Journal ArticleDOI
Ontogeny and mechanisms of action for the stimulatory effect of kisspeptin on gonadotropin-releasing hormone system of the rat.
Juan M. Castellano,Víctor M. Navarro,R. Fernández-Fernández,Justo P. Castaño,María M. Malagón,Enrique Aguilar,Carlos Dieguez,Paolo Magni,Leonor Pinilla,Manuel Tena-Sempere +9 more
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TLDR
The present data document the ontogeny, sensitivity and intracellular signals for the stimulatory action of kisspeptin on the GnRH/LH axis in the rat and stress the essential role ofkisspeptin in normal, and eventually pathological, timing of puberty.About:
This article is published in Molecular and Cellular Endocrinology.The article was published on 2006-09-26. It has received 173 citations till now. The article focuses on the topics: Kisspeptin & Gonadotropin-releasing hormone.read more
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Journal ArticleDOI
Kisspeptin Signaling in the Brain
TL;DR: Kisspeptin signaling in the brain has been implicated in mediating the negative feedback action of sex steroids on gonadotropin secretion, generating the preovulatory GnRH/LH surge, triggering and guiding the tempo of sexual maturation at puberty, controlling seasonal reproduction, and restraining reproductive activity during lactation.
Journal ArticleDOI
Kisspeptins and Reproduction: Physiological Roles and Regulatory Mechanisms
TL;DR: This review aims to provide a comprehensive account of the state-of-the-art in the field of kisspeptin physiology by covering in-depth the consensus knowledge on the major molecular features, biological effects, and mechanisms of action ofkisspeptins in mammals and, to a lesser extent, in nonmammalian vertebrates.
Journal ArticleDOI
New frontiers in kisspeptin/GPR54 physiology as fundamental gatekeepers of reproductive function.
Juan Carlos Roa,Enrique Aguilar,Enrique Aguilar,Carlos Dieguez,Carlos Dieguez,Leonor Pinilla,Leonor Pinilla,Manuel Tena-Sempere,Manuel Tena-Sempere +8 more
TL;DR: Novel aspects of kisspeptin/GPR54 physiology have emerged, including their involvement in the neuroendocrine control of ovulation and the metabolic gating of reproductive function.
Journal ArticleDOI
Kisspeptin excites gonadotropin-releasing hormone neurons through a phospholipase C/calcium-dependent pathway regulating multiple ion channels.
TL;DR: Electrophysiology and calcium imaging studies indicate that kisspeptin activates G protein-coupled receptor 54 (GPR54) to initiate a PLC-IP3R-calcium cascade that modulates both potassium and NSC channels to initiate depolarization in GnRH neurons.
Journal ArticleDOI
Kisspeptin Depolarizes Gonadotropin-Releasing Hormone Neurons through Activation of TRPC-Like Cationic Channels
TL;DR: It appears that kisspeptin depolarizes GnRH neurons through activating TRPC-like channels and, to a lesser extent, inhibition of Kir channels, which contribute to the pronounced excitation of Gn RH neurons that is critical for mammalian reproduction.
References
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Journal ArticleDOI
Leptin signaling in the hypothalamus of normal rats in vivo
TL;DR: It remains unclear how signaling is propagated downstream from the leptin receptor to STAT3, but this may involve novel signaling intermediates, and results differ from findings in cultured cells and in vitro systems.
Journal ArticleDOI
Melatonin receptor activation regulates GnRH gene expression and secretion in GT1-7 GnRH neurons. Signal transduction mechanisms.
TL;DR: In this paper, the authors examined the potential signal transduction pathways activated by melatonin directly at the level of the GT1-7 neuron and found that melatonin inhibited forskolin-stimulated adenosine 3'-, 5'-cyclic monophosphate accumulation in GT 1-7 cells through an inhibitory G protein.
Journal ArticleDOI
Reproductive disturbances, pituitary lactotrope adenomas, and mammary gland tumors in transgenic female mice producing high levels of human chorionic gonadotropin.
Susana B Rulli,Aino Kuorelahti,Oznur Karaer,Lauri J. Pelliniemi,Matti Poutanen,Ilpo Huhtaniemi +5 more
TL;DR: Findings suggest that the hCG-induced aberrations of ovarian function are clearly responsible for the extragonadal tumors observed in these TG mice.
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In vivo gonadotropin-releasing hormone secretion in female rats during peripubertal development and on proestrus.
TL;DR: It is demonstrated that pubertal maturation in the female rat is associated with an acceleration of GnRH pulse generator activity and that later stages of pubertAL maturation are characterized by the appearance of afternoon increases in GnRH release that may underlie previously reported mini-surges in LH.
Journal ArticleDOI
Corticotropin-Releasing Hormone Stimulates Ca2+ Entry through L= and P-Type Ca2+ Channels in Rat Corticotropes*
Abstract: CRH induces corticotrope membrane depolarization and facilitates action potential firing The increase in electrical excitability causes large oscillatory increases in cytosolic Ca”- levels In this study on highly enriched populations of cultured rat corticotropes, inhibitors were used to determine the contribution ofthe Na’ channel and Ca” channel subtypes to membrane excitability and cytosolic Ca”+ levels Tetrodotoxin, an inhibitor of the voltage-dependent Na’ channel, inhibited a rapid initial component of the action potential, but generally did not influence spontaneous or CRH-induced firing frequency Tetrodotoxin also had no effect on spontaneous or CRHinduced cytosolic Ca*’ levels The L-type Ca“ channel inhibitor nifedipine abolished spontaneous and CRH-induced action potentials and cytosolic Ca’ + transients, but did not eliminate the CRH-induced membrane depolarization or completely restore cytosolic Ca”’ to basal levels Inhibition of P-type Ca”’ channels with w-agatoxin-IVA decreased action potential firing frequency and reduced the CRHinduced increase in cytosolic Ca” The combination of nifedipine and w-agatoxin-IVA abolished the CRH-induced rise in Ca2- but did not abolish the membrane depolarization Thus, cytosolic Ca’ + is mainly increased by CRH-induced action potentials that are completely dependent on L-type Ca” channels and partially regulated by P-type Ca”- channels CRH-induced Ca” entry also occurs independently of action potentials and is due to P-type, and possibly L-type, Ca”’ channels activated by the CRH-induced membrane depolarization
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