Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon
Background Short‐chain fatty acids (SCFA) are microbial fermentation products absorbed by the colon. We recently reported that activation of the SCFA receptor termed free fatty acid receptor 3 (FFA3), expressed on cholinergic nerves, suppresses nicotinic acetylcholine receptor (nAChR)‐mediated trans...
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| Veröffentlicht in: | Neurogastroenterology and motility 2018-01, Vol.30 (1), p.n/a |
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| description | Background
Short‐chain fatty acids (SCFA) are microbial fermentation products absorbed by the colon. We recently reported that activation of the SCFA receptor termed free fatty acid receptor 3 (FFA3), expressed on cholinergic nerves, suppresses nicotinic acetylcholine receptor (nAChR)‐mediated transepithelial anion secretion. This study aimed to clarify how activation of neurally expressed FFA3 affects colonic motor function.
Methods
FFA3‐expressing myenteric neurons were identified by immunostaining; contractions of isolated circular muscle strips obtained from rat proximal colon were measured by isometric transducers. The effect of FFA3 agonists on defecation in vivo was examined in an exogenous serotonin‐induced defecation model.
Key Results
FFA3 immunoreactivity was located in nitrergic and cholinergic neurons in the myenteric plexus. In isolated circular muscle strips without mucosa and submucosa, the addition of nicotine (10 μM) or serotonin transiently relaxed the muscle through nitrergic neurons, whereas high concentrations of nicotine (100 μM) induced large‐amplitude contractions that were mediated by cholinergic neurons. Pretreatment with FFA3 agonists inhibited nicotine‐ or serotonin‐induced motility changes but had no effect on bethanechol‐induced direct muscle contractions. The Gi/o inhibitor pertussis toxin reversed the inhibitory effect of an FFA3 agonist AR420626 on nicotine‐evoked contractions, suggesting that FFA3 activation suppresses nAChR‐mediated neural activity in myenteric neurons, consistent with an FFA3‐mediated antisecretory effect. In conscious rats, exogenous serotonin increased the volume of fecal output, compared with the vehicle‐ or AR420626‐treated groups. Pretreatment with AR420626 significantly suppressed serotonin‐induced fecal output.
Conclusion and Inferences
FFA3 is a promising target for the treatment of neurogenic diarrheal disorders by suppressing nAChR‐mediated neural pathways.
Short‐chain fatty acids produced by the gut microbiota contribute to the colonic motility regulation in health and disease. We identified the expression of a short‐chain fatty acid receptor, free fatty acid receptor 3 (FFA3), in inhibitory and excitatory myenteric neurons. The activation of FFA3 inhibited nicotine‐ or serotonin‐induced circular muscle activities ex vivo, and prevented serotonin‐induced defecation in vivo. |
| doi_str_mv | 10.1111/nmo.13157 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5739952</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1978557048</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5097-85a950da5886c0462bfca8dfaca1f85cb0e80811a7a1e789e663b805f1f87eb63</originalsourceid><addsrcrecordid>eNp1kUtv3CAUhVHUqJNHF_kDFVI3zcITsI2BTaVqlJeUxybddIMwcz0lssEFnGT-fUgmidJKYXO5ut89OnAQOqBkTvM5coOf04oyvoV2aNWwopSi_PR0Z6SgsmQztBvjLSGkKevmM5qVgtO65HwH_T4JALjTKa2xNnaJAxgYkw-4yn2ydzpZ73CcxjFAjBCxgyn4FThr8OCT7W3etA4HnfAY_IMddI-N773bR9ud7iN8eal76NfJ8c3irLi4Pj1f_LwoDCOSF4JpychSMyEaQ-qmbDujxbLTRtNOMNMSEERQqrmmwIWEpqlaQViXpxzaptpDPza649QOsDTgUtC9GkO2EtbKa6v-nTj7R638nWK8kpKVWeD7i0DwfyeISQ02Guh77cBPUeUfJFQyLuuMfvsPvfVTcPl5meKCMU5qkanDDWWCjzFA92aGEvWUmMqJqefEMvv1vfs38jWiDBxtgHvbw_pjJXV1eb2RfAToy6HU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1978557048</pqid></control><display><type>article</type><title>Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Wiley Online Library Free Content</source><creator>Kaji, I. ; Akiba, Y. ; Furuyama, T. ; Adelson, D. W. ; Iwamoto, K. ; Watanabe, M. ; Kuwahara, A. ; Kaunitz, J. D.</creator><creatorcontrib>Kaji, I. ; Akiba, Y. ; Furuyama, T. ; Adelson, D. W. ; Iwamoto, K. ; Watanabe, M. ; Kuwahara, A. ; Kaunitz, J. D.</creatorcontrib><description>Background
Short‐chain fatty acids (SCFA) are microbial fermentation products absorbed by the colon. We recently reported that activation of the SCFA receptor termed free fatty acid receptor 3 (FFA3), expressed on cholinergic nerves, suppresses nicotinic acetylcholine receptor (nAChR)‐mediated transepithelial anion secretion. This study aimed to clarify how activation of neurally expressed FFA3 affects colonic motor function.
