Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice
Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of tra...
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| description | Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of transient receptor potential (TRP) channels. To further test this mechanism, the mouse provides an ideal model in which genetic tools could be applied. However, whether CCK acts by similar mechanism(s) in mice has not been determined. In the present study we explored the actions of CCK on nodose neurons isolated from Sprague Dawley (SD) rat and two strains of mice; C57BL/6 and BalbC using fluorescence-based calcium imaging. With minor exceptions nodose neurons isolated from all species/strains behaved similarly. They all respond to brief depolarization with a large calcium transient. A significant subset of neurons responded to capsaicin (CAP), a TRPV1 agonist, although neurons from C57BL/6 were 10-fold more sensitive to CAP than SD rats or BalbC mice, and a significantly smaller fraction of neurons from BalbC mice responded to CAP. CCK-8 dose-dependently activated a subpopulation of neurons with similar dose dependency, percent responders, and overlap between CCK and CAP responsiveness. In all species/strains CCK-8 induced activation was significantly attenuated (but not completely blocked) by pretreatment with the TRPV channel blocker RuR. Surprisingly, the CCK analogue JMV-180, which is reported to have pure antagonistic properties in rat but mixed agonist/antagonist properties in mice, behaved as a pure antagonist to CCK in both rat and mouse neurons. The pure antagonistic action of JMV-180 in this in vitro preparation suggests that prior reported differential effects of JMV-180 on satiation in rats versus mouse must be mediated by a site other than vagal afferent activation. |
| doi_str_mv | 10.1371/journal.pone.0034755 |
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Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of transient receptor potential (TRP) channels. To further test this mechanism, the mouse provides an ideal model in which genetic tools could be applied. However, whether CCK acts by similar mechanism(s) in mice has not been determined. In the present study we explored the actions of CCK on nodose neurons isolated from Sprague Dawley (SD) rat and two strains of mice; C57BL/6 and BalbC using fluorescence-based calcium imaging. With minor exceptions nodose neurons isolated from all species/strains behaved similarly. They all respond to brief depolarization with a large calcium transient. A significant subset of neurons responded to capsaicin (CAP), a TRPV1 agonist, although neurons from C57BL/6 were 10-fold more sensitive to CAP than SD rats or BalbC mice, and a significantly smaller fraction of neurons from BalbC mice responded to CAP. CCK-8 dose-dependently activated a subpopulation of neurons with similar dose dependency, percent responders, and overlap between CCK and CAP responsiveness. In all species/strains CCK-8 induced activation was significantly attenuated (but not completely blocked) by pretreatment with the TRPV channel blocker RuR. Surprisingly, the CCK analogue JMV-180, which is reported to have pure antagonistic properties in rat but mixed agonist/antagonist properties in mice, behaved as a pure antagonist to CCK in both rat and mouse neurons. The pure antagonistic action of JMV-180 in this in vitro preparation suggests that prior reported differential effects of JMV-180 on satiation in rats versus mouse must be mediated by a site other than vagal afferent activation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0034755</identifier><identifier>PMID: 22514663</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Anatomy & physiology ; Animals ; Binding sites ; Biology ; Calcium ; Calcium imaging ; Capsaicin ; Capsaicin receptors ; Cells, Cultured ; Cholecystokinin ; Cholecystokinin - pharmacology ; Cloning ; Depolarization ; Dose dependency ; Fluorescence ; Gastrointestinal system ; Gastrointestinal tract ; House mouse ; Kinases ; Male ; Medicine ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neurons ; Neurons, Afferent - cytology ; Neurons, Afferent - drug effects ; Neurons, Afferent - metabolism ; Neurosciences ; Nodose Ganglion - cytology ; Nodose Ganglion - drug effects ; Nodose Ganglion - metabolism ; Pharmacology ; Physiology ; Platinum group compounds ; Pretreatment ; Rats ; Rats, Sprague-Dawley ; Rodents ; Ruthenium ; Ruthenium red ; Satiety ; Sensory neurons ; Signal transduction ; Transient receptor potential proteins ; Vagus nerve ; Vagus Nerve - drug effects</subject><ispartof>PloS one, 2012-04, Vol.7 (4), p.e34755-e34755</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c718t-1a096b9606fadacefe2cc66d3a5c6c2c64d19c8c0797e360d27ba1715fa8152c3</citedby><cites>FETCH-LOGICAL-c718t-1a096b9606fadacefe2cc66d3a5c6c2c64d19c8c0797e360d27ba1715fa8152c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326049/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326049/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22514663$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Tache, Yvette</contributor><creatorcontrib>Kinch, Dallas C</creatorcontrib><creatorcontrib>Peters, James H</creatorcontrib><creatorcontrib>Simasko, Steven M</creatorcontrib><title>Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of transient receptor potential (TRP) channels. To further test this mechanism, the mouse provides an ideal model in which genetic tools could be applied. However, whether CCK acts by similar mechanism(s) in mice has not been determined. In the present study we explored the actions of CCK on nodose neurons isolated from Sprague Dawley (SD) rat and two strains of mice; C57BL/6 and BalbC using fluorescence-based calcium imaging. With minor exceptions nodose neurons isolated from all species/strains behaved similarly. They all respond to brief depolarization with a large calcium transient. A significant subset of neurons responded to capsaicin (CAP), a TRPV1 agonist, although neurons from C57BL/6 were 10-fold more sensitive to CAP than SD rats or BalbC mice, and a significantly smaller fraction of neurons from BalbC mice responded to CAP. CCK-8 dose-dependently activated a subpopulation of neurons with similar dose dependency, percent responders, and overlap between CCK and CAP responsiveness. In all species/strains CCK-8 induced activation was significantly attenuated (but not completely blocked) by pretreatment with the TRPV channel blocker RuR. Surprisingly, the CCK analogue JMV-180, which is reported to have pure antagonistic properties in rat but mixed agonist/antagonist properties in mice, behaved as a pure antagonist to CCK in both rat and mouse neurons. The pure antagonistic action of JMV-180 in this in vitro preparation suggests that prior reported differential effects of JMV-180 on satiation in rats versus mouse must be mediated by a site other than vagal afferent activation.</description><subject>Activation</subject><subject>Anatomy & physiology</subject><subject>Animals</subject><subject>Binding sites</subject><subject>Biology</subject><subject>Calcium</subject><subject>Calcium imaging</subject><subject>Capsaicin</subject><subject>Capsaicin receptors</subject><subject>Cells, Cultured</subject><subject>Cholecystokinin</subject><subject>Cholecystokinin - pharmacology</subject><subject>Cloning</subject><subject>Depolarization</subject><subject>Dose dependency</subject><subject>Fluorescence</subject><subject>Gastrointestinal system</subject><subject>Gastrointestinal tract</subject><subject>House mouse</subject><subject>Kinases</subject><subject>Male</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Neurons</subject><subject>Neurons, Afferent - cytology</subject><subject>Neurons, Afferent - drug effects</subject><subject>Neurons, Afferent - metabolism</subject><subject>Neurosciences</subject><subject>Nodose Ganglion - cytology</subject><subject>Nodose Ganglion - drug effects</subject><subject>Nodose Ganglion - metabolism</subject><subject>Pharmacology</subject><subject>Physiology</subject><subject>Platinum group compounds</subject><subject>Pretreatment</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Ruthenium</subject><subject>Ruthenium red</subject><subject>Satiety</subject><subject>Sensory neurons</subject><subject>Signal transduction</subject><subject>Transient receptor potential proteins</subject><subject>Vagus nerve</subject><subject>Vagus Nerve - drug effects</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1tr2zAUx83YWLtu32BshsHYHpLpZtl-GZSwS6BQ2O1VHEtyokyWUskOy7ef0rglHn0YfrA5_v3_RzqXLHuJ0RzTEn_Y-CE4sPOtd3qOEGVlUTzKznFNyYwTRB-ffJ9lz2LcIFTQivOn2RkhBWac0_OsX_huCwF6s9P5dg2hA-mtX-1z3-Zy7a2W-9j738YZlxunBqlVDjLhSeLdLTXYfggpvIMV2BzaVgft-tzpIXgX8zb4Lk8ZYg5O5Z2R-nn2pAUb9YvxfZH9_Pzpx-Lr7Or6y3JxeTWTJa76GQZU86bmiLegQOpWEyk5VxQKySWRnClcy0qisi415UiRsgFc4qKFChdE0ovs9dF3a30UY8GiwJQwxipekUQsj4TysBHbYDoIe-HBiNuADysBoTfSakFpg7mSNWaVZByaCjeU1pw2tKy0qnTy-jhmG5pOK5lqEMBOTKd_nFmLld8lZ8IRq5PBu9Eg-JtBx150JkptLTjth3RuhKqKEVKihL75B334diOV-qKFca1PeeXBVFyyssQUcXpIO3-ASo_SqVlpulqT4hPB-4kgMb3-069giFEsv3_7f_b615R9e8KuNdh-Hb0dDoMWpyA7gjL4GINu74uMkTgsx101xGE5xLgcSfbqtEH3orttoH8BupMLwg</recordid><startdate>20120413</startdate><enddate>20120413</enddate><creator>Kinch, Dallas C</creator><creator>Peters, James H</creator><creator>Simasko, Steven M</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120413</creationdate><title>Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice</title><author>Kinch, Dallas C ; Peters, James H ; Simasko, Steven M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c718t-1a096b9606fadacefe2cc66d3a5c6c2c64d19c8c0797e360d27ba1715fa8152c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Activation</topic><topic>Anatomy & physiology</topic><topic>Animals</topic><topic>Binding sites</topic><topic>Biology</topic><topic>Calcium</topic><topic>Calcium imaging</topic><topic>Capsaicin</topic><topic>Capsaicin receptors</topic><topic>Cells, Cultured</topic><topic>Cholecystokinin</topic><topic>Cholecystokinin - pharmacology</topic><topic>Cloning</topic><topic>Depolarization</topic><topic>Dose dependency</topic><topic>Fluorescence</topic><topic>Gastrointestinal system</topic><topic>Gastrointestinal tract</topic><topic>House mouse</topic><topic>Kinases</topic><topic>Male</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Neurons</topic><topic>Neurons, Afferent - cytology</topic><topic>Neurons, Afferent - drug effects</topic><topic>Neurons, Afferent - metabolism</topic><topic>Neurosciences</topic><topic>Nodose Ganglion - cytology</topic><topic>Nodose Ganglion - drug effects</topic><topic>Nodose Ganglion - metabolism</topic><topic>Pharmacology</topic><topic>Physiology</topic><topic>Platinum group compounds</topic><topic>Pretreatment</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Ruthenium</topic><topic>Ruthenium red</topic><topic>Satiety</topic><topic>Sensory neurons</topic><topic>Signal transduction</topic><topic>Transient receptor potential proteins</topic><topic>Vagus nerve</topic><topic>Vagus Nerve - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kinch, Dallas C</creatorcontrib><creatorcontrib>Peters, James H</creatorcontrib><creatorcontrib>Simasko, Steven M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kinch, Dallas C</au><au>Peters, James H</au><au>Simasko, Steven M</au><au>Tache, Yvette</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-04-13</date><risdate>2012</risdate><volume>7</volume><issue>4</issue><spage>e34755</spage><epage>e34755</epage><pages>e34755-e34755</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of transient receptor potential (TRP) channels. To further test this mechanism, the mouse provides an ideal model in which genetic tools could be applied. However, whether CCK acts by similar mechanism(s) in mice has not been determined. In the present study we explored the actions of CCK on nodose neurons isolated from Sprague Dawley (SD) rat and two strains of mice; C57BL/6 and BalbC using fluorescence-based calcium imaging. With minor exceptions nodose neurons isolated from all species/strains behaved similarly. They all respond to brief depolarization with a large calcium transient. A significant subset of neurons responded to capsaicin (CAP), a TRPV1 agonist, although neurons from C57BL/6 were 10-fold more sensitive to CAP than SD rats or BalbC mice, and a significantly smaller fraction of neurons from BalbC mice responded to CAP. CCK-8 dose-dependently activated a subpopulation of neurons with similar dose dependency, percent responders, and overlap between CCK and CAP responsiveness. In all species/strains CCK-8 induced activation was significantly attenuated (but not completely blocked) by pretreatment with the TRPV channel blocker RuR. Surprisingly, the CCK analogue JMV-180, which is reported to have pure antagonistic properties in rat but mixed agonist/antagonist properties in mice, behaved as a pure antagonist to CCK in both rat and mouse neurons. The pure antagonistic action of JMV-180 in this in vitro preparation suggests that prior reported differential effects of JMV-180 on satiation in rats versus mouse must be mediated by a site other than vagal afferent activation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22514663</pmid><doi>10.1371/journal.pone.0034755</doi><tpages>e34755</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Activation Anatomy & physiology Animals Binding sites Biology Calcium Calcium imaging Capsaicin Capsaicin receptors Cells, Cultured Cholecystokinin Cholecystokinin - pharmacology Cloning Depolarization Dose dependency Fluorescence Gastrointestinal system Gastrointestinal tract House mouse Kinases Male Medicine Mice Mice, Inbred BALB C Mice, Inbred C57BL Neurons Neurons, Afferent - cytology Neurons, Afferent - drug effects Neurons, Afferent - metabolism Neurosciences Nodose Ganglion - cytology Nodose Ganglion - drug effects Nodose Ganglion - metabolism Pharmacology Physiology Platinum group compounds Pretreatment Rats Rats, Sprague-Dawley Rodents Ruthenium Ruthenium red Satiety Sensory neurons Signal transduction Transient receptor potential proteins Vagus nerve Vagus Nerve - drug effects |
| title | Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice |
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