Astrocytes in the Ventromedial Hypothalamus Involve Chronic Stress-Induced Anxiety and Bone Loss in Mice

Copyright © 2021 Yunhui Liu et al.

Détails bibliographiques
Publié dans:Neural plasticity. - 1998. - 2021(2021) vom: 01., Seite 7806370
Auteur principal: Liu, Yunhui (Auteur)
Autres auteurs: Shao, Jie, Gao, Dashuang, Zhang, Lu, Yang, Fan
Format: Article en ligne
Langue:English
Publié: 2021
Accès à la collection:Neural plasticity
Sujets:Journal Article Research Support, Non-U.S. Gov't Proto-Oncogene Proteins c-fos Receptors, N-Methyl-D-Aspartate GTP-Binding Protein alpha Subunits, Gi-Go EC 3.6.5.1 GTP-Binding Protein alpha Subunits, Gq-G11 Clozapine J60AR2IKIC
Description
Résumé:Copyright © 2021 Yunhui Liu et al.
Chronic stress is one of the main risk factors of bone loss. While the neurons and neural circuits of the ventromedial hypothalamus (VMH) mediate bone loss induced by chronic stress, the detailed intrinsic mechanisms within the VMH nucleus still need to be explored. Astrocytes in brain regions play important roles in the regulation of metabolism and anxiety-like behavior through interactions with surrounding neurons. However, whether astrocytes in the VMH affect neuronal activity and therefore regulate chronic stress-induced anxiety and bone loss remain elusive. In this study, we found that VMH astrocytes were activated during chronic stress-induced anxiety and bone loss. Pharmacogenetic activation of the Gi and Gq pathways in VMH astrocytes reduced and increased the levels of anxiety and bone loss, respectively. Furthermore, activation of VMH astrocytes by optogenetics induced depolarization in neighboring steroidogenic factor-1 (SF-1) neurons, which was diminished by administration of N-methyl-D-aspartic acid (NMDA) receptor blocker but not by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor blocker. These results suggest that there may be a functional "glial-neuron microcircuit" in VMH nuclei that mediates anxiety and bone loss induced by chronic stress. This study not only advances our understanding of glial cell function but also provides a potential intervention target for chronic stress-induced anxiety and bone loss therapy
Description:Date Completed 18.01.2022
Date Revised 18.01.2022
published: Electronic-eCollection
Citation Status MEDLINE
ISSN:1687-5443
DOI:10.1155/2021/7806370