Electrophysiological characterization of sodium-activated potassium channels in NG108-15 and NSC-34 motor neuron-like cells
Aims The electrical properties of Na+‐activated K+ current (IK(Na)) and its contribution to spike firing has not been characterized in motor neurons. Methods We evaluated how activation of voltage‐gated K+ current (IK) at the cellular level could be coupled to Na+ influx through voltage‐gated Na+ cu...
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| Veröffentlicht in: | Acta Physiologica 2012-10, Vol.206 (2), p.120-134 |
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| creator | Wu, S.-N. Yeh, C.-C. Huang, H.-C. So, E. C. Lo, Y.-C. |
| description | Aims
The electrical properties of Na+‐activated K+ current (IK(Na)) and its contribution to spike firing has not been characterized in motor neurons.
Methods
We evaluated how activation of voltage‐gated K+ current (IK) at the cellular level could be coupled to Na+ influx through voltage‐gated Na+ current (INa) in two motor neuron‐like cells (NG108‐15 and NSC‐34 cells).
Results
Increasing stimulation frequency altered the amplitudes of both INa and IK simultaneously. With changes in stimulation frequency, the kinetics of both INa inactivation and IK activation were well correlated at the same cell. Addition of tetrodotoxin or ranolazine reduced the amplitudes of both INa and IK simultaneously. Tefluthrin (Tef) increased the amplitudes of both INa and IK throughout the voltages ranging from −30 to + 10 mV. In cell‐attached recordings, single‐channel conductance from a linear current‐voltage relation was 94 ± 3 pS (n = 7). Tef (10 μm) enhanced channel activity with no change in single‐channel conductance. Tef increased spike firing accompanied by enhanced facilitation of spike‐frequency adaptation. Riluzole (10 μm) reversed Tef‐stimulated activity of KNa channels. In motor neuron‐like NSC‐34 cells, increasing stimulation frequency altered the kinetics of both INa and IK. Modelling studies of motor neurons were simulated to demonstrate that the magnitude of IK(Na) modulates AP firing.
Conclusions
There is a direct association of Na+ and KNa channels which can provide the rapid activation of KNa channels required to regulate AP firing occurring in motor neurons. |
| doi_str_mv | 10.1111/j.1748-1716.2012.02438.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_1419363594</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3957298291</sourcerecordid><originalsourceid>FETCH-LOGICAL-i3958-cf271bb11f3f789f74e879b0f3bb1d6b9fab472a251743a8da3f3b44f3bfb4a23</originalsourceid><addsrcrecordid>eNqFkl1v0zAUhiMEYtO2v4AsISRuEvyVOL5BqsrWIaaCBohLy0ls5s6xi51s7fbncdZSJG7whX10zqPj9_h1lgEEC5TWu1WBGK1zxFBVYIhwATEldbF5lh0fCs8PMayPsrMYVxAmFBGK8cvsCOOSkArXx9njuVXtEPz6ZhuNt_6naaUF7Y0Msh1UMA9yMN4Br0H0nRn7PKXNnRxUB9Z-kDGm3IQ7p2wExoHlAsF0bwmk68Dy6zwnFPR-8AE4NQbvcmtuFWiVtfE0e6Gljepsf55k3y_Ov80v86vPi4_z2VVuCC_rvNWYoaZBSBPNaq4ZVTXjDdQkJbuq4Vo2lGGJyzQykXUnSSpRmjbdUInJSfZ213cd_K9RxUH0Jk4KpFN-jAJRxElFSk7_j0JSQzbZkNDX_6ArPwaXBhGIVRXmOIlK1Ks9NTa96sQ6mF6GrfjjQALe7AEZ09PrIF1r4l8u6YIc8sS933H3xqrtoY6gmNSIlZj8FpP3YvoU4ulTiI2YfbmcTWFqkO8amDiozaGBDLeiYoSV4sdyIT5dX3wgy2soIPkNv_a4GA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1766292472</pqid></control><display><type>article</type><title>Electrophysiological characterization of sodium-activated potassium channels in NG108-15 and NSC-34 motor neuron-like cells</title><source>MEDLINE</source><source>Wiley Journals</source><creator>Wu, S.-N. ; Yeh, C.-C. ; Huang, H.-C. ; So, E. C. ; Lo, Y.-C.</creator><creatorcontrib>Wu, S.-N. ; Yeh, C.-C. ; Huang, H.-C. ; So, E. C. ; Lo, Y.-C.</creatorcontrib><description>Aims
The electrical properties of Na+‐activated K+ current (IK(Na)) and its contribution to spike firing has not been characterized in motor neurons.