Methods
FFA3‐expressing myenteric neurons were identified by immunostaining; contractions of isolated circular muscle strips obtained from rat proximal colon were measured by isometric transducers. The effect of FFA3 agonists on defecation in vivo was examined in an exogenous serotonin‐induced defecation model.
Key Results
FFA3 immunoreactivity was located in nitrergic and cholinergic neurons in the myenteric plexus. In isolated circular muscle strips without mucosa and submucosa, the addition of nicotine (10 μM) or serotonin transiently relaxed the muscle through nitrergic neurons, whereas high concentrations of nicotine (100 μM) induced large‐amplitude contractions that were mediated by cholinergic neurons. Pretreatment with FFA3 agonists inhibited nicotine‐ or serotonin‐induced motility changes but had no effect on bethanechol‐induced direct muscle contractions. The Gi/o inhibitor pertussis toxin reversed the inhibitory effect of an FFA3 agonist AR420626 on nicotine‐evoked contractions, suggesting that FFA3 activation suppresses nAChR‐mediated neural activity in myenteric neurons, consistent with an FFA3‐mediated antisecretory effect. In conscious rats, exogenous serotonin increased the volume of fecal output, compared with the vehicle‐ or AR420626‐treated groups. Pretreatment with AR420626 significantly suppressed serotonin‐induced fecal output.
Conclusion and Inferences
FFA3 is a promising target for the treatment of neurogenic diarrheal disorders by suppressing nAChR‐mediated neural pathways.
Short‐chain fatty acids produced by the gut microbiota contribute to the colonic motility regulation in health and disease. We identified the expression of a short‐chain fatty acid receptor, free fatty acid receptor 3 (FFA3), in inhibitory and excitatory myenteric neurons. The activation of FFA3 inhibited nicotine‐ or serotonin‐induced circular muscle activities ex vivo, and prevented serotonin‐induced defecation in vivo.</description><identifier>ISSN: 1350-1925</identifier><identifier>EISSN: 1365-2982</identifier><identifier>DOI: 10.1111/nmo.13157</identifier><identifier>PMID: 28714277</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Acetylcholine receptors (nicotinic) ; Animals ; Cholinergic nerves ; Cholinergic Neurons - metabolism ; circular muscle contraction ; Colon ; Colon - metabolism ; Colon - physiology ; Defecation ; Diarrhea ; Enteric nervous system ; enteric neural pathway ; Fatty acids ; Fermentation ; free fatty acid receptor 3 ; Gastrointestinal Motility ; Immunoreactivity ; Male ; Motility ; Mucosa ; Muscle Contraction ; Myenteric plexus ; Myenteric Plexus - physiology ; Nerves ; Neurons ; Neurons - metabolism ; Neurons - physiology ; Nicotine ; Nicotine - administration & dosage ; Nicotinic Agonists - administration & dosage ; Nitrergic Neurons - metabolism ; Pertussis ; Pertussis toxin ; proximal colon ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled - agonists ; Receptors, G-Protein-Coupled - metabolism ; Receptors, G-Protein-Coupled - physiology ; Rodents ; Serotonin ; Serotonin - administration & dosage ; Serotonin Antagonists - administration & dosage</subject><ispartof>Neurogastroenterology and motility, 2018-01, Vol.30 (1), p.n/a</ispartof><rights>2017 John Wiley & Sons Ltd</rights><rights>2017 John Wiley & Sons Ltd.