Drugs acting at TRPM7 channels inhibit seizure‐like activity

Author:

Khalil Aytakin1,Shekh‐Ahmad Tawfeeq12ORCID,Kovac Stjepana13,Wykes Robert C.14ORCID,Horgen F. David5,Fleig Andrea6,Walker Matthew C.1ORCID

Affiliation:

1. Department of Clinical and Experimental Epilepsy UCL Queen Square Institute of Neurology, University College London London UK

2. The Institute for Drug Research, The School of Pharmacy, Faculty of Medicine The Hebrew University of Jerusalem Jerusalem Israel

3. Department of Neurology University of Münster Münster Germany

4. Nanomedicine Lab, Division of Neuroscience University of Manchester Manchester UK

5. Department of Natural Sciences Hawaii Pacific University Kaneohe Hawaii USA

6. The Queen's Medical Center and John A. Burns School of Medicine and Cancer Center University of Hawaii Honolulu Hawaii USA

Abstract

AbstractTransient receptor potential cation subfamily M7 (TRPM7) channels are ion channels permeable to divalent cations. They are abundantly expressed with particularly high expression in the brain. Previous studies have highlighted the importance of TRPM7 channels in brain diseases such as stroke and traumatic brain injury, yet evidence for a role in seizures and epilepsy is lacking. Here, we show that carvacrol, a food additive that inhibits TRPM7 channels, and waixenicin A, a novel selective and potent TRPM7 inhibitor, completely suppressed seizure‐like activity in rodent hippocampal‐entorhinal brain slices exposed to pentylenetetrazole or low magnesium. These findings support inhibition of TRPM7 channels as a novel target for antiseizure medications.

Funder

National Institutes of Health

Publisher

Wiley

Subject

Neurology (clinical),Neurology

Cited by 3 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3