ASIC1a affects hypothalamic signaling and regulates the daily rhythm of body temperature in mice.

Détails

Ressource 1Télécharger: Peng_circ_s42003-023-05221-2-t.pdf (1589.08 [Ko])
Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_B248EF4DD49B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
ASIC1a affects hypothalamic signaling and regulates the daily rhythm of body temperature in mice.
Périodique
Communications biology
Auteur⸱e⸱s
Peng Z., Ziros P.G., Martini T., Liao X.H., Stoop R., Refetoff S., Albrecht U., Sykiotis G.P., Kellenberger S.
ISSN
2399-3642 (Electronic)
ISSN-L
2399-3642
Statut éditorial
Publié
Date de publication
17/08/2023
Peer-reviewed
Oui
Volume
6
Numéro
1
Pages
857
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
Publication Status: epublish
Résumé
The body temperature of mice is higher at night than during the day. We show here that global deletion of acid-sensing ion channel 1a (ASIC1a) results in lower body temperature during a part of the night. ASICs are pH sensors that modulate neuronal activity. The deletion of ASIC1a decreased the voluntary activity at night of mice that had access to a running wheel but did not affect their spontaneous activity. Daily rhythms of thyrotropin-releasing hormone mRNA in the hypothalamus and of thyroid-stimulating hormone β mRNA in the pituitary, and of prolactin mRNA in the hypothalamus and pituitary were suppressed in ASIC1a <sup>-/-</sup> mice. The serum thyroid hormone levels were however not significantly changed by ASIC1a deletion. Our findings indicate that ASIC1a regulates activity and signaling in the hypothalamus and pituitary. This likely leads to the observed changes in body temperature by affecting the metabolism or energy expenditure.
Mots-clé
Animals, Mice, Acid Sensing Ion Channels/genetics, Body Temperature, Energy Metabolism/genetics, Hypothalamus, RNA, Messenger
Pubmed
Web of science
Open Access
Oui
Financement(s)
Fonds national suisse / 31003A_172968
Fonds national suisse / 310030_212558
Création de la notice
18/08/2023 17:40
Dernière modification de la notice
30/09/2023 6:55
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