ERNEST COST action overview on the (patho)physiology of GPCRs and orphan GPCRs in the nervous system.

IF 6.8 2区 医学 Q1 PHARMACOLOGY & PHARMACY British Journal of Pharmacology Pub Date : 2024-06-02 DOI:10.1111/bph.16389
Necla Birgül Iyison, Clauda Abboud, Dayana Abboud, Abdulrasheed O Abdulrahman, Ana-Nicoleta Bondar, Julie Dam, Zafiroula Georgoussi, Jesús Giraldo, Anemari Horvat, Christos Karoussiotis, Alba Paz-Castro, Miriam Scarpa, Hannes Schihada, Nicole Scholz, Bilge Güvenc Tuna, Nina Vardjan
{"title":"ERNEST COST action overview on the (patho)physiology of GPCRs and orphan GPCRs in the nervous system.","authors":"Necla Birgül Iyison, Clauda Abboud, Dayana Abboud, Abdulrasheed O Abdulrahman, Ana-Nicoleta Bondar, Julie Dam, Zafiroula Georgoussi, Jesús Giraldo, Anemari Horvat, Christos Karoussiotis, Alba Paz-Castro, Miriam Scarpa, Hannes Schihada, Nicole Scholz, Bilge Güvenc Tuna, Nina Vardjan","doi":"10.1111/bph.16389","DOIUrl":null,"url":null,"abstract":"<p><p>G protein-coupled receptors (GPCRs) are a large family of cell surface receptors that play a critical role in nervous system function by transmitting signals between cells and their environment. They are involved in many, if not all, nervous system processes, and their dysfunction has been linked to various neurological disorders representing important drug targets. This overview emphasises the GPCRs of the nervous system, which are the research focus of the members of ERNEST COST action (CA18133) working group 'Biological roles of signal transduction'. First, the (patho)physiological role of the nervous system GPCRs in the modulation of synapse function is discussed. We then debate the (patho)physiology and pharmacology of opioid, acetylcholine, chemokine, melatonin and adhesion GPCRs in the nervous system. Finally, we address the orphan GPCRs, their implication in the nervous system function and disease, and the challenges that need to be addressed to deorphanize them.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.8000,"publicationDate":"2024-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"British Journal of Pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/bph.16389","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0

Abstract

G protein-coupled receptors (GPCRs) are a large family of cell surface receptors that play a critical role in nervous system function by transmitting signals between cells and their environment. They are involved in many, if not all, nervous system processes, and their dysfunction has been linked to various neurological disorders representing important drug targets. This overview emphasises the GPCRs of the nervous system, which are the research focus of the members of ERNEST COST action (CA18133) working group 'Biological roles of signal transduction'. First, the (patho)physiological role of the nervous system GPCRs in the modulation of synapse function is discussed. We then debate the (patho)physiology and pharmacology of opioid, acetylcholine, chemokine, melatonin and adhesion GPCRs in the nervous system. Finally, we address the orphan GPCRs, their implication in the nervous system function and disease, and the challenges that need to be addressed to deorphanize them.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
ERNEST COST 行动概述神经系统中 GPCR 和孤儿 GPCR 的(病理)生理学。
G 蛋白偶联受体(GPCR)是细胞表面受体的一个大家族,通过在细胞与其环境之间传递信号,在神经系统功能中发挥着至关重要的作用。它们参与了许多甚至所有神经系统过程,其功能障碍与各种神经系统疾病有关,是重要的药物靶点。本综述重点介绍神经系统的 GPCR,这是 ERNEST COST 行动(CA18133)"信号转导的生物学作用 "工作组成员的研究重点。首先,我们讨论了神经系统 GPCR 在调节突触功能方面的(病理)生理作用。然后,我们讨论神经系统中阿片类、乙酰胆碱、趋化因子、褪黑激素和粘附 GPCR 的(病理)生理学和药理学。最后,我们讨论了孤儿 GPCR、它们在神经系统功能和疾病中的影响,以及使它们非形态化所面临的挑战。
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 去求助
来源期刊
CiteScore
15.40
自引率
12.30%
发文量
270
审稿时长
2.0 months
期刊介绍: The British Journal of Pharmacology (BJP) is a biomedical science journal offering comprehensive international coverage of experimental and translational pharmacology. It publishes original research, authoritative reviews, mini reviews, systematic reviews, meta-analyses, databases, letters to the Editor, and commentaries. Review articles, databases, systematic reviews, and meta-analyses are typically commissioned, but unsolicited contributions are also considered, either as standalone papers or part of themed issues. In addition to basic science research, BJP features translational pharmacology research, including proof-of-concept and early mechanistic studies in humans. While it generally does not publish first-in-man phase I studies or phase IIb, III, or IV studies, exceptions may be made under certain circumstances, particularly if results are combined with preclinical studies.
期刊最新文献
Vortioxetine reduces the development of pain-related behaviour in a knee osteoarthritis model in rats: Involvement of nerve growth factor (NGF) down-regulation Selective modulation of epileptic tissue by an adenosine A3 receptor-activating drug Contribution of T-type calcium channel isoforms to cold and mechanical sensitivity in naïve and oxaliplatin-treated mice of both sexes Mitigating off-target effects of small RNAs: conventional approaches, network theory and artificial intelligence Immune regulatory and anti-resorptive activities of tanshinone IIA sulfonate attenuates rheumatoid arthritis in mice
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1