Ethanol Enhances Human Hyperpolarization-Activated Cyclic Nucleotide-Gated Currents
Background There is a clear association between excessive ethanol ( EtOH ) consumption and the risk of sudden cardiac death. The hyperpolarization‐activated cyclic nucleotide‐gated (HCN) current, I f, is known to contribute to spontaneous pacemaker activity of sinoatrial (SA) node cells. However, th...
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| description | Background
There is a clear association between excessive ethanol (
EtOH
) consumption and the risk of sudden cardiac death. The hyperpolarization‐activated cyclic nucleotide‐gated (HCN) current, I
f, is known to contribute to spontaneous pacemaker activity of sinoatrial (SA) node cells. However, the exact mechanisms of
EtOH
on arrhythmia induction are not well understood.
Methods
The preparations of SA node were excised from rabbit heart, transmembrane potentials were recorded by standard glass microelectrode technique, and a whole‐cell patch clamp technique was used to record I
f in enzymatically isolated rabbit SA node pacemaker cells. Human HCN2 (hHCN2) and HCN4 channels were heterologously expressed in
Xenopus oocytes and studied using 2‐electrode voltage clamp technique.
Results
Superfusion of
EtOH
increased the spontaneous firing frequency of SA node cells in a reversible fashion. Treatment with ivabradine irreversibly depressed basal firing frequency and markedly attenuated the enhancement effect of
EtOH
on firing. The stimulatory effects of
EtOH
on I
f were concentration‐dependent in the range of 1 to 100 mM, with an average EC
50 value of 20.81 ± 6.71 mM and Hill coefficient of 1.19 ± 0.10. Furthermore,
EtOH
reversibly enhanced the HCN currents in a concentration‐dependent fashion with an EC
50 value of 18.41 ± 2.75 mM for the HCN2 channel and 21.98 ± 3.54 mM for the HCN4 channel, which was accompanied by the acceleration of activation and deactivation kinetics. In addition,
EtOH
, at both moderate and high doses, caused a shift in the voltage dependence of hHCN4 channel activation to more depolarizing potentials. However, superfusion of high, not moderate, concentration of
EtOH
caused a shift in the voltage dependence of hHCN2 channel activation to more hyperpolarizing potentials.
Conclusions
This study provides insight into the molecular interaction of
EtOH
and the hHCN channels, which may shed light on elucidating the potentially proarrhythmic mechanism of
EtOH
. |
| doi_str_mv | 10.1111/j.1530-0277.2012.01826.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1323800050</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2950981201</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5496-560c4d23d6ef38af590391fb689783d11531bf0c0686f23cf996c44a501ea44c3</originalsourceid><addsrcrecordid>eNqNkV2LEzEUhoMobl39CzIggjcznnxO5kYopdsKyyqrspchzSSYOp2pyYy2--s349QK3mhuTkie8yaHB6EMQ4HTerstMKeQAynLggAmBWBJRHF4hGbni8doBpjxXADIC_Qsxi0AMCnEU3RBCK8wpniGPi37r7rtmmzZpmpszNbDTrfZ-ri3Yd81Ovh73fuuzeem9z90b-tscTSNN9nNYBrb9b62-Wo6H0KwbR-foydON9G-ONVL9OVq-Xmxzq8_rN4v5te54awSORdgWE1oLayjUjteAa2w2whZlZLWOE2CNw4MCCkcocZVlTCMaQ7YasYMvURvptx96L4PNvZq56OxTaNb2w1RYUqoTENz-DeaSAysBJ7QV3-h224IbRokBVJSSUF5mSg5USZ0MQbr1D74nQ5HhUGNjtRWjSrUqEKNjtQvR-qQWl-eHhg2O1ufG39LScDrE6Cj0Y0LSYyPfzhRci4YS9y7ifvpG3v87w-o-WJ5O25TQD4F-NjbwzlAh29KlLTk6u5mpW7h45Xk9C5N_wAaWLl4</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1332986357</pqid></control><display><type>article</type><title>Ethanol Enhances Human Hyperpolarization-Activated Cyclic Nucleotide-Gated Currents</title><source>Wiley Online Library - AutoHoldings Journals</source><source>MEDLINE</source><source>Journals@Ovid Complete</source><creator>Chen, Yongjun ; Wu, Pan ; Fan, Xinrong ; Chen, Hui ; Yang, Jing ; Song, Tao ; Huang, Congxin</creator><creatorcontrib>Chen, Yongjun ; Wu, Pan ; Fan, Xinrong ; Chen, Hui ; Yang, Jing ; Song, Tao ; Huang, Congxin</creatorcontrib><description>Background
There is a clear association between excessive ethanol (
EtOH
) consumption and the risk of sudden cardiac death. The hyperpolarization‐activated cyclic nucleotide‐gated (HCN) current, I
f, is known to contribute to spontaneous pacemaker activity of sinoatrial (SA) node cells. However, the exact mechanisms of
EtOH
on arrhythmia induction are not well understood.
