Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells
Tramadol is a centrally acting analgesic drug used mainly in the moderate to severe pain control. In this study, the effects of this agent on ion currents of NG108-15 neuronal cells were investigated. This cell line expresses Kv3.1a mRNAs and exhibits the activity of delayed rectifier K + (K DR) cha...
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| Veröffentlicht in: | European journal of pain 2006-10, Vol.10 (7), p.597-597 |
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| creator | Tsai, Tung-Ying Tsai, Yu-Chuan Wu, Sheng-Nan Liu, Yen-Chin |
| description | Tramadol is a centrally acting analgesic drug used mainly in the moderate to severe pain control. In this study, the effects of this agent on ion currents of NG108-15 neuronal cells were investigated. This cell line expresses Kv3.1a mRNAs and exhibits the activity of delayed rectifier K
+ (K
DR) channels. Tramadol suppressed the amplitude of delayed rectifier K
+ current (
I
K(DR)) in a concentration-dependent manner with an IC
50 values of 25
μM. Tramadol (30
μM) also shifted the steady-state inactivation of
I
K(DR) to a more negative membrane potential by approximately −15
mV. The role of the K
DR channel, particularly as a member of the Kv3 superfamily, is to stabilize the resting potential and to reduce the width of action potentials in the time-coding neurons. Tramadol-induced block of
I
K(DR) observed in this study could be partly responsible for its anti-depressant action. |
| doi_str_mv | 10.1016/j.ejpain.2005.09.001 |
| format | Article |
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+ (K
DR) channels. Tramadol suppressed the amplitude of delayed rectifier K
+ current (
I
K(DR)) in a concentration-dependent manner with an IC
50 values of 25
μM. Tramadol (30
μM) also shifted the steady-state inactivation of
I
K(DR) to a more negative membrane potential by approximately −15
mV. The role of the K
DR channel, particularly as a member of the Kv3 superfamily, is to stabilize the resting potential and to reduce the width of action potentials in the time-coding neurons. Tramadol-induced block of
I
K(DR) observed in this study could be partly responsible for its anti-depressant action.</description><identifier>ISSN: 1090-3801</identifier><identifier>EISSN: 1532-2149</identifier><identifier>DOI: 10.1016/j.ejpain.2005.09.001</identifier><identifier>PMID: 16226908</identifier><language>eng</language><publisher>Oxford, UK: Elsevier Ltd</publisher><subject>Action Potentials - drug effects ; Action Potentials - physiology ; Analgesics, Opioid - pharmacology ; Animals ; Cell Line, Tumor ; Cell Membrane - drug effects ; Cell Membrane - metabolism ; Central Nervous System - drug effects ; Central Nervous System - physiopathology ; Delayed rectifier K + current ; Hybridomas ; Male ; Neural Inhibition - drug effects ; Neural Inhibition - physiology ; Neurons - drug effects ; Neurons - metabolism ; NG108-15 neuronal cells ; Pain - drug therapy ; Pain - physiopathology ; Potassium Channel Blockers - pharmacology ; Potassium Channels - drug effects ; Potassium Channels - metabolism ; Rats ; Tramadol ; Tramadol - pharmacology</subject><ispartof>European journal of pain, 2006-10, Vol.10 (7), p.597-597</ispartof><rights>2005 European Federation of Chapters of the International Association for the Study of Pain</rights><rights>2006 European Federation of Chapters of the International Association for the Study of Pain</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5397-c3939f2a071cd60869677e6bc86e32e6dabc839aeb2971834323b1e377fb73f23</citedby><cites>FETCH-LOGICAL-c5397-c3939f2a071cd60869677e6bc86e32e6dabc839aeb2971834323b1e377fb73f23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.ejpain.2005.09.001$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1016%2Fj.ejpain.2005.09.001$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16226908$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsai, Tung-Ying</creatorcontrib><creatorcontrib>Tsai, Yu-Chuan</creatorcontrib><creatorcontrib>Wu, Sheng-Nan</creatorcontrib><creatorcontrib>Liu, Yen-Chin</creatorcontrib><title>Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells</title><title>European journal of pain</title><addtitle>Eur J Pain</addtitle><description>Tramadol is a centrally acting analgesic drug used mainly in the moderate to severe pain control. In this study, the effects of this agent on ion currents of NG108-15 neuronal cells were investigated. This cell line expresses Kv3.1a mRNAs and exhibits the activity of delayed rectifier K
+ (K
DR) channels. Tramadol suppressed the amplitude of delayed rectifier K
+ current (
I
K(DR)) in a concentration-dependent manner with an IC
50 values of 25
μM. Tramadol (30
μM) also shifted the steady-state inactivation of
I
K(DR) to a more negative membrane potential by approximately −15
mV. The role of the K
DR channel, particularly as a member of the Kv3 superfamily, is to stabilize the resting potential and to reduce the width of action potentials in the time-coding neurons. Tramadol-induced block of
I