</rights><rights>Copyright © 2018 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5097-85a950da5886c0462bfca8dfaca1f85cb0e80811a7a1e789e663b805f1f87eb63</citedby><cites>FETCH-LOGICAL-c5097-85a950da5886c0462bfca8dfaca1f85cb0e80811a7a1e789e663b805f1f87eb63</cites><orcidid>0000-0001-5395-0497</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fnmo.13157$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnmo.13157$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28714277$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kaji, I.</creatorcontrib><creatorcontrib>Akiba, Y.</creatorcontrib><creatorcontrib>Furuyama, T.</creatorcontrib><creatorcontrib>Adelson, D. W.</creatorcontrib><creatorcontrib>Iwamoto, K.</creatorcontrib><creatorcontrib>Watanabe, M.</creatorcontrib><creatorcontrib>Kuwahara, A.</creatorcontrib><creatorcontrib>Kaunitz, J. D.</creatorcontrib><title>Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon</title><title>Neurogastroenterology and motility</title><addtitle>Neurogastroenterol Motil</addtitle><description>Background
Short‐chain fatty acids (SCFA) are microbial fermentation products absorbed by the colon. We recently reported that activation of the SCFA receptor termed free fatty acid receptor 3 (FFA3), expressed on cholinergic nerves, suppresses nicotinic acetylcholine receptor (nAChR)‐mediated transepithelial anion secretion. This study aimed to clarify how activation of neurally expressed FFA3 affects colonic motor function.
Methods
FFA3‐expressing myenteric neurons were identified by immunostaining; contractions of isolated circular muscle strips obtained from rat proximal colon were measured by isometric transducers. The effect of FFA3 agonists on defecation in vivo was examined in an exogenous serotonin‐induced defecation model.
Key Results
FFA3 immunoreactivity was located in nitrergic and cholinergic neurons in the myenteric plexus. In isolated circular muscle strips without mucosa and submucosa, the addition of nicotine (10 μM) or serotonin transiently relaxed the muscle through nitrergic neurons, whereas high concentrations of nicotine (100 μM) induced large‐amplitude contractions that were mediated by cholinergic neurons. Pretreatment with FFA3 agonists inhibited nicotine‐ or serotonin‐induced motility changes but had no effect on bethanechol‐induced direct muscle contractions. The Gi/o inhibitor pertussis toxin reversed the inhibitory effect of an FFA3 agonist AR420626 on nicotine‐evoked contractions, suggesting that FFA3 activation suppresses nAChR‐mediated neural activity in myenteric neurons, consistent with an FFA3‐mediated antisecretory effect. In conscious rats, exogenous serotonin increased the volume of fecal output, compared with the vehicle‐ or AR420626‐treated groups. Pretreatment with AR420626 significantly suppressed serotonin‐induced fecal output.
Conclusion and Inferences
FFA3 is a promising target for the treatment of neurogenic diarrheal disorders by suppressing nAChR‐mediated neural pathways.