Methods
The preparations of SA node were excised from rabbit heart, transmembrane potentials were recorded by standard glass microelectrode technique, and a whole‐cell patch clamp technique was used to record I
f in enzymatically isolated rabbit SA node pacemaker cells. Human HCN2 (hHCN2) and HCN4 channels were heterologously expressed in
Xenopus oocytes and studied using 2‐electrode voltage clamp technique.
Results
Superfusion of
EtOH
increased the spontaneous firing frequency of SA node cells in a reversible fashion. Treatment with ivabradine irreversibly depressed basal firing frequency and markedly attenuated the enhancement effect of
EtOH
on firing. The stimulatory effects of
EtOH
on I
f were concentration‐dependent in the range of 1 to 100 mM, with an average EC
50 value of 20.81 ± 6.71 mM and Hill coefficient of 1.19 ± 0.10. Furthermore,
EtOH
reversibly enhanced the HCN currents in a concentration‐dependent fashion with an EC
50 value of 18.41 ± 2.75 mM for the HCN2 channel and 21.98 ± 3.54 mM for the HCN4 channel, which was accompanied by the acceleration of activation and deactivation kinetics. In addition,
EtOH
, at both moderate and high doses, caused a shift in the voltage dependence of hHCN4 channel activation to more depolarizing potentials. However, superfusion of high, not moderate, concentration of
EtOH
caused a shift in the voltage dependence of hHCN2 channel activation to more hyperpolarizing potentials.
Conclusions
This study provides insight into the molecular interaction of
EtOH
and the hHCN channels, which may shed light on elucidating the potentially proarrhythmic mechanism of
EtOH
.</description><identifier>ISSN: 0145-6008</identifier><identifier>EISSN: 1530-0277</identifier><identifier>DOI: 10.1111/j.1530-0277.2012.01826.x</identifier><identifier>PMID: 22591131</identifier><identifier>CODEN: ACRSDM</identifier><language>eng</language><publisher>Hoboken, NJ: Blackwell Publishing Ltd</publisher><subject>Action Potentials - drug effects ; Action Potentials - physiology ; Alcoholism ; Alcoholism and acute alcohol poisoning ; Animals ; Arrhythmia ; Benzazepines - pharmacology ; Biological and medical sciences ; Biological Clocks - drug effects ; Biological Clocks - physiology ; Cyclic Nucleotide-Gated Cation Channels - drug effects ; Cyclic Nucleotide-Gated Cation Channels - physiology ; Deactivation ; Depolarization ; Dose-Response Relationship, Drug ; Drug abuse ; Ethanol ; Ethanol - pharmacology ; Firing rate ; Heart ; hHCN Current ; Humans ; ion channels (cyclic nucleotide-gated) ; Kinetics ; Male ; Medical sciences ; Membrane potential ; Microelectrodes ; Nodes ; Oocytes ; Oocytes - drug effects ; Oocytes - physiology ; Pacemaker Current (I f) ; Pacemaker Current (If) ; Pacemakers ; Patch-Clamp Techniques ; Rabbits ; Sinoatrial Node ; Sinoatrial Node - cytology ; Sinoatrial Node - drug effects ; Sinoatrial Node - physiology ; Spontaneous Action Potential ; Toxicology ; Xenopus</subject><ispartof>Alcoholism, clinical and experimental research, 2012-12, Vol.36 (12), p.2036-2046</ispartof><rights>Copyright © 2012 by the Research Society on Alcoholism</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 by the Research Society on Alcoholism.</rights><rights>Copyright 2012 Research Society on Alcoholism</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5496-560c4d23d6ef38af590391fb689783d11531bf0c0686f23cf996c44a501ea44c3</citedby><cites>FETCH-LOGICAL-c5496-560c4d23d6ef38af590391fb689783d11531bf0c0686f23cf996c44a501ea44c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1530-0277.2012.01826.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1530-0277.2012.01826.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26755644$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22591131$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Yongjun</creatorcontrib><creatorcontrib>Wu, Pan</creatorcontrib><creatorcontrib>Fan, Xinrong</creatorcontrib><creatorcontrib>Chen, Hui</creatorcontrib><creatorcontrib>Yang, Jing</creatorcontrib><creatorcontrib>Song, Tao</creatorcontrib><creatorcontrib>Huang, Congxin</creatorcontrib><title>Ethanol Enhances Human Hyperpolarization-Activated Cyclic Nucleotide-Gated Currents</title><title>Alcoholism, clinical and experimental research</title><addtitle>Alcohol Clin Exp Res</addtitle><description>Background
