KCNQ1/KCNE1 K+ channel and P2Y4 receptor are co-expressed from the time of birth in the apical membrane of rat strial marginal cells.

Acta oto-laryngologica. Supplementum Pub Date : 2007-10-01 DOI:10.1080/03655230701624830

Dong Gu Hur, Jun Ho Lee, Seung-Ha Oh, Young Ho Kim, Jin Hee Lee, Dong Hoon Shin, Sun O Chang, Chong-Sun Kim

{"title":"KCNQ1/KCNE1 K+ channel and P2Y4 receptor are co-expressed from the time of birth in the apical membrane of rat strial marginal cells.","authors":"Dong Gu Hur, Jun Ho Lee, Seung-Ha Oh, Young Ho Kim, Jin Hee Lee, Dong Hoon Shin, Sun O Chang, Chong-Sun Kim","doi":"10.1080/03655230701624830","DOIUrl":null,"url":null,"abstract":"Conclusion: KCNQ1/KCNE1 K(+) channels and P2Y(4) receptors are expressed in the apical membrane of rat strial marginal cells from postnatal day 1 (P1) and maintained throughout development.Objectives: The purpose of the present study was to investigate the developmental expression of KCNQ1/KCNE1 K(+) channel and of P2Y(4), which is an important metabotropic regulator of KCNQ1/KCNE1 K(+) channel in strial marginal cells.Materials and methods: Sprague-Dawley rats at different stages of development (P1, P3, P5, P7, P14, and P21) were studied. The spiral ligament with the stria vascularis was detached from the cartilaginous or bony cochlea and prepared for a voltage-sensitive vibrating probe and immunohistochemistry.Results: Chromanol 293B, a blocker of KCNQ1/KCNE1 K(+) channel, inhibited short-circuit currents (I ( sc )) from P1 to P21. Similarly, I ( sc ) were found to be decreased by uridine 5'-triphosphate at all ages. The antagonist profiles indicated that the apical P2Y receptor is P2Y(4) subtype. KCNQ1, KCNE1, and P2Y(4) were immunolocalized in the apical region of stria vascularis at P1.","PeriodicalId":7027,"journal":{"name":"Acta oto-laryngologica. Supplementum","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2007-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/03655230701624830","citationCount":"12","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta oto-laryngologica. Supplementum","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/03655230701624830","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 12

Abstract

Conclusion: KCNQ1/KCNE1 K(+) channels and P2Y(4) receptors are expressed in the apical membrane of rat strial marginal cells from postnatal day 1 (P1) and maintained throughout development.

Objectives: The purpose of the present study was to investigate the developmental expression of KCNQ1/KCNE1 K(+) channel and of P2Y(4), which is an important metabotropic regulator of KCNQ1/KCNE1 K(+) channel in strial marginal cells.

Materials and methods: Sprague-Dawley rats at different stages of development (P1, P3, P5, P7, P14, and P21) were studied. The spiral ligament with the stria vascularis was detached from the cartilaginous or bony cochlea and prepared for a voltage-sensitive vibrating probe and immunohistochemistry.

Results: Chromanol 293B, a blocker of KCNQ1/KCNE1 K(+) channel, inhibited short-circuit currents (I ( sc )) from P1 to P21. Similarly, I ( sc ) were found to be decreased by uridine 5'-triphosphate at all ages. The antagonist profiles indicated that the apical P2Y receptor is P2Y(4) subtype. KCNQ1, KCNE1, and P2Y(4) were immunolocalized in the apical region of stria vascularis at P1.

查看原文本刊更多论文

KCNQ1/KCNE1 K+通道和P2Y4受体从出生时起就在大鼠试体边缘细胞的顶膜中共同表达。

结论:KCNQ1/KCNE1 K(+)通道和P2Y(4)受体从出生第1天(P1)开始在大鼠试体边缘细胞顶膜中表达，并在整个发育过程中维持。目的:研究KCNQ1/KCNE1 K(+)通道和KCNQ1/KCNE1 K(+)通道重要代谢调节因子P2Y(4)在试验边缘细胞中的发育表达。材料与方法:以不同发育阶段(P1、P3、P5、P7、P14、P21)的Sprague-Dawley大鼠为研究对象。将带血管纹的螺旋韧带从软骨耳蜗或骨耳蜗上分离出来，准备用于电压敏感振动探针和免疫组织化学。结果:KCNQ1/KCNE1 K(+)通道阻断剂Chromanol 293B抑制P1至P21的短路电流(I (sc))。同样，尿苷5′-三磷酸在所有年龄段均能降低I (sc)。拮抗剂谱显示顶端P2Y受体为P2Y(4)亚型。KCNQ1、KCNE1和P2Y(4)免疫定位于P1的血管纹顶端区。

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

Acta oto-laryngologica. Supplementum

自引率

0.00%

发文量