Methods
We evaluated how activation of voltage‐gated K+ current (IK) at the cellular level could be coupled to Na+ influx through voltage‐gated Na+ current (INa) in two motor neuron‐like cells (NG108‐15 and NSC‐34 cells).
Results
Increasing stimulation frequency altered the amplitudes of both INa and IK simultaneously. With changes in stimulation frequency, the kinetics of both INa inactivation and IK activation were well correlated at the same cell. Addition of tetrodotoxin or ranolazine reduced the amplitudes of both INa and IK simultaneously. Tefluthrin (Tef) increased the amplitudes of both INa and IK throughout the voltages ranging from −30 to + 10 mV. In cell‐attached recordings, single‐channel conductance from a linear current‐voltage relation was 94 ± 3 pS (n = 7). Tef (10 μm) enhanced channel activity with no change in single‐channel conductance. Tef increased spike firing accompanied by enhanced facilitation of spike‐frequency adaptation. Riluzole (10 μm) reversed Tef‐stimulated activity of KNa channels. In motor neuron‐like NSC‐34 cells, increasing stimulation frequency altered the kinetics of both INa and IK. Modelling studies of motor neurons were simulated to demonstrate that the magnitude of IK(Na) modulates AP firing.
Conclusions
There is a direct association of Na+ and KNa channels which can provide the rapid activation of KNa channels required to regulate AP firing occurring in motor neurons.</description><identifier>ISSN: 1748-1708</identifier><identifier>EISSN: 1748-1716</identifier><identifier>DOI: 10.1111/j.1748-1716.2012.02438.x</identifier><identifier>PMID: 22533628</identifier><language>eng</language><publisher>Oxford: Blackwell Publishing Ltd</publisher><subject>Acetanilides - pharmacology ; Action Potentials ; Animals ; Biological and medical sciences ; Cell Line, Tumor ; Cyclopropanes - pharmacology ; Electric Stimulation ; Fundamental and applied biological sciences. Psychology ; Hydrocarbons, Fluorinated - pharmacology ; Ion Channel Gating - drug effects ; K+ current ; Kinetics ; Mice ; Models, Neurological ; motor neurons ; Motor Neurons - metabolism ; Na+ current ; Na+-activated K+ channels ; Patch-Clamp Techniques ; Piperazines - pharmacology ; Potassium - metabolism ; Potassium Channels, Voltage-Gated - drug effects ; Potassium Channels, Voltage-Gated - metabolism ; pyrethroid ; Ranolazine ; Rats ; Riluzole - pharmacology ; simulation ; Sodium - metabolism ; Sodium Channel Blockers - pharmacology ; Tetrodotoxin - pharmacology ; Vertebrates: anatomy and physiology, studies on body, several organs or systems ; Voltage-Gated Sodium Channels - drug effects ; Voltage-Gated Sodium Channels - metabolism</subject><ispartof>Acta Physiologica, 2012-10, Vol.206 (2), p.120-134</ispartof><rights>2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society</rights><rights>2015 INIST-CNRS</rights><rights>2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.</rights><rights>Copyright © 2012 Scandinavian Physiological Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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.1748-1716.2012.02438.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1748-1716.2012.02438.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26350909$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22533628$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, S.-N.</creatorcontrib><creatorcontrib>Yeh, C.-C.</creatorcontrib><creatorcontrib>Huang, H.-C.</creatorcontrib><creatorcontrib>So, E. C.</creatorcontrib><creatorcontrib>Lo, Y.-C.</creatorcontrib><title>Electrophysiological characterization of sodium-activated potassium channels in NG108-15 and NSC-34 motor neuron-like cells</title><title>Acta Physiologica</title><addtitle>Acta Physiol</addtitle><description>Aims
The electrical properties of Na+‐activated K+ current (IK(Na)) and its contribution to spike firing has not been characterized in motor neurons.
Methods
We evaluated how activation of voltage‐gated K+ current (IK) at the cellular level could be coupled to Na+ influx through voltage‐gated Na+ current (INa) in two motor neuron‐like cells (NG108‐15 and NSC‐34 cells).