There is a clear association between excessive ethanol (
EtOH
) consumption and the risk of sudden cardiac death. The hyperpolarization‐activated cyclic nucleotide‐gated (HCN) current, I
f, is known to contribute to spontaneous pacemaker activity of sinoatrial (SA) node cells. However, the exact mechanisms of
EtOH
on arrhythmia induction are not well understood.
Methods
The preparations of SA node were excised from rabbit heart, transmembrane potentials were recorded by standard glass microelectrode technique, and a whole‐cell patch clamp technique was used to record I
f in enzymatically isolated rabbit SA node pacemaker cells. Human HCN2 (hHCN2) and HCN4 channels were heterologously expressed in
Xenopus oocytes and studied using 2‐electrode voltage clamp technique.
Results
Superfusion of
EtOH
increased the spontaneous firing frequency of SA node cells in a reversible fashion. Treatment with ivabradine irreversibly depressed basal firing frequency and markedly attenuated the enhancement effect of
EtOH
on firing. The stimulatory effects of
EtOH
on I
f were concentration‐dependent in the range of 1 to 100 mM, with an average EC
50 value of 20.81 ± 6.71 mM and Hill coefficient of 1.19 ± 0.10. Furthermore,
EtOH
reversibly enhanced the HCN currents in a concentration‐dependent fashion with an EC
50 value of 18.41 ± 2.75 mM for the HCN2 channel and 21.98 ± 3.54 mM for the HCN4 channel, which was accompanied by the acceleration of activation and deactivation kinetics. In addition,
EtOH
, at both moderate and high doses, caused a shift in the voltage dependence of hHCN4 channel activation to more depolarizing potentials. However, superfusion of high, not moderate, concentration of
EtOH
caused a shift in the voltage dependence of hHCN2 channel activation to more hyperpolarizing potentials.
Conclusions
This study provides insight into the molecular interaction of
EtOH
and the hHCN channels, which may shed light on elucidating the potentially proarrhythmic mechanism of
EtOH
.</description><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Alcoholism</subject><subject>Alcoholism and acute alcohol poisoning</subject><subject>Animals</subject><subject>Arrhythmia</subject><subject>Benzazepines - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biological Clocks - drug effects</subject><subject>Biological Clocks - physiology</subject><subject>Cyclic Nucleotide-Gated Cation Channels - drug effects</subject><subject>Cyclic Nucleotide-Gated Cation Channels - physiology</subject><subject>Deactivation</subject><subject>Depolarization</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug abuse</subject><subject>Ethanol</subject><subject>Ethanol - pharmacology</subject><subject>Firing rate</subject><subject>Heart</subject><subject>hHCN Current</subject><subject>Humans</subject><subject>ion channels (cyclic nucleotide-gated)</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane potential</subject><subject>Microelectrodes</subject><subject>Nodes</subject><subject>Oocytes</subject><subject>Oocytes - drug effects</subject><subject>Oocytes - physiology</subject><subject>Pacemaker Current (I f)</subject><subject>Pacemaker Current (If)</subject><subject>Pacemakers</subject><subject>Patch-Clamp Techniques</subject><subject>Rabbits</subject><subject>Sinoatrial Node</subject><subject>Sinoatrial Node - cytology</subject><subject>Sinoatrial Node - drug effects</subject><subject>Sinoatrial Node - physiology</subject><subject>Spontaneous Action