VGLUT2-expressing neurons in the vestibular nuclear complex mediate gravitational stress-induced hypothermia in mice.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
08 05 2020
Historique:
received: 23 11 2019
accepted: 17 04 2020
entrez: 10 5 2020
pubmed: 10 5 2020
medline: 12 6 2021
Statut: epublish

Résumé

The vestibular system, which is essential for maintaining balance, contributes to the sympathetic response. Although this response is involved in hypergravity load-induced hypothermia in mice, the underlying mechanism remains unknown. This study showed that hypergravity (2g) decreased plasma catecholamines, which resulted in hypoactivity of the interscapular brown adipose tissue (iBAT). Hypothermia induced by 2g load was significantly suppressed by administration of beta-adrenergic receptor agonists, suggesting the involvement of decrease in iBAT activity through sympathoinhibition. Bilateral chemogenetic activation of vesicular glutamate transporter 2 (VGLUT2)-expressing neurons in the vestibular nuclear complex (VNC) induced hypothermia. The VGLUT2-expressing neurons contributed to 2g load-induced hypothermia, since their deletion suppressed hypothermia. Although activation of vesicular gamma-aminobutyric acid transporter-expressing neurons in the VNC induced slight hypothermia instead of hyperthermia, their deletion did not affect 2g load-induced hypothermia. Thus, we concluded that 2g load-induced hypothermia resulted from sympathoinhibition via the activation of VGLUT2-expressing neurons in the VNC.

Identifiants

pubmed: 32385401
doi: 10.1038/s42003-020-0950-0
pii: 10.1038/s42003-020-0950-0
pmc: PMC7210111
doi:

Substances chimiques

Slc17a6 protein, mouse 0
Vesicular Glutamate Transport Protein 2 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

227

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Auteurs

Chikara Abe (C)

Department of Physiology, Gifu University Graduate School of Medicine, Gifu, Japan. chikara@gifu-u.ac.jp.

Yusuke Yamaoka (Y)

Department of Physiology, Gifu University Graduate School of Medicine, Gifu, Japan.

Yui Maejima (Y)

Department of Physiology, Gifu University Graduate School of Medicine, Gifu, Japan.

Tomoe Mikami (T)

Department of Physiology, Gifu University Graduate School of Medicine, Gifu, Japan.

Shigefumi Yokota (S)

Department of Anatomy and Neuroscience, Shimane University School of Medicine, Izumo, Shimane, Japan.

Akihiro Yamanaka (A)

Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.

Hironobu Morita (H)

Department of Physiology, Gifu University Graduate School of Medicine, Gifu, Japan. zunzunmorita@gmail.com.

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