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Title: Direct Actions of Kisspeptins on GnRH Neurons Permit Attainment of Fertility but are Insufficient to Fully Preserve Gonadotropic Axis Activity.
Authors: León, Silvia
Barroso, Alexia
Vázquez, María J
García-Galiano, David
Manfredi-Lozano, María
Ruiz-Pino, Francisco
Heras, Violeta
Romero-Ruiz, Antonio
Roa, Juan
Schutz, Günther
Kirilov, Milen
Gaytan, Francisco
Pinilla, Leonor
Tena-Sempere, Manuel
metadata.dc.subject.mesh: Animals
Feedback, Physiological
Gonadotropin-Releasing Hormone
Mice, Knockout
Receptors, G-Protein-Coupled
Receptors, Kisspeptin-1
Issue Date: 12-Jan-2016
Abstract: Kisspeptins, ligands of the receptor, Gpr54, are potent stimulators of puberty and fertility. Yet, whether direct kisspeptin actions on GnRH neurons are sufficient for the whole repertoire of their reproductive effects remains debatable. To dissect out direct vs. indirect effects of kisspeptins on GnRH neurons in vivo, we report herein the detailed reproductive/gonadotropic characterization of a Gpr54 null mouse line with selective re-introduction of Gpr54 expression only in GnRH cells (Gpr54(-/-)Tg; rescued). Despite preserved fertility, adult rescued mice displayed abnormalities in gonadal microstructure, with signs of precocious ageing in females and elevated LH levels with normal-to-low testosterone secretion in males. Gpr54(-/-)Tg rescued mice showed also altered gonadotropin responses to negative feedback withdrawal, while luteinizing hormone responses to various gonadotropic regulators were variably affected, with partially blunted relative (but not absolute) responses to kisspeptin-10, NMDA and the agonist of tachykinin receptors, NK2R. Our data confirm that direct effects of kisspeptins on GnRH cells are sufficient to attain fertility. Yet, such direct actions appear to be insufficient to completely preserve proper functionality of gonadotropic axis, suggesting a role of kisspeptin signaling outside GnRH cells.
metadata.dc.identifier.doi: 10.1038/srep19206
Appears in Collections:Producción 2020

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