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Status: Bibliographieeintrag

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Verfasst von:Blum, Thomas [VerfasserIn]   i
 Moreno-Pérez, Ana [VerfasserIn]   i
 Pyrski, Martina [VerfasserIn]   i
 Bufe, Bernd [VerfasserIn]   i
 Arifovic, Anela [VerfasserIn]   i
 Weißgerber, Petra [VerfasserIn]   i
 Freichel, Marc [VerfasserIn]   i
 Zufall, Frank [VerfasserIn]   i
 Leinders-Zufall, Trese [VerfasserIn]   i
Titel:Trpc5 deficiency causes hypoprolactinemia and altered function of oscillatory dopamine neurons in the arcuate nucleus
Verf.angabe:Thomas Blum, Ana Moreno-Pérez, Martina Pyrski, Bernd Bufe, Anela Arifovic, Petra Weissgerber, Marc Freichel, Frank Zufall, and Trese Leinders-Zufall
E-Jahr:2019
Jahr:July 23, 2019
Umfang:8 S.
Fussnoten:Gesehen am 13.12.2019
Titel Quelle:Enthalten in: National Academy of Sciences (Washington, DC)Proceedings of the National Academy of Sciences of the United States of America
Ort Quelle:Washington, DC : National Acad. of Sciences, 1915
Jahr Quelle:2019
Band/Heft Quelle:116(2019), 30, Seite 15236-15243
ISSN Quelle:1091-6490
Abstract:Dopamine neurons of the hypothalamic arcuate nucleus (ARC) tonically inhibit the release of the protein hormone prolactin from lactotropic cells in the anterior pituitary gland and thus play a central role in prolactin homeostasis of the body. Prolactin, in turn, orchestrates numerous important biological functions such as maternal behavior, reproduction, and sexual arousal. Here, we identify the canonical transient receptor potential channel Trpc5 as an essential requirement for normal function of dopamine ARC neurons and prolactin homeostasis. By analyzing female mice carrying targeted mutations in the Trpc5 gene including a conditional Trpc5 deletion, we show that Trpc5 is required for maintaining highly stereotyped infraslow membrane potential oscillations of dopamine ARC neurons. Trpc5 is also required for eliciting prolactin-evoked tonic plateau potentials in these neurons that are part of a regulatory feedback circuit. Trpc5 mutant females show severe prolactin deficiency or hypoprolactinemia that is associated with irregular reproductive cyclicity, gonadotropin imbalance, and impaired reproductive capabilities. These results reveal a previously unknown role for the cation channel Trpc5 in prolactin homeostasis of female mice and provide strategies to explore the genetic basis of reproductive disorders and other malfunctions associated with defective prolactin regulation in humans.
DOI:doi:10.1073/pnas.1905705116
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1073/pnas.1905705116
 Volltext: https://www.pnas.org/content/116/30/15236
 DOI: https://doi.org/10.1073/pnas.1905705116
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:dopamine
 HC-070
 hypothalamus
 prolactin
 Trpc5 channelopathy
K10plus-PPN:1685452779
Verknüpfungen:→ Zeitschrift

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