Results
Increasing stimulation frequency altered the amplitudes of both INa and IK simultaneously. With changes in stimulation frequency, the kinetics of both INa inactivation and IK activation were well correlated at the same cell. Addition of tetrodotoxin or ranolazine reduced the amplitudes of both INa and IK simultaneously. Tefluthrin (Tef) increased the amplitudes of both INa and IK throughout the voltages ranging from −30 to + 10 mV. In cell‐attached recordings, single‐channel conductance from a linear current‐voltage relation was 94 ± 3 pS (n = 7). Tef (10 μm) enhanced channel activity with no change in single‐channel conductance. Tef increased spike firing accompanied by enhanced facilitation of spike‐frequency adaptation. Riluzole (10 μm) reversed Tef‐stimulated activity of KNa channels. In motor neuron‐like NSC‐34 cells, increasing stimulation frequency altered the kinetics of both INa and IK. Modelling studies of motor neurons were simulated to demonstrate that the magnitude of IK(Na) modulates AP firing.
Conclusions
There is a direct association of Na+ and KNa channels which can provide the rapid activation of KNa channels required to regulate AP firing occurring in motor neurons.</description><subject>Acetanilides - pharmacology</subject><subject>Action Potentials</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>Cyclopropanes - pharmacology</subject><subject>Electric Stimulation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hydrocarbons, Fluorinated - pharmacology</subject><subject>Ion Channel Gating - drug effects</subject><subject>K+ current</subject><subject>Kinetics</subject><subject>Mice</subject><subject>Models, Neurological</subject><subject>motor neurons</subject><subject>Motor Neurons - metabolism</subject><subject>Na+ current</subject><subject>Na+-activated K+ channels</subject><subject>Patch-Clamp Techniques</subject><subject>Piperazines - pharmacology</subject><subject>Potassium - metabolism</subject><subject>Potassium Channels, Voltage-Gated - drug effects</subject><subject>Potassium Channels, Voltage-Gated - metabolism</subject><subject>pyrethroid</subject><subject>Ranolazine</subject><subject>Rats</subject><subject>Riluzole - pharmacology</subject><subject>simulation</subject><subject>Sodium - metabolism</subject><subject>Sodium Channel Blockers - pharmacology</subject><subject>Tetrodotoxin - pharmacology</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><subject>Voltage-Gated Sodium Channels - drug effects</subject><subject>Voltage-Gated Sodium Channels - metabolism</subject><issn>1748-1708</issn><issn>1748-1716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkl1v0zAUhiMEYtO2v4AsISRuEvyVOL5BqsrWIaaCBohLy0ls5s6xi51s7fbncdZSJG7whX10zqPj9_h1lgEEC5TWu1WBGK1zxFBVYIhwATEldbF5lh0fCs8PMayPsrMYVxAmFBGK8cvsCOOSkArXx9njuVXtEPz6ZhuNt_6naaUF7Y0Msh1UMA9yMN4Br0H0nRn7PKXNnRxUB9Z-kDGm3IQ7p2wExoHlAsF0bwmk68Dy6zwnFPR-8AE4NQbvcmtuFWiVtfE0e6Gljepsf55k3y_Ov80v86vPi4_z2VVuCC_rvNWYoaZBSBPNaq4ZVTXjDdQkJbuq4Vo2lGGJyzQykXUnSSpRmjbdUInJSfZ213cd_K9RxUH0Jk4KpFN-jAJRxElFSk7_j0JSQzbZkNDX_6ArPwaXBhGIVRXmOIlK1Ks9NTa96sQ6mF6GrfjjQALe7AEZ09PrIF1r4l8u6YIc8sS933H3xqrtoY6gmNSIlZj8FpP3YvoU4ulTiI2YfbmcTWFqkO8amDiozaGBDLeiYoSV4sdyIT5dX3wgy2soIPkNv_a4GA</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Wu, S.-N.</creator><creator>Yeh, C.-C.</creator><creator>Huang, H.-C.</creator><creator>So, E. C.</creator><creator>Lo, Y.-C.</creator><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</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>7TK</scope><scope>7TS</scope><scope>7X8</scope></search><sort><creationdate>201210</creationdate><title>Electrophysiological characterization of sodium-activated potassium channels in NG108-15 and NSC-34 motor neuron-like cells</title><author>Wu, S.-N. ; Yeh, C.-C. ; Huang, H.-C. ; So, E. C. ; Lo, Y.-C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i3958-cf271bb11f3f789f74e879b0f3bb1d6b9fab472a251743a8da3f3b44f3bfb4a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acetanilides - pharmacology</topic><topic>Action Potentials</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>Cyclopropanes - pharmacology</topic><topic>Electric Stimulation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hydrocarbons, Fluorinated - pharmacology</topic><topic>Ion Channel Gating - drug effects</topic><topic>K+ current</topic><topic>Kinetics</topic><topic>Mice</topic><topic>Models, Neurological</topic><topic>motor neurons</topic><topic>Motor Neurons - metabolism</topic><topic>Na+ current</topic><topic>Na+-activated