Short‐chain fatty acids produced by the gut microbiota contribute to the colonic motility regulation in health and disease. We identified the expression of a short‐chain fatty acid receptor, free fatty acid receptor 3 (FFA3), in inhibitory and excitatory myenteric neurons. The activation of FFA3 inhibited nicotine‐ or serotonin‐induced circular muscle activities ex vivo, and prevented serotonin‐induced defecation in vivo.</description><subject>Acetylcholine receptors (nicotinic)</subject><subject>Animals</subject><subject>Cholinergic nerves</subject><subject>Cholinergic Neurons - metabolism</subject><subject>circular muscle contraction</subject><subject>Colon</subject><subject>Colon - metabolism</subject><subject>Colon - physiology</subject><subject>Defecation</subject><subject>Diarrhea</subject><subject>Enteric nervous system</subject><subject>enteric neural pathway</subject><subject>Fatty acids</subject><subject>Fermentation</subject><subject>free fatty acid receptor 3</subject><subject>Gastrointestinal Motility</subject><subject>Immunoreactivity</subject><subject>Male</subject><subject>Motility</subject><subject>Mucosa</subject><subject>Muscle Contraction</subject><subject>Myenteric plexus</subject><subject>Myenteric Plexus - physiology</subject><subject>Nerves</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>Nicotine</subject><subject>Nicotine - administration & dosage</subject><subject>Nicotinic Agonists - administration & dosage</subject><subject>Nitrergic Neurons - metabolism</subject><subject>Pertussis</subject><subject>Pertussis toxin</subject><subject>proximal colon</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Receptors, G-Protein-Coupled - physiology</subject><subject>Rodents</subject><subject>Serotonin</subject><subject>Serotonin - administration & dosage</subject><subject>Serotonin Antagonists - administration & dosage</subject><issn>1350-1925</issn><issn>1365-2982</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUtv3CAUhVHUqJNHF_kDFVI3zcITsI2BTaVqlJeUxybddIMwcz0lssEFnGT-fUgmidJKYXO5ut89OnAQOqBkTvM5coOf04oyvoV2aNWwopSi_PR0Z6SgsmQztBvjLSGkKevmM5qVgtO65HwH_T4JALjTKa2xNnaJAxgYkw-4yn2ydzpZ73CcxjFAjBCxgyn4FThr8OCT7W3etA4HnfAY_IMddI-N773bR9ud7iN8eal76NfJ8c3irLi4Pj1f_LwoDCOSF4JpychSMyEaQ-qmbDujxbLTRtNOMNMSEERQqrmmwIWEpqlaQViXpxzaptpDPza649QOsDTgUtC9GkO2EtbKa6v-nTj7R638nWK8kpKVWeD7i0DwfyeISQ02Guh77cBPUeUfJFQyLuuMfvsPvfVTcPl5meKCMU5qkanDDWWCjzFA92aGEvWUmMqJqefEMvv1vfs38jWiDBxtgHvbw_pjJXV1eb2RfAToy6HU</recordid><startdate>201801</startdate><enddate>201801</enddate><creator>Kaji, I.</creator><creator>Akiba, Y.</creator><creator>Furuyama, T.</creator><creator>Adelson, D. W.</creator><creator>Iwamoto, K.</creator><creator>Watanabe, M.</creator><creator>Kuwahara, A.</creator><creator>Kaunitz, J. D.</creator><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5395-0497</orcidid></search><sort><creationdate>201801</creationdate><title>Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon</title><author>Kaji, I. ; Akiba, Y. ; Furuyama, T. ; Adelson, D. W. ; Iwamoto, K. ; Watanabe, M. ; Kuwahara, A. ; Kaunitz, J. D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5097-85a950da5886c0462bfca8dfaca1f85cb0e80811a7a1e789e663b805f1f87eb63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetylcholine receptors (nicotinic)</topic><topic>Animals</topic><topic>Cholinergic nerves</topic><topic>Cholinergic Neurons - metabolism</topic><topic>circular muscle contraction</topic><topic>Colon</topic><topic>Colon - metabolism</topic><topic>Colon - physiology</topic><topic>Defecation</topic><topic>Diarrhea</topic><topic>Enteric nervous system</topic><topic>enteric neural pathway</topic><topic>Fatty acids</topic><topic>Fermentation</topic><topic>free fatty acid receptor 3</topic><topic>Gastrointestinal Motility</topic><topic>Immunoreactivity</topic><topic>Male</topic><topic>Motility</topic><topic>Mucosa</topic><topic>Muscle Contraction</topic><topic>Myenteric plexus</topic><topic>Myenteric Plexus - physiology</topic><topic>Nerves</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>Nicotine</topic><topic>Nicotine - administration & dosage</topic><topic>Nicotinic Agonists - administration & dosage</topic><topic>Nitrergic Neurons - metabolism</topic><topic>Pertussis</topic><topic>Pertussis toxin</topic><topic>proximal colon</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, G-Protein-Coupled - agonists</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Receptors, G-Protein-Coupled - physiology</topic><topic>Rodents</topic><topic>Serotonin</topic><topic>Serotonin - administration & dosage</topic><topic>Serotonin Antagonists - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kaji, I.