评估IKCa通道在CA1海马锥体细胞产生sAHP中的作用

IF 3.3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Channels Pub Date : 2016-03-07 DOI:10.1080/19336950.2016.1161988

R. W. Turner, Hadhimulya Asmara, J. Engbers, J. Miclat, Arsalan P. Rizwan, Giriraj Sahu, G. Zamponi

{"title":"评估IKCa通道在CA1海马锥体细胞产生sAHP中的作用","authors":"R. W. Turner, Hadhimulya Asmara, J. Engbers, J. Miclat, Arsalan P. Rizwan, Giriraj Sahu, G. Zamponi","doi":"10.1080/19336950.2016.1161988","DOIUrl":null,"url":null,"abstract":"ABSTRACT Our previous work reported that KCa3.1 (IKCa) channels are expressed in CA1 hippocampal pyramidal cells and contribute to the slow afterhyperpolarization that regulates spike accommodation in these cells. The current report presents data from single cell RT-PCR that further reveals mRNA in CA1 cells that corresponds to the sequence of an IKCa channel from transmembrane segments 5 through 6 including the pore region, revealing the established binding sites for 4 different IKCa channel blockers. A comparison of methods to internally apply the IKCa channel blocker TRAM-34 shows that including the drug in an electrode from the onset of an experiment is unviable given the speed of drug action upon gaining access for whole-cell recordings. Together the data firmly establish IKCa channel expression in CA1 neurons and clarify methodological requirements to obtain a block of IKCa channel activity through internal application of TRAM-34.","PeriodicalId":9750,"journal":{"name":"Channels","volume":"379 1","pages":"313 - 319"},"PeriodicalIF":3.3000,"publicationDate":"2016-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"21","resultStr":"{\"title\":\"Assessing the role of IKCa channels in generating the sAHP of CA1 hippocampal pyramidal cells\",\"authors\":\"R. W. Turner, Hadhimulya Asmara, J. Engbers, J. Miclat, Arsalan P. Rizwan, Giriraj Sahu, G. Zamponi\",\"doi\":\"10.1080/19336950.2016.1161988\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"ABSTRACT Our previous work reported that KCa3.1 (IKCa) channels are expressed in CA1 hippocampal pyramidal cells and contribute to the slow afterhyperpolarization that regulates spike accommodation in these cells. The current report presents data from single cell RT-PCR that further reveals mRNA in CA1 cells that corresponds to the sequence of an IKCa channel from transmembrane segments 5 through 6 including the pore region, revealing the established binding sites for 4 different IKCa channel blockers. A comparison of methods to internally apply the IKCa channel blocker TRAM-34 shows that including the drug in an electrode from the onset of an experiment is unviable given the speed of drug action upon gaining access for whole-cell recordings. Together the data firmly establish IKCa channel expression in CA1 neurons and clarify methodological requirements to obtain a block of IKCa channel activity through internal application of TRAM-34.\",\"PeriodicalId\":9750,\"journal\":{\"name\":\"Channels\",\"volume\":\"379 1\",\"pages\":\"313 - 319\"},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2016-03-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"21\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Channels\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/19336950.2016.1161988\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Channels","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/19336950.2016.1161988","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 21

摘要

我们之前的研究报道了KCa3.1 (IKCa)通道在CA1海马锥体细胞中表达，并参与调节这些细胞中尖峰调节的缓慢后超极化。目前的报告提供了来自单细胞RT-PCR的数据，进一步揭示了CA1细胞中与IKCa通道序列相对应的跨膜片段5至6(包括孔区)的mRNA，揭示了4种不同IKCa通道阻滞剂的建立结合位点。对内部应用IKCa通道阻滞剂TRAM-34的方法的比较表明，考虑到获得全细胞记录后药物作用的速度，从实验开始就将药物包括在电极中是不可行的。总之，这些数据牢固地确立了IKCa通道在CA1神经元中的表达，并阐明了通过内部应用TRAM-34获得IKCa通道活性块的方法要求。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

Assessing the role of IKCa channels in generating the sAHP of CA1 hippocampal pyramidal cells

ABSTRACT Our previous work reported that KCa3.1 (IKCa) channels are expressed in CA1 hippocampal pyramidal cells and contribute to the slow afterhyperpolarization that regulates spike accommodation in these cells. The current report presents data from single cell RT-PCR that further reveals mRNA in CA1 cells that corresponds to the sequence of an IKCa channel from transmembrane segments 5 through 6 including the pore region, revealing the established binding sites for 4 different IKCa channel blockers. A comparison of methods to internally apply the IKCa channel blocker TRAM-34 shows that including the drug in an electrode from the onset of an experiment is unviable given the speed of drug action upon gaining access for whole-cell recordings. Together the data firmly establish IKCa channel expression in CA1 neurons and clarify methodological requirements to obtain a block of IKCa channel activity through internal application of TRAM-34.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Channels 生物-生化与分子生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Channels is an open access journal for all aspects of ion channel research. The journal publishes high quality papers that shed new light on ion channel and ion transporter/exchanger function, structure, biophysics, pharmacology, and regulation in health and disease. Channels welcomes interdisciplinary approaches that address ion channel physiology in areas such as neuroscience, cardiovascular sciences, cancer research, endocrinology, and gastroenterology. Our aim is to foster communication among the ion channel and transporter communities and facilitate the advancement of the field.