Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors
KCNQ1-4 potassium channels were expressed in mammalian Chinese hamster ovary (CHO) cells stably transfected with M 1 muscarinic acetylcholine receptors and currents were recorded using the whole-cell perforated patch technique and cell-attached patch recording. Stimulation of M 1 receptors by 10 μ...
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Veröffentlicht in: | The Journal of physiology 2000-02, Vol.522 (3), p.349-355 |
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creator | Selyanko, A. A. Hadley, J. K. Wood, I. C. Abogadie, F. C. Jentsch, T. J. Brown, D. A. |
description | KCNQ1-4 potassium channels were expressed in mammalian Chinese hamster ovary (CHO) cells stably transfected with M 1 muscarinic acetylcholine receptors and currents were recorded using the whole-cell perforated patch technique and cell-attached
patch recording.
Stimulation of M 1 receptors by 10 μ m oxotremorine-M (Oxo-M) strongly reduced (to 0â10%) currents produced by KCNQ1-4 subunits expressed individually and also
those produced by KCNQ2+KCNQ3 and KCNQ1+KCNE1 heteromers, which are thought to generate neuronal M-currents ( I K,M ) and cardiac slow delayed rectifier currents ( I K,s ), respectively.
The activity of KCNQ2+KCNQ3, KCNQ2 and KCNQ3 channels recorded with cell-attached pipettes was strongly and reversibly reduced
by Oxo-M applied to the extra-patch membrane.
It is concluded that M 1 receptors couple to all known KCNQ subunits and that inhibition of KCNQ2+KCNQ3 channels, like that of native M-channels,
requires a diffusible second messenger. |
doi_str_mv | 10.1111/j.1469-7793.2000.t01-2-00349.x |
format | Article |
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patch recording.
Stimulation of M 1 receptors by 10 μ m oxotremorine-M (Oxo-M) strongly reduced (to 0â10%) currents produced by KCNQ1-4 subunits expressed individually and also
those produced by KCNQ2+KCNQ3 and KCNQ1+KCNE1 heteromers, which are thought to generate neuronal M-currents ( I K,M ) and cardiac slow delayed rectifier currents ( I K,s ), respectively.
The activity of KCNQ2+KCNQ3, KCNQ2 and KCNQ3 channels recorded with cell-attached pipettes was strongly and reversibly reduced
by Oxo-M applied to the extra-patch membrane.
It is concluded that M 1 receptors couple to all known KCNQ subunits and that inhibition of KCNQ2+KCNQ3 channels, like that of native M-channels,
requires a diffusible second messenger.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1111/j.1469-7793.2000.t01-2-00349.x</identifier><identifier>PMID: 10713961</identifier><language>eng</language><publisher>Oxford, UK: The Physiological Society</publisher><subject>Animals ; CHO Cells ; Cricetinae ; KCNQ Potassium Channels ; KCNQ1 Potassium Channel ; KCNQ2 Potassium Channel ; KCNQ3 Potassium Channel ; Muscarinic Agonists - pharmacology ; Oxotremorine - analogs & derivatives ; Oxotremorine - pharmacology ; Patch-Clamp Techniques ; Potassium Channel Blockers ; Potassium Channels - genetics ; Potassium Channels - metabolism ; Potassium Channels, Voltage-Gated ; Rapid Report ; Receptor, Muscarinic M1 ; Receptors, Muscarinic - drug effects ; Receptors, Muscarinic - metabolism ; Stimulation, Chemical ; Transfection</subject><ispartof>The Journal of physiology, 2000-02, Vol.522 (3), p.349-355</ispartof><rights>2000 The Journal of Physiology © 2000 The Physiological Society</rights><rights>The Physiological Society 2000 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2269765/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2269765/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10713961$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Selyanko, A. A.</creatorcontrib><creatorcontrib>Hadley, J. K.</creatorcontrib><creatorcontrib>Wood, I. C.</creatorcontrib><creatorcontrib>Abogadie, F. C.</creatorcontrib><creatorcontrib>Jentsch, T. J.</creatorcontrib><creatorcontrib>Brown, D. A.</creatorcontrib><title>Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>KCNQ1-4 potassium channels were expressed in mammalian Chinese hamster ovary (CHO) cells stably transfected with M 1 muscarinic acetylcholine receptors and currents were recorded using the whole-cell perforated patch technique and cell-attached
patch recording.
Stimulation of M 1 receptors by 10 μ m oxotremorine-M (Oxo-M) strongly reduced (to 0â10%) currents produced by KCNQ1-4 subunits expressed individually and also
those produced by KCNQ2+KCNQ3 and KCNQ1+KCNE1 heteromers, which are thought to generate neuronal M-currents ( I K,M ) and cardiac slow delayed rectifier currents ( I K,s ), respectively.
The activity of KCNQ2+KCNQ3, KCNQ2 and KCNQ3 channels recorded with cell-attached pipettes was strongly and reversibly reduced
by Oxo-M applied to the extra-patch membrane.