K(DR) observed in this study could be partly responsible for its anti-depressant action.</description><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Analgesics, Opioid - pharmacology</subject><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - metabolism</subject><subject>Central Nervous System - drug effects</subject><subject>Central Nervous System - physiopathology</subject><subject>Delayed rectifier K + current</subject><subject>Hybridomas</subject><subject>Male</subject><subject>Neural Inhibition - drug effects</subject><subject>Neural Inhibition - physiology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>NG108-15 neuronal cells</subject><subject>Pain - drug therapy</subject><subject>Pain - physiopathology</subject><subject>Potassium Channel Blockers - pharmacology</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels - metabolism</subject><subject>Rats</subject><subject>Tramadol</subject><subject>Tramadol - pharmacology</subject><issn>1090-3801</issn><issn>1532-2149</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0Eoj_wBghlxS7h2p74Z4MEVRkYqlJQEQsWluPcSJ4m8dROKPP2eJQR7BArX1nfubK_Q8gLChUFKl5vK9zurB8rBlBXoCsA-oic0pqzktGVfpxn0FByBfSEnKW0BYCVBP6UnFDBmNCgTsmP22gH24a-9GM7O2yLpg_uzrZYhK5osbf7fBfRTb7zGItdmGxKfh4KN8eI41T4sbheU1AlrYsR5xhG2xcO-z49I0862yd8fjzPybf3l7cXH8qrz-uPF2-vSldzLUvHNdcdsyCpawUooYWUKBqnBHKGorV55Npiw7Skiq844w1FLmXXSN4xfk5eLXt3MdzPmCYz-HR4gR0xzMkIJVWtBM3gagFdDClF7Mwu-sHGvaFgDlLN1ixSzUGqAW2y1Bx7edw_NwO2f0NHixnQC_Dge9z_11JzublhgsucLZesTxP--pO18c4IyWVtvl-vzc3XzfrTu400XzL_ZuExG_2ZKzHJeRxzc_7QkmmD__dvfgPSmqqK</recordid><startdate>200610</startdate><enddate>200610</enddate><creator>Tsai, Tung-Ying</creator><creator>Tsai, Yu-Chuan</creator><creator>Wu, Sheng-Nan</creator><creator>Liu, Yen-Chin</creator><general>Elsevier Ltd</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>200610</creationdate><title>Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells</title><author>Tsai, Tung-Ying ; Tsai, Yu-Chuan ; Wu, Sheng-Nan ; Liu, Yen-Chin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5397-c3939f2a071cd60869677e6bc86e32e6dabc839aeb2971834323b1e377fb73f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Analgesics, Opioid - pharmacology</topic><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Cell Membrane - drug effects</topic><topic>Cell Membrane - metabolism</topic><topic>Central Nervous System - drug effects</topic><topic>Central Nervous System - physiopathology</topic><topic>Delayed rectifier K + current</topic><topic>Hybridomas</topic><topic>Male</topic><topic>Neural Inhibition - drug effects</topic><topic>Neural Inhibition - physiology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>NG108-15 neuronal cells</topic><topic>Pain - drug therapy</topic><topic>Pain - physiopathology</topic><topic>Potassium Channel Blockers - pharmacology</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels - metabolism</topic><topic>Rats</topic><topic>Tramadol</topic><topic>Tramadol - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsai, Tung-Ying</creatorcontrib><creatorcontrib>Tsai, Yu-Chuan</creatorcontrib><creatorcontrib>Wu, Sheng-Nan</creatorcontrib><creatorcontrib>Liu, Yen-Chin</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pain</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsai, Tung-Ying</au><au>Tsai, Yu-Chuan</au><au>Wu, Sheng-Nan</au><au>Liu, Yen-Chin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells</atitle><jtitle>European journal of pain</jtitle><addtitle>Eur J Pain</addtitle><date>2006-10</date><risdate>2006</risdate><volume>10</volume><issue>7</issue><spage>597</spage><epage>597</epage><pages>597-597</pages><issn>1090-3801</issn><eissn>1532-2149</eissn><abstract>Tramadol is a centrally acting analgesic drug used mainly in the moderate to severe pain control. In this study, the effects of this agent on ion currents of NG108-15 neuronal cells were investigated. This cell line expresses Kv3.1a mRNAs and exhibits the activity of delayed rectifier K
+ (K
DR) channels. Tramadol suppressed the amplitude of delayed rectifier K
+ current (
I
K(DR)) in a concentration-dependent manner with an IC
50 values of 25
μM. Tramadol (30
μM) also shifted the steady-state inactivation of
I
K(DR) to a more negative membrane potential by approximately −15
mV. The role of the K
DR channel, particularly as a member of the Kv3 superfamily, is to stabilize the resting potential and to reduce the width of action potentials in the time-coding neurons. Tramadol-induced block of
I
K(DR) observed in this study could be partly responsible for its anti-depressant action.</abstract><cop>Oxford, UK</cop><pub>Elsevier Ltd</pub><pmid>16226908</pmid><doi>10.1016/j.ejpain.2005.09.001</doi></addata></record> |
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| ispartof | European journal of pain, 2006-10, Vol.10 (7), p.597-597 |
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| subjects | Action Potentials - drug effects Action Potentials - physiology Analgesics, Opioid - pharmacology Animals Cell Line, Tumor Cell Membrane - drug effects Cell Membrane - metabolism Central Nervous System - drug effects Central Nervous System - physiopathology Delayed rectifier K + current Hybridomas Male Neural Inhibition - drug effects Neural Inhibition - physiology Neurons - drug effects Neurons - metabolism NG108-15 neuronal cells Pain - drug therapy Pain - physiopathology Potassium Channel Blockers - pharmacology Potassium Channels - drug effects Potassium Channels - metabolism Rats Tramadol Tramadol - pharmacology |
| title | Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells |
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