Abstract
Kisspeptins are products of the KiSS-1 gene, which bind to a G protein-coupled receptor known as GPR54. Mutations or targeted disruptions in the GPR54 gene cause hypogonadotropic hypogonadism in humans and mice, suggesting that kisspeptin signaling may be important for the regulation of gonadotropin secretion. To examine the effects of kisspeptin-54 (metastin) and kisspeptin-10 (the biologically active C-terminal decapeptide) on gonadotropin secretion in the mouse, we administered the kisspeptins directly into the lateral cerebral ventricle of the brain and demonstrated that both peptides stimulate LH secretion. Further characterization of kisspeptin-54 demonstrated that it stimulated both LH and FSH secretion, at doses as low as 1 fmol; moreover, this effect was shown to be blocked by pretreatment with acyline, a potent GnRH antagonist. To learn more about the functional anatomy of kisspeptins, we mapped the distribution of KiSS-1 mRNA in the hypothalamus. We observed that KiSS-1 mRNA is expressed in areas of the hypothalamus implicated in the neuroendocrine regulation of gonadotropin secretion, including the anteroventral periventricular nucleus, the periventricular nucleus, and the arcuate nucleus. We conclude that kisspeptin-GPR54 signaling may be part of the hypothalamic circuitry that governs the hypothalamic secretion of GnRH.

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Journal ArticleDOI

Recent advances in mammalian RFamide peptides : The discovery and functional analyses of PrRP, RFRPs and QRFP

TL;DR: The strategies employed for the identification of these mammalian RFamide peptides are reviewed and, the most recently identified, pyroglutamylatedRFamide peptide (QRFP), the discovery of all of which the authors were at least partly involved in is reviewed.
Journal ArticleDOI

Role of Neurokinin B in the Control of Female Puberty and Its Modulation by Metabolic Status

TL;DR: The regulation of Tac2 and Tacr3 mRNAs in female rats is investigated and it is demonstrated that their hypothalamic expression is increased along postnatal maturation, suggesting that NKB–NK3R signaling plays a role in pubertal maturation and that its alterations may contribute to Pubertal disorders linked to metabolic stress and negative energy balance.
Journal ArticleDOI

RFamide-Related Peptide-3 Receptor Gene Expression in GnRH and Kisspeptin Neurons and GnRH-Dependent Mechanism of Action

TL;DR: Data reveal that RFRP-3 can act at two levels of the GnRH neuronal network to modulate reproduction but is unable to inhibit gonadotropin secretion independently of GnRH.
Journal ArticleDOI

Circadian Control of Kisspeptin and a Gated GnRH Response Mediate the Preovulatory Luteinizing Hormone Surge

TL;DR: A novel mechanism of ovulatory control with interactions among the circadian system, kisspeptin signaling, and a GnRH gating mechanism of control is revealed.
References
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Book

The Physiology of Reproduction

Ernst Knobil, +1 more
TL;DR: The gametes, fertilization and early embryogenesis the reproductive systems - the female, the male the pituitary and the hypothalmus, and the reproductive processes and their control.
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

Comparative distribution of estrogen receptor-alpha and -beta mRNA in the rat central nervous system.

TL;DR: Comparing the distribution of the classical and novel forms of ER mRNA‐expressing neurons in the central nervous system (CNS) of the rat with in situ hybridization histochemistry provides evidence that the region‐specific expression of ER‐α, ER‐β, or both may be important in determining the physiological responses of neuronal populations to estrogen action.
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.
Journal ArticleDOI

Distribution of androgen and estrogen receptor mRNA‐containing cells in the rat brain: An in situ hybridization study

TL;DR: AR and ER may modulate nonolfactory sensory information as well since labeled cells were found in regions involved in the central relay of somatosensory information, including the mesencephalic nucleus of the trigeminal nerve, the ventral thalamic nuclear group, and the dorsal horn of the spinal cord.
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