It is concluded that M 1 receptors couple to all known KCNQ subunits and that inhibition of KCNQ2+KCNQ3 channels, like that of native M-channels,
requires a diffusible second messenger.</description><subject>Animals</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>KCNQ Potassium Channels</subject><subject>KCNQ1 Potassium Channel</subject><subject>KCNQ2 Potassium Channel</subject><subject>KCNQ3 Potassium Channel</subject><subject>Muscarinic Agonists - pharmacology</subject><subject>Oxotremorine - analogs & derivatives</subject><subject>Oxotremorine - pharmacology</subject><subject>Patch-Clamp Techniques</subject><subject>Potassium Channel Blockers</subject><subject>Potassium Channels - genetics</subject><subject>Potassium Channels - metabolism</subject><subject>Potassium Channels, Voltage-Gated</subject><subject>Rapid Report</subject><subject>Receptor, Muscarinic M1</subject><subject>Receptors, Muscarinic - drug effects</subject><subject>Receptors, Muscarinic - metabolism</subject><subject>Stimulation, Chemical</subject><subject>Transfection</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkVtv1DAQhS0EokvhLyA_lacE3xLHL0iw4lIoN6k8j7xeZ-NVYgc7aXf_PQ5bquKXsXTOnNHMh9AFJSXN7_W-pKJWhZSKl4wQUk6EFqwghAtVHh6h1b38GK0IYazgsqJn6FlKe0IoJ0o9RWeUSMpVTVcoXPrObdzkgsehxV_W337SQuAxTDolNw_YdNp72ydsD2O0Kdktdh4Pehh077THxvZZvHEaf6V4mJPR0XlnsDZ2OvamC73zFkdr7DiFmJ6jJ63uk31xV8_Rrw_vr9efiqvvHy_Xb6-KnRBCFUxy2ghpqZR1y1rSaCGFYRvOVaVroZVupGiU5LrhlWy3rNlwZq2ocrfgjebn6M0pd5w3g90a66eoexijG3Q8QtAO_le862AXboCxWsm6ygEXdwEx_J5tmmBwaVlWexvmBJKoqlFVnY0vH066H_Hvxtnw7mS4db09PtBhIQp7WJDBggwWopCJAoO_ROEA159_5E8OeXUK6dyuu3XRwtgdkwspGJcPDRVjwGFx_gGV_KQZ</recordid><startdate>200002</startdate><enddate>200002</enddate><creator>Selyanko, A. A.</creator><creator>Hadley, J. K.</creator><creator>Wood, I. C.</creator><creator>Abogadie, F. C.</creator><creator>Jentsch, T. J.</creator><creator>Brown, D. A.</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Blackwell Science Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200002</creationdate><title>Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors</title><author>Selyanko, A. A. ; Hadley, J. K. ; Wood, I. C. ; Abogadie, F. C. ; Jentsch, T. J. ; Brown, D. A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g4449-2731847e1776f2f08a474c2b3395a64a9a8748973a8357fd28b32ee45444438a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>KCNQ Potassium Channels</topic><topic>KCNQ1 Potassium Channel</topic><topic>KCNQ2 Potassium Channel</topic><topic>KCNQ3 Potassium Channel</topic><topic>Muscarinic Agonists - pharmacology</topic><topic>Oxotremorine - analogs & derivatives</topic><topic>Oxotremorine - pharmacology</topic><topic>Patch-Clamp Techniques</topic><topic>Potassium Channel Blockers</topic><topic>Potassium Channels - genetics</topic><topic>Potassium Channels - metabolism</topic><topic>Potassium Channels, Voltage-Gated</topic><topic>Rapid Report</topic><topic>Receptor, Muscarinic M1</topic><topic>Receptors, Muscarinic - drug effects</topic><topic>Receptors, Muscarinic - metabolism</topic><topic>Stimulation, Chemical</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Selyanko, A. A.</creatorcontrib><creatorcontrib>Hadley, J. K.</creatorcontrib><creatorcontrib>Wood, I. C.</creatorcontrib><creatorcontrib>Abogadie, F. C.</creatorcontrib><creatorcontrib>Jentsch, T. J.</creatorcontrib><creatorcontrib>Brown, D. A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Selyanko, A. A.</au><au>Hadley, J. K.</au><au>Wood, I. C.</au><au>Abogadie, F. C.</au><au>Jentsch, T. J.</au><au>Brown, D. A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2000-02</date><risdate>2000</risdate><volume>522</volume><issue>3</issue><spage>349</spage><epage>355</epage><pages>349-355</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>KCNQ1-4 potassium channels were expressed in mammalian Chinese hamster ovary (CHO) cells stably transfected with M 1 muscarinic acetylcholine receptors and currents were recorded using the whole-cell perforated patch technique and cell-attached
patch recording.
Stimulation of M 1 receptors by 10 μ m oxotremorine-M (Oxo-M) strongly reduced (to 0â10%) currents produced by KCNQ1-4 subunits expressed individually and also
those produced by KCNQ2+KCNQ3 and KCNQ1+KCNE1 heteromers, which are thought to generate neuronal M-currents ( I K,M ) and cardiac slow delayed rectifier currents ( I K,s ), respectively.
The activity of KCNQ2+KCNQ3, KCNQ2 and KCNQ3 channels recorded with cell-attached pipettes was strongly and reversibly reduced
by Oxo-M applied to the extra-patch membrane.
It is concluded that M 1 receptors couple to all known KCNQ subunits and that inhibition of KCNQ2+KCNQ3 channels, like that of native M-channels,
requires a diffusible second messenger.</abstract><cop>Oxford, UK</cop><pub>The Physiological Society</pub><pmid>10713961</pmid><doi>10.1111/j.1469-7793.2000.t01-2-00349.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals CHO Cells Cricetinae KCNQ Potassium Channels KCNQ1 Potassium Channel KCNQ2 Potassium Channel KCNQ3 Potassium Channel Muscarinic Agonists - pharmacology Oxotremorine - analogs & derivatives Oxotremorine - pharmacology Patch-Clamp Techniques Potassium Channel Blockers Potassium Channels - genetics Potassium Channels - metabolism Potassium Channels, Voltage-Gated Rapid Report Receptor, Muscarinic M1 Receptors, Muscarinic - drug effects Receptors, Muscarinic - metabolism Stimulation, Chemical Transfection |
title | Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors |
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