Potential</subject><subject>Toxicology</subject><subject>Xenopus</subject><issn>0145-6008</issn><issn>1530-0277</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV2LEzEUhoMobl39CzIggjcznnxO5kYopdsKyyqrspchzSSYOp2pyYy2--s349QK3mhuTkie8yaHB6EMQ4HTerstMKeQAynLggAmBWBJRHF4hGbni8doBpjxXADIC_Qsxi0AMCnEU3RBCK8wpniGPi37r7rtmmzZpmpszNbDTrfZ-ri3Yd81Ovh73fuuzeem9z90b-tscTSNN9nNYBrb9b62-Wo6H0KwbR-foydON9G-ONVL9OVq-Xmxzq8_rN4v5te54awSORdgWE1oLayjUjteAa2w2whZlZLWOE2CNw4MCCkcocZVlTCMaQ7YasYMvURvptx96L4PNvZq56OxTaNb2w1RYUqoTENz-DeaSAysBJ7QV3-h224IbRokBVJSSUF5mSg5USZ0MQbr1D74nQ5HhUGNjtRWjSrUqEKNjtQvR-qQWl-eHhg2O1ufG39LScDrE6Cj0Y0LSYyPfzhRci4YS9y7ifvpG3v87w-o-WJ5O25TQD4F-NjbwzlAh29KlLTk6u5mpW7h45Xk9C5N_wAaWLl4</recordid><startdate>201212</startdate><enddate>201212</enddate><creator>Chen, Yongjun</creator><creator>Wu, Pan</creator><creator>Fan, Xinrong</creator><creator>Chen, Hui</creator><creator>Yang, Jing</creator><creator>Song, Tao</creator><creator>Huang, Congxin</creator><general>Blackwell Publishing Ltd</general><general>Wiley</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>K7.</scope><scope>K9.</scope><scope>7X8</scope><scope>7TM</scope></search><sort><creationdate>201212</creationdate><title>Ethanol Enhances Human Hyperpolarization-Activated Cyclic Nucleotide-Gated Currents</title><author>Chen, Yongjun ; Wu, Pan ; Fan, Xinrong ; Chen, Hui ; Yang, Jing ; Song, Tao ; Huang, Congxin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5496-560c4d23d6ef38af590391fb689783d11531bf0c0686f23cf996c44a501ea44c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Alcoholism</topic><topic>Alcoholism and acute alcohol poisoning</topic><topic>Animals</topic><topic>Arrhythmia</topic><topic>Benzazepines - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biological Clocks - drug effects</topic><topic>Biological Clocks - physiology</topic><topic>Cyclic Nucleotide-Gated Cation Channels - drug effects</topic><topic>Cyclic Nucleotide-Gated Cation Channels - physiology</topic><topic>Deactivation</topic><topic>Depolarization</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug abuse</topic><topic>Ethanol</topic><topic>Ethanol - pharmacology</topic><topic>Firing rate</topic><topic>Heart</topic><topic>hHCN Current</topic><topic>Humans</topic><topic>ion channels (cyclic nucleotide-gated)</topic><topic>Kinetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane potential</topic><topic>Microelectrodes</topic><topic>Nodes</topic><topic>Oocytes</topic><topic>Oocytes - drug effects</topic><topic>Oocytes - physiology</topic><topic>Pacemaker Current (I f)</topic><topic>Pacemaker Current (If)</topic><topic>Pacemakers</topic><topic>Patch-Clamp Techniques</topic><topic>Rabbits</topic><topic>Sinoatrial Node</topic><topic>Sinoatrial Node - cytology</topic><topic>Sinoatrial Node - drug effects</topic><topic>Sinoatrial Node - physiology</topic><topic>Spontaneous Action Potential</topic><topic>Toxicology</topic><topic>Xenopus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yongjun</creatorcontrib><creatorcontrib>Wu, Pan</creatorcontrib><creatorcontrib>Fan, Xinrong</creatorcontrib><creatorcontrib>Chen, Hui</creatorcontrib><creatorcontrib>Yang, Jing</creatorcontrib><creatorcontrib>Song, Tao</creatorcontrib><creatorcontrib>Huang, Congxin</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Criminal Justice (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Alcoholism, clinical and experimental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Yongjun</au><au>Wu, Pan</au><au>Fan, Xinrong</au><au>Chen, Hui</au><au>Yang, Jing</au><au>Song, Tao</au><au>Huang, Congxin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ethanol Enhances Human Hyperpolarization-Activated Cyclic Nucleotide-Gated Currents</atitle><jtitle>Alcoholism, clinical and experimental research</jtitle><addtitle>Alcohol Clin Exp Res</addtitle><date>2012-12</date><risdate>2012</risdate><volume>36</volume><issue>12</issue><spage>2036</spage><epage>2046</epage><pages>2036-2046</pages><issn>0145-6008</issn><eissn>1530-0277</eissn><coden>ACRSDM</coden><abstract>Background
There is a clear association between excessive ethanol (
EtOH
) consumption and the risk of sudden cardiac death. The hyperpolarization‐activated cyclic nucleotide‐gated (HCN) current, I
f, is known to contribute to spontaneous pacemaker activity of sinoatrial (SA) node cells. However, the exact mechanisms of
EtOH
on arrhythmia induction are not well understood.
