PKC regulates capsaicin-induced currents of dorsal root ganglion neurons in rats
Capsaicin activates a non-specific cation conductance in a subset of dorsal root ganglion (DRG) neurons. The inward current and membrane potential of acutely isolated DRG neurons were examined using whole-cell patch recording methods. We report here that the current and voltage responses activated b...
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Veröffentlicht in: | Neuropharmacology 2001-10, Vol.41 (5), p.601-608 |
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description | Capsaicin activates a non-specific cation conductance in a subset of dorsal root ganglion (DRG) neurons. The inward current and membrane potential of acutely isolated DRG neurons were examined using whole-cell patch recording methods. We report here that the current and voltage responses activated by capsaicin were markedly increased by phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC). The mean current, after application of 0.3
μM PMA, was 153.5±5.7% of control (
n=32) in Ca
2+-free external solution and 181.6±6.8% of control (
n=15) in standard external solution. Under current-clamp conditions, 0.3
μM PMA facilitated capsaicin-induced depolarization and action potential generation. Bindolylmaleimide I (BIM), a specific inhibitor of PKC activity, abolished the effect of PMA. In addition, capsaicin-evoked current was attenuated to 68.3±5.0% of control (
n=13) by individual administration of 1
μM BIM in standard external solution, while 0.3
μM BIM did not have this effect. These data suggest that PKC can directly regulate the capsaicin response in DRG neurons, which could increase nociceptive sensory transmission and contribute to hyperalgesia. |
doi_str_mv | 10.1016/S0028-3908(01)00106-X |
format | Article |
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μM PMA, was 153.5±5.7% of control (
n=32) in Ca
2+-free external solution and 181.6±6.8% of control (
n=15) in standard external solution. Under current-clamp conditions, 0.3
μM PMA facilitated capsaicin-induced depolarization and action potential generation. Bindolylmaleimide I (BIM), a specific inhibitor of PKC activity, abolished the effect of PMA. In addition, capsaicin-evoked current was attenuated to 68.3±5.0% of control (
n=13) by individual administration of 1
μM BIM in standard external solution, while 0.3
μM BIM did not have this effect. These data suggest that PKC can directly regulate the capsaicin response in DRG neurons, which could increase nociceptive sensory transmission and contribute to hyperalgesia.</description><identifier>ISSN: 0028-3908</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/S0028-3908(01)00106-X</identifier><identifier>PMID: 11587715</identifier><identifier>CODEN: NEPHBW</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Biological and medical sciences ; Capsaicin ; Capsaicin - pharmacology ; Cells, Cultured ; Central nervous system ; Dorsal root ganglion ; Electrophysiology ; Fundamental and applied biological sciences. Psychology ; Ganglia, Spinal - drug effects ; Ganglia, Spinal - enzymology ; Ganglia, Spinal - physiology ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Neurons - drug effects ; Neurons - enzymology ; Neurons - physiology ; Protein kinase C ; Protein Kinase C - physiology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors ; Vertebrates: nervous system and sense organs ; Whole-cell patch</subject><ispartof>Neuropharmacology, 2001-10, Vol.41 (5), p.601-608</ispartof><rights>2001 Elsevier Science Ltd</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-55576074a6e6037816cd2af01914198f8a36855304630335fbd91342551d57d3</citedby><cites>FETCH-LOGICAL-c447t-55576074a6e6037816cd2af01914198f8a36855304630335fbd91342551d57d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0028-3908(01)00106-X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1132260$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11587715$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Yu</creatorcontrib><creatorcontrib>Zhou, Zhi-Shang</creatorcontrib><creatorcontrib>Zhao, Zhi-Qi</creatorcontrib><title>PKC regulates capsaicin-induced currents of dorsal root ganglion neurons in rats</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>Capsaicin activates a non-specific cation conductance in a subset of dorsal root ganglion (DRG) neurons. The inward current and membrane potential of acutely isolated DRG neurons were examined using whole-cell patch recording methods. We report here that the current and voltage responses activated by capsaicin were markedly increased by phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC). The mean current, after application of 0.3
μM PMA, was 153.5±5.7% of control (
n=32) in Ca
2+-free external solution and 181.6±6.8% of control (
n=15) in standard external solution. Under current-clamp conditions, 0.3
μM PMA facilitated capsaicin-induced depolarization and action potential generation. Bindolylmaleimide I (BIM), a specific inhibitor of PKC activity, abolished the effect of PMA. In addition, capsaicin-evoked current was attenuated to 68.3±5.0% of control (
n=13) by individual administration of 1
μM BIM in standard external solution, while 0.3
