GPER-Deficient Rats Exhibit Lower Serum Corticosterone Level and Increased Anxiety-Like Behavior

Copyright © 2020 Yi Zheng et al.

Détails bibliographiques
Publié dans:Neural plasticity. - 1998. - 2020(2020) vom: 15., Seite 8866187
Auteur principal: Zheng, Yi (Auteur)
Autres auteurs: Wu, Meimei, Gao, Ting, Meng, Li, Ding, Xiaowei, Meng, Youqiang, Jiao, Yingfu, Luo, Ping, He, Zhenquan, Sun, Tao, Zhang, Guohua, Shi, Xueyin, Rong, Weifang
Format: Article en ligne
Langue:English
Publié: 2020
Accès à la collection:Neural plasticity
Sujets:Journal Article Research Support, Non-U.S. Gov't Gper1 protein, rat Receptors, G-Protein-Coupled Adrenocorticotropic Hormone 9002-60-2 Corticosterone W980KJ009P
Description
Résumé:Copyright © 2020 Yi Zheng et al.
Ample evidence suggests that estrogens have strong influences on the occurrence of stress-related mood disorders, but the underlying mechanisms remain poorly understood. Through multiple approaches, we demonstrate that the G protein-coupled estrogen receptor (GPER) is widely distributed along the HPA axis and in brain structures critically involved in mood control. Genetic ablation of GPER in the rat resulted in significantly lower basal serum corticosterone level but enhanced ACTH release in response to acute restraint stress, especially in the female. GPER-/- rats of either sex displayed increased anxiety-like behaviors and deficits in learning and memory. Additionally, GPER deficiency led to aggravation of anxiety-like behaviors following single-prolonged stress (SPS). SPS caused significant decreases in serum corticosterone in WT but not in GPER-deficient rats. The results highlight an important role of GPER at multiple sites in regulation of the HPA axis and mood
Description:Date Completed 03.08.2021
Date Revised 03.08.2021
published: Electronic-eCollection
Citation Status MEDLINE
ISSN:1687-5443
DOI:10.1155/2020/8866187