Methods
The preparations of SA node were excised from rabbit heart, transmembrane potentials were recorded by standard glass microelectrode technique, and a whole‐cell patch clamp technique was used to record I
f in enzymatically isolated rabbit SA node pacemaker cells. Human HCN2 (hHCN2) and HCN4 channels were heterologously expressed in
Xenopus oocytes and studied using 2‐electrode voltage clamp technique.
Results
Superfusion of
EtOH
increased the spontaneous firing frequency of SA node cells in a reversible fashion. Treatment with ivabradine irreversibly depressed basal firing frequency and markedly attenuated the enhancement effect of
EtOH
on firing. The stimulatory effects of
EtOH
on I
f were concentration‐dependent in the range of 1 to 100 mM, with an average EC
50 value of 20.81 ± 6.71 mM and Hill coefficient of 1.19 ± 0.10. Furthermore,
EtOH
reversibly enhanced the HCN currents in a concentration‐dependent fashion with an EC
50 value of 18.41 ± 2.75 mM for the HCN2 channel and 21.98 ± 3.54 mM for the HCN4 channel, which was accompanied by the acceleration of activation and deactivation kinetics. In addition,
EtOH
, at both moderate and high doses, caused a shift in the voltage dependence of hHCN4 channel activation to more depolarizing potentials. However, superfusion of high, not moderate, concentration of
EtOH
caused a shift in the voltage dependence of hHCN2 channel activation to more hyperpolarizing potentials.
Conclusions
This study provides insight into the molecular interaction of
EtOH
and the hHCN channels, which may shed light on elucidating the potentially proarrhythmic mechanism of
EtOH
.</abstract><cop>Hoboken, NJ</cop><pub>Blackwell Publishing Ltd</pub><pmid>22591131</pmid><doi>10.1111/j.1530-0277.2012.01826.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0145-6008 |
| ispartof | Alcoholism, clinical and experimental research, 2012-12, Vol.36 (12), p.2036-2046 |
| issn | 0145-6008 1530-0277 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1323800050 |
| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; Journals@Ovid Complete |
| subjects | Action Potentials - drug effects Action Potentials - physiology Alcoholism Alcoholism and acute alcohol poisoning Animals Arrhythmia Benzazepines - pharmacology Biological and medical sciences Biological Clocks - drug effects Biological Clocks - physiology Cyclic Nucleotide-Gated Cation Channels - drug effects Cyclic Nucleotide-Gated Cation Channels - physiology Deactivation Depolarization Dose-Response Relationship, Drug Drug abuse Ethanol Ethanol - pharmacology Firing rate Heart hHCN Current Humans ion channels (cyclic nucleotide-gated) Kinetics Male Medical sciences Membrane potential Microelectrodes Nodes Oocytes Oocytes - drug effects Oocytes - physiology Pacemaker Current (I f) Pacemaker Current (If) Pacemakers Patch-Clamp Techniques Rabbits Sinoatrial Node Sinoatrial Node - cytology Sinoatrial Node - drug effects Sinoatrial Node - physiology Spontaneous Action Potential Toxicology Xenopus |
| title | Ethanol Enhances Human Hyperpolarization-Activated Cyclic Nucleotide-Gated Currents |
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