Gper1 inhibition exacerbates traumatic brain injury-induced neurological impairments in mice.

IF 3.3 2区 心理学 Q1 BEHAVIORAL SCIENCES
Ya-Fei Xue, Ying-Xi Wu, Yun-Ze Zhang, Tian-Zhi Zhao
{"title":"Gper1 inhibition exacerbates traumatic brain injury-induced neurological impairments in mice.","authors":"Ya-Fei Xue, Ying-Xi Wu, Yun-Ze Zhang, Tian-Zhi Zhao","doi":"10.1186/s12993-025-00281-2","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>G protein-coupled estrogen receptor 1 (Gper1) is widely expressed in the brain, while its function in traumatic brain injury (TBI) remains poorly understood. This study aims to investigate the role of Gper1 in TBI pathology and the underlying mechanisms using a mouse model.</p><p><strong>Methods: </strong>Gper1 knockout (Gper1<sup>KO</sup>) mice were generated, and TBI was induced via controlled cortical impact (CCI). Brain water content, cell apoptosis, and neuroinflammation were assessed using real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and TUNEL staining. Behavioral outcomes, including cognitive and anxiety-related behaviors, were evaluated using the open field test and Y-maze test.</p><p><strong>Results: </strong>Gper1 expression was significantly upregulated in the brain tissues of TBI mice. Knockout of Gper1 led to exacerbated TBI-induced outcomes, including increased brain edema, blood-brain barrier disruption, and aggravated cell apoptosis and neuroinflammation in the cortex. Behaviorally, Gper1<sup>KO</sup> mice displayed more severe cognitive impairments and anxiety-like behaviors compared to wild-type mice.</p><p><strong>Conclusions: </strong>Gper1 inhibition exacerbates TBI-induced neurological and behavioral impairments, which suggests that Gper1 may be a potential therapeutic target for mitigating TBI-associated brain injury.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"19"},"PeriodicalIF":3.3000,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224363/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Behavioral and Brain Functions","FirstCategoryId":"102","ListUrlMain":"https://doi.org/10.1186/s12993-025-00281-2","RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BEHAVIORAL SCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Background: G protein-coupled estrogen receptor 1 (Gper1) is widely expressed in the brain, while its function in traumatic brain injury (TBI) remains poorly understood. This study aims to investigate the role of Gper1 in TBI pathology and the underlying mechanisms using a mouse model.

Methods: Gper1 knockout (Gper1KO) mice were generated, and TBI was induced via controlled cortical impact (CCI). Brain water content, cell apoptosis, and neuroinflammation were assessed using real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and TUNEL staining. Behavioral outcomes, including cognitive and anxiety-related behaviors, were evaluated using the open field test and Y-maze test.

Results: Gper1 expression was significantly upregulated in the brain tissues of TBI mice. Knockout of Gper1 led to exacerbated TBI-induced outcomes, including increased brain edema, blood-brain barrier disruption, and aggravated cell apoptosis and neuroinflammation in the cortex. Behaviorally, Gper1KO mice displayed more severe cognitive impairments and anxiety-like behaviors compared to wild-type mice.

Conclusions: Gper1 inhibition exacerbates TBI-induced neurological and behavioral impairments, which suggests that Gper1 may be a potential therapeutic target for mitigating TBI-associated brain injury.

Gper1抑制加剧了小鼠创伤性脑损伤引起的神经损伤。
背景:G蛋白偶联雌激素受体1 (Gper1)在大脑中广泛表达,但其在创伤性脑损伤(TBI)中的功能尚不清楚。本研究旨在通过小鼠模型探讨Gper1在TBI病理中的作用及其潜在机制。方法:制备Gper1基因敲除(Gper1KO)小鼠,通过控制性皮质冲击(CCI)诱导TBI。采用实时聚合酶链反应、酶联免疫吸附试验和TUNEL染色评估脑含水量、细胞凋亡和神经炎症。行为结果,包括认知和焦虑相关行为,采用开放场测试和y迷宫测试进行评估。结果:Gper1在脑外伤小鼠脑组织中的表达明显上调。敲除Gper1导致tbi诱导的结果加重,包括脑水肿加重、血脑屏障破坏、皮质细胞凋亡和神经炎症加重。行为上,与野生型小鼠相比,Gper1KO小鼠表现出更严重的认知障碍和焦虑样行为。结论:Gper1抑制加重了tbi引起的神经和行为损伤,这表明Gper1可能是减轻tbi相关脑损伤的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Behavioral and Brain Functions
Behavioral and Brain Functions 医学-行为科学
CiteScore
5.90
自引率
0.00%
发文量
11
审稿时长
6-12 weeks
期刊介绍: A well-established journal in the field of behavioral and cognitive neuroscience, Behavioral and Brain Functions welcomes manuscripts which provide insight into the neurobiological mechanisms underlying behavior and brain function, or dysfunction. The journal gives priority to manuscripts that combine both neurobiology and behavior in a non-clinical manner.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信