Mechanism of antinociceptive action of clonidine in nonmyelinated nerve fibres
Despite a large body of clinical evidence in favour of a local anesthetic effect of clonidine, the underlying mechanism has not yet been elucidated. In this study we have used the sucrose-gap method to measure the effects of clonidine on the electrophysiological properties of nonmyelinated nerve fib...
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| Veröffentlicht in: | European journal of pharmacology 1999-10, Vol.383 (1), p.1-8 |
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| container_title | European journal of pharmacology |
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| creator | Erne-Brand, Françoise Jirounek, Petr Drewe, Jürgen Hampl, Karl Schneider, Markus C |
| description | Despite a large body of clinical evidence in favour of a local anesthetic effect of clonidine, the underlying mechanism has not yet been elucidated. In this study we have used the sucrose-gap method to measure the effects of clonidine on the electrophysiological properties of nonmyelinated nerve fibers in the rabbit vagus nerve. The results showed that clonidine enhanced the hyperpolarizing and reduced the depolarizing afterpotential that follow compound action potentials during electrical activity. We showed that summation of these afterpotentials shifts the membrane potential toward more negative values, thus creating a region of low safety conduction, where the local circuit currents might fail to depolarize the axonal membrane to the threshold value needed to open voltage-dependent Na
+ channels. Yohimbine did not reverse the inhibitory effects of clonidine on impulse propagation, indicating that the observed effects of clonidine relies on mechanisms not mediated by α
2-adrenoceptors. |
| doi_str_mv | 10.1016/S0014-2999(99)00620-2 |
| format | Article |
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+ channels. Yohimbine did not reverse the inhibitory effects of clonidine on impulse propagation, indicating that the observed effects of clonidine relies on mechanisms not mediated by α
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+ channels. Yohimbine did not reverse the inhibitory effects of clonidine on impulse propagation, indicating that the observed effects of clonidine relies on mechanisms not mediated by α
2-adrenoceptors.</description><subject>Action Potentials - drug effects</subject><subject>Adrenergic alpha-Antagonists - pharmacology</subject><subject>Afterpotential</subject><subject>Analgesics - pharmacology</subject><subject>Anesthetics, Local - pharmacology</subject><subject>Anesthetics. Neuromuscular blocking agents</subject><subject>Animals</subject><subject>Antinociception</subject><subject>Biological and medical sciences</subject><subject>C-fibre</subject><subject>Clonidine</subject><subject>Clonidine - pharmacology</subject><subject>Electric Stimulation</subject><subject>Electrophysiology</subject><subject>In Vitro Techniques</subject><subject>Medical sciences</subject><subject>Myelin Sheath - physiology</subject><subject>Nerve Fibers - drug effects</subject><subject>Nerve Fibers - physiology</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rabbits</subject><subject>Receptors, Adrenergic, alpha-2 - drug effects</subject><subject>Receptors, Adrenergic, alpha-2 - physiology</subject><subject>Sodium Channels - drug effects</subject><subject>Sucrose-gap</subject><subject>Time Factors</subject><subject>Vagus Nerve - drug effects</subject><subject>Vagus Nerve - ultrastructure</subject><subject>Yohimbine - pharmacology</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1v1DAQQC0EotvCTwDlgCo4pIyd2I5PCFUUkFo4AGfLHk-EUWIvdrZS_32z3RVwQxrNHObNhx5jLzhccODq7TcA3rfCGPPamDcASkArHrENH7RpQXPxmG3-ICfstNZfACCNkE_ZCQcpldL9hn25IfzpUqxzk8fGpSWmjBFpu8RbahwuMad9B6ecYoiJmpialNN8R1NMbqHQJCorOkZfqD5jT0Y3VXp-rGfsx9WH75ef2uuvHz9fvr9use_F0oZA3nMc-s4PvB8NdsoD8iBMP0q1Jo0KPHhjpOu0GSQXmnNFXncGQwfdGTs_7N2W_HtHdbFzrEjT5BLlXbXKCC17NaygPIBYcq2FRrstcXblznKwe5H2QaTdW7JrPIi0Yp17eTyw8zOFf6YO5lbg1RFwFd00Fpcw1r-c0VpIvWLvDhitNm4jFVsxUkIKsRAuNuT4n0_uAf1uj3Y</recordid><startdate>19991021</startdate><enddate>19991021</enddate><creator>Erne-Brand, Françoise</creator><creator>Jirounek, Petr</creator><creator>Drewe, Jürgen</creator><creator>Hampl, Karl</creator><creator>Schneider, Markus C</creator><general>Elsevier