μM BIM did not have this effect. These data suggest that PKC can directly regulate the capsaicin response in DRG neurons, which could increase nociceptive sensory transmission and contribute to hyperalgesia.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Capsaicin</subject><subject>Capsaicin - pharmacology</subject><subject>Cells, Cultured</subject><subject>Central nervous system</subject><subject>Dorsal root ganglion</subject><subject>Electrophysiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ganglia, Spinal - drug effects</subject><subject>Ganglia, Spinal - enzymology</subject><subject>Ganglia, Spinal - physiology</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Neurons - drug effects</subject><subject>Neurons - enzymology</subject><subject>Neurons - physiology</subject><subject>Protein kinase C</subject><subject>Protein Kinase C - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Whole-cell patch</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi1ERZfCTwD5gBAcAjNx_JFThVZAq1aiEj30Zrm2szLK2osnQeLfk-2ugFtPc3nemVfPMPYK4QMCqo_fAVrTiB7MO8D3AAiquXvCVmi0aDSo7ilb_UVO2XOiHwDQGTTP2CmiNFqjXLGbm6s1r3Ezj26KxL3bkUs-5SblMPsYuJ9rjXkiXgYeSiU38lrKxDcub8ZUMs9xriUTT5lXN9ELdjK4keLL4zxjt18-364vmutvXy_Xn64b33V6aqSUWoHunIoKhDaofGjdANhjh70ZjBPKSCmgUwKEkMN96FF0rZQYpA7ijL09rN3V8nOONNltIh_H0eVYZrK6Rd2rFh4F0WCvNIoFlAfQ10JU42B3NW1d_W0R7F65fVBu9z4toH1Qbu-W3Ovjgfl-G8O_1NHxArw5Ao68G4fqsk_0HyfaVu2Lnh-wuFj7lWK15FPMyw9SjX6yoaRHmvwBAwObUA</recordid><startdate>20011001</startdate><enddate>20011001</enddate><creator>Zhou, Yu</creator><creator>Zhou, Zhi-Shang</creator><creator>Zhao, Zhi-Qi</creator><general>Elsevier Ltd</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20011001</creationdate><title>PKC regulates capsaicin-induced currents of dorsal root ganglion neurons in rats</title><author>Zhou, Yu ; Zhou, Zhi-Shang ; Zhao, Zhi-Qi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-55576074a6e6037816cd2af01914198f8a36855304630335fbd91342551d57d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Capsaicin</topic><topic>Capsaicin - pharmacology</topic><topic>Cells, Cultured</topic><topic>Central nervous system</topic><topic>Dorsal root ganglion</topic><topic>Electrophysiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Ganglia, Spinal - drug effects</topic><topic>Ganglia, Spinal - enzymology</topic><topic>Ganglia, Spinal - physiology</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>Neurons - drug effects</topic><topic>Neurons - enzymology</topic><topic>Neurons - physiology</topic><topic>Protein kinase C</topic><topic>Protein Kinase C - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>Whole-cell patch</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Yu</creatorcontrib><creatorcontrib>Zhou, Zhi-Shang</creatorcontrib><creatorcontrib>Zhao, Zhi-Qi</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Yu</au><au>Zhou, Zhi-Shang</au><au>Zhao, Zhi-Qi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PKC regulates capsaicin-induced currents of dorsal root ganglion neurons in rats</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>2001-10-01</date><risdate>2001</risdate><volume>41</volume><issue>5</issue><spage>601</spage><epage>608</epage><pages>601-608</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><coden>NEPHBW</coden><abstract>Capsaicin activates a non-specific cation conductance in a subset of dorsal root ganglion (DRG) neurons. The inward current and membrane potential of acutely isolated DRG neurons were examined using whole-cell patch recording methods. We report here that the current and voltage responses activated by capsaicin were markedly increased by phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC). The mean current, after application of 0.3
μM PMA, was 153.5±5.7% of control (
n=32) in Ca
2+-free external solution and 181.6±6.8% of control (
n=15) in standard external solution. Under current-clamp conditions, 0.3
μM PMA facilitated capsaicin-induced depolarization and action potential generation. Bindolylmaleimide I (BIM), a specific inhibitor of PKC activity, abolished the effect of PMA. In addition, capsaicin-evoked current was attenuated to 68.3±5.0% of control (
n=13) by individual administration of 1
μM BIM in standard external solution, while 0.3
μM BIM did not have this effect. These data suggest that PKC can directly regulate the capsaicin response in DRG neurons, which could increase nociceptive sensory transmission and contribute to hyperalgesia.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>11587715</pmid><doi>10.1016/S0028-3908(01)00106-X</doi><tpages>8</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Capsaicin Capsaicin - pharmacology Cells, Cultured Central nervous system Dorsal root ganglion Electrophysiology Fundamental and applied biological sciences. Psychology Ganglia, Spinal - drug effects Ganglia, Spinal - enzymology Ganglia, Spinal - physiology Membrane Potentials - drug effects Membrane Potentials - physiology Neurons - drug effects Neurons - enzymology Neurons - physiology Protein kinase C Protein Kinase C - physiology Rats Rats, Sprague-Dawley Signal Transduction - drug effects Signal Transduction - physiology Somesthesis and somesthetic pathways (proprioception, exteroception, nociception) interoception electrolocation. Sensory receptors Vertebrates: nervous system and sense organs Whole-cell patch |
title | PKC regulates capsaicin-induced currents of dorsal root ganglion neurons in rats |
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