Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes

Dihydropyridines (DHPs) are well known for their effects on L-type voltage-dependent Ca2+ channels. However, these drugs also affect other voltage-dependent ion channels, including Shaker K+ channels. We examined the effects of DHPs on the Shaker K+ channels expressed in Xenopus oocytes. Intracellul...

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Main Authors: Avdonin, Vladimir, Shibata, Erwin F., Hoshi, Toshinori
Format: Online
Language:English
Published: The Rockefeller University Press 1997
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2220064/
id pubmed-2220064
recordtype oai_dc
spelling pubmed-22200642008-04-22 Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes Avdonin, Vladimir Shibata, Erwin F. Hoshi, Toshinori Article Dihydropyridines (DHPs) are well known for their effects on L-type voltage-dependent Ca2+ channels. However, these drugs also affect other voltage-dependent ion channels, including Shaker K+ channels. We examined the effects of DHPs on the Shaker K+ channels expressed in Xenopus oocytes. Intracellular applications of DHPs quickly and reversibly induced apparent inactivation in the Shaker K+ mutant channels with disrupted N- and C-type inactivation. We found that DHPs interact with the open state of the channel as evidenced by the decreased mean open time. The DHPs effects are voltage-dependent, becoming more effective with hyperpolarization. A model which involves binding of two DHP molecules to the channel is consistent with the results obtained in our experiments. The Rockefeller University Press 1997-02-01 /pmc/articles/PMC2220064/ /pubmed/9041446 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Avdonin, Vladimir
Shibata, Erwin F.
Hoshi, Toshinori
spellingShingle Avdonin, Vladimir
Shibata, Erwin F.
Hoshi, Toshinori
Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes
author_facet Avdonin, Vladimir
Shibata, Erwin F.
Hoshi, Toshinori
author_sort Avdonin, Vladimir
title Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes
title_short Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes
title_full Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes
title_fullStr Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes
title_full_unstemmed Dihydropyridine Action on Voltage-dependent Potassium Channels Expressed in Xenopus Oocytes
title_sort dihydropyridine action on voltage-dependent potassium channels expressed in xenopus oocytes
description Dihydropyridines (DHPs) are well known for their effects on L-type voltage-dependent Ca2+ channels. However, these drugs also affect other voltage-dependent ion channels, including Shaker K+ channels. We examined the effects of DHPs on the Shaker K+ channels expressed in Xenopus oocytes. Intracellular applications of DHPs quickly and reversibly induced apparent inactivation in the Shaker K+ mutant channels with disrupted N- and C-type inactivation. We found that DHPs interact with the open state of the channel as evidenced by the decreased mean open time. The DHPs effects are voltage-dependent, becoming more effective with hyperpolarization. A model which involves binding of two DHP molecules to the channel is consistent with the results obtained in our experiments.
publisher The Rockefeller University Press
publishDate 1997
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2220064/
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