K+ channels</topic><topic>Patch-Clamp Techniques</topic><topic>Piperazines - pharmacology</topic><topic>Potassium - metabolism</topic><topic>Potassium Channels, Voltage-Gated - drug effects</topic><topic>Potassium Channels, Voltage-Gated - metabolism</topic><topic>pyrethroid</topic><topic>Ranolazine</topic><topic>Rats</topic><topic>Riluzole - pharmacology</topic><topic>simulation</topic><topic>Sodium - metabolism</topic><topic>Sodium Channel Blockers - pharmacology</topic><topic>Tetrodotoxin - pharmacology</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><topic>Voltage-Gated Sodium Channels - drug effects</topic><topic>Voltage-Gated Sodium Channels - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, S.-N.</creatorcontrib><creatorcontrib>Yeh, C.-C.</creatorcontrib><creatorcontrib>Huang, H.-C.</creatorcontrib><creatorcontrib>So, E. C.</creatorcontrib><creatorcontrib>Lo, Y.-C.</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>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>MEDLINE - Academic</collection><jtitle>Acta Physiologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, S.-N.</au><au>Yeh, C.-C.</au><au>Huang, H.-C.</au><au>So, E. C.</au><au>Lo, Y.-C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electrophysiological characterization of sodium-activated potassium channels in NG108-15 and NSC-34 motor neuron-like cells</atitle><jtitle>Acta Physiologica</jtitle><addtitle>Acta Physiol</addtitle><date>2012-10</date><risdate>2012</risdate><volume>206</volume><issue>2</issue><spage>120</spage><epage>134</epage><pages>120-134</pages><issn>1748-1708</issn><eissn>1748-1716</eissn><abstract>Aims
The electrical properties of Na+‐activated K+ current (IK(Na)) and its contribution to spike firing has not been characterized in motor neurons.
Methods
We evaluated how activation of voltage‐gated K+ current (IK) at the cellular level could be coupled to Na+ influx through voltage‐gated Na+ current (INa) in two motor neuron‐like cells (NG108‐15 and NSC‐34 cells).
Results
Increasing stimulation frequency altered the amplitudes of both INa and IK simultaneously. With changes in stimulation frequency, the kinetics of both INa inactivation and IK activation were well correlated at the same cell. Addition of tetrodotoxin or ranolazine reduced the amplitudes of both INa and IK simultaneously. Tefluthrin (Tef) increased the amplitudes of both INa and IK throughout the voltages ranging from −30 to + 10 mV. In cell‐attached recordings, single‐channel conductance from a linear current‐voltage relation was 94 ± 3 pS (n = 7). Tef (10 μm) enhanced channel activity with no change in single‐channel conductance. Tef increased spike firing accompanied by enhanced facilitation of spike‐frequency adaptation. Riluzole (10 μm) reversed Tef‐stimulated activity of KNa channels. In motor neuron‐like NSC‐34 cells, increasing stimulation frequency altered the kinetics of both INa and IK. Modelling studies of motor neurons were simulated to demonstrate that the magnitude of IK(Na) modulates AP firing.
Conclusions
There is a direct association of Na+ and KNa channels which can provide the rapid activation of KNa channels required to regulate AP firing occurring in motor neurons.</abstract><cop>Oxford</cop><pub>Blackwell Publishing Ltd</pub><pmid>22533628</pmid><doi>10.1111/j.1748-1716.2012.02438.x</doi><tpages>15</tpages></addata></record> |
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| subjects | Acetanilides - pharmacology Action Potentials Animals Biological and medical sciences Cell Line, Tumor Cyclopropanes - pharmacology Electric Stimulation Fundamental and applied biological sciences. Psychology Hydrocarbons, Fluorinated - pharmacology Ion Channel Gating - drug effects K+ current Kinetics Mice Models, Neurological motor neurons Motor Neurons - metabolism Na+ current Na+-activated K+ channels Patch-Clamp Techniques Piperazines - pharmacology Potassium - metabolism Potassium Channels, Voltage-Gated - drug effects Potassium Channels, Voltage-Gated - metabolism pyrethroid Ranolazine Rats Riluzole - pharmacology simulation Sodium - metabolism Sodium Channel Blockers - pharmacology Tetrodotoxin - pharmacology Vertebrates: anatomy and physiology, studies on body, several organs or systems Voltage-Gated Sodium Channels - drug effects Voltage-Gated Sodium Channels - metabolism |
| title | Electrophysiological characterization of sodium-activated potassium channels in NG108-15 and NSC-34 motor neuron-like cells |
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