B.V</general><general>Elsevier</general><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>7X8</scope></search><sort><creationdate>19991021</creationdate><title>Mechanism of antinociceptive action of clonidine in nonmyelinated nerve fibres</title><author>Erne-Brand, Françoise ; Jirounek, Petr ; Drewe, Jürgen ; Hampl, Karl ; Schneider, Markus C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-ddebb1c843b814f9c36b0c1d294f5694f7c60b0b995a37985127116eb739cd303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Action Potentials - drug effects</topic><topic>Adrenergic alpha-Antagonists - pharmacology</topic><topic>Afterpotential</topic><topic>Analgesics - pharmacology</topic><topic>Anesthetics, Local - pharmacology</topic><topic>Anesthetics. Neuromuscular blocking agents</topic><topic>Animals</topic><topic>Antinociception</topic><topic>Biological and medical sciences</topic><topic>C-fibre</topic><topic>Clonidine</topic><topic>Clonidine - pharmacology</topic><topic>Electric Stimulation</topic><topic>Electrophysiology</topic><topic>In Vitro Techniques</topic><topic>Medical sciences</topic><topic>Myelin Sheath - physiology</topic><topic>Nerve Fibers - drug effects</topic><topic>Nerve Fibers - physiology</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rabbits</topic><topic>Receptors, Adrenergic, alpha-2 - drug effects</topic><topic>Receptors, Adrenergic, alpha-2 - physiology</topic><topic>Sodium Channels - drug effects</topic><topic>Sucrose-gap</topic><topic>Time Factors</topic><topic>Vagus Nerve - drug effects</topic><topic>Vagus Nerve - ultrastructure</topic><topic>Yohimbine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Erne-Brand, Françoise</creatorcontrib><creatorcontrib>Jirounek, Petr</creatorcontrib><creatorcontrib>Drewe, Jürgen</creatorcontrib><creatorcontrib>Hampl, Karl</creatorcontrib><creatorcontrib>Schneider, Markus C</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Erne-Brand, Françoise</au><au>Jirounek, Petr</au><au>Drewe, Jürgen</au><au>Hampl, Karl</au><au>Schneider, Markus C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism of antinociceptive action of clonidine in nonmyelinated nerve fibres</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1999-10-21</date><risdate>1999</risdate><volume>383</volume><issue>1</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Despite a large body of clinical evidence in favour of a local anesthetic effect of clonidine, the underlying mechanism has not yet been elucidated. In this study we have used the sucrose-gap method to measure the effects of clonidine on the electrophysiological properties of nonmyelinated nerve fibers in the rabbit vagus nerve. The results showed that clonidine enhanced the hyperpolarizing and reduced the depolarizing afterpotential that follow compound action potentials during electrical activity. We showed that summation of these afterpotentials shifts the membrane potential toward more negative values, thus creating a region of low safety conduction, where the local circuit currents might fail to depolarize the axonal membrane to the threshold value needed to open voltage-dependent Na
+ channels. Yohimbine did not reverse the inhibitory effects of clonidine on impulse propagation, indicating that the observed effects of clonidine relies on mechanisms not mediated by α
2-adrenoceptors.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10556674</pmid><doi>10.1016/S0014-2999(99)00620-2</doi><tpages>8</tpages></addata></record> |
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| subjects | Action Potentials - drug effects Adrenergic alpha-Antagonists - pharmacology Afterpotential Analgesics - pharmacology Anesthetics, Local - pharmacology Anesthetics. Neuromuscular blocking agents Animals Antinociception Biological and medical sciences C-fibre Clonidine Clonidine - pharmacology Electric Stimulation Electrophysiology In Vitro Techniques Medical sciences Myelin Sheath - physiology Nerve Fibers - drug effects Nerve Fibers - physiology Neuropharmacology Pharmacology. Drug treatments Rabbits Receptors, Adrenergic, alpha-2 - drug effects Receptors, Adrenergic, alpha-2 - physiology Sodium Channels - drug effects Sucrose-gap Time Factors Vagus Nerve - drug effects Vagus Nerve - ultrastructure Yohimbine - pharmacology |
| title | Mechanism of antinociceptive action of clonidine in nonmyelinated nerve fibres |
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