</creatorcontrib><creatorcontrib>Akiba, Y.</creatorcontrib><creatorcontrib>Furuyama, T.</creatorcontrib><creatorcontrib>Adelson, D. W.</creatorcontrib><creatorcontrib>Iwamoto, K.</creatorcontrib><creatorcontrib>Watanabe, M.</creatorcontrib><creatorcontrib>Kuwahara, A.</creatorcontrib><creatorcontrib>Kaunitz, J. D.</creatorcontrib><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>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurogastroenterology and motility</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kaji, I.</au><au>Akiba, Y.</au><au>Furuyama, T.</au><au>Adelson, D. W.</au><au>Iwamoto, K.</au><au>Watanabe, M.</au><au>Kuwahara, A.</au><au>Kaunitz, J. D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon</atitle><jtitle>Neurogastroenterology and motility</jtitle><addtitle>Neurogastroenterol Motil</addtitle><date>2018-01</date><risdate>2018</risdate><volume>30</volume><issue>1</issue><epage>n/a</epage><issn>1350-1925</issn><eissn>1365-2982</eissn><abstract>Background
Short‐chain fatty acids (SCFA) are microbial fermentation products absorbed by the colon. We recently reported that activation of the SCFA receptor termed free fatty acid receptor 3 (FFA3), expressed on cholinergic nerves, suppresses nicotinic acetylcholine receptor (nAChR)‐mediated transepithelial anion secretion. This study aimed to clarify how activation of neurally expressed FFA3 affects colonic motor function.
Methods
FFA3‐expressing myenteric neurons were identified by immunostaining; contractions of isolated circular muscle strips obtained from rat proximal colon were measured by isometric transducers. The effect of FFA3 agonists on defecation in vivo was examined in an exogenous serotonin‐induced defecation model.
Key Results
FFA3 immunoreactivity was located in nitrergic and cholinergic neurons in the myenteric plexus. In isolated circular muscle strips without mucosa and submucosa, the addition of nicotine (10 μM) or serotonin transiently relaxed the muscle through nitrergic neurons, whereas high concentrations of nicotine (100 μM) induced large‐amplitude contractions that were mediated by cholinergic neurons. Pretreatment with FFA3 agonists inhibited nicotine‐ or serotonin‐induced motility changes but had no effect on bethanechol‐induced direct muscle contractions. The Gi/o inhibitor pertussis toxin reversed the inhibitory effect of an FFA3 agonist AR420626 on nicotine‐evoked contractions, suggesting that FFA3 activation suppresses nAChR‐mediated neural activity in myenteric neurons, consistent with an FFA3‐mediated antisecretory effect. In conscious rats, exogenous serotonin increased the volume of fecal output, compared with the vehicle‐ or AR420626‐treated groups. Pretreatment with AR420626 significantly suppressed serotonin‐induced fecal output.
Conclusion and Inferences
FFA3 is a promising target for the treatment of neurogenic diarrheal disorders by suppressing nAChR‐mediated neural pathways.
Short‐chain fatty acids produced by the gut microbiota contribute to the colonic motility regulation in health and disease. We identified the expression of a short‐chain fatty acid receptor, free fatty acid receptor 3 (FFA3), in inhibitory and excitatory myenteric neurons. The activation of FFA3 inhibited nicotine‐ or serotonin‐induced circular muscle activities ex vivo, and prevented serotonin‐induced defecation in vivo.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28714277</pmid><doi>10.1111/nmo.13157</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-5395-0497</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Neurogastroenterology and motility, 2018-01, Vol.30 (1), p.n/a |
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| subjects | Acetylcholine receptors (nicotinic) Animals Cholinergic nerves Cholinergic Neurons - metabolism circular muscle contraction Colon Colon - metabolism Colon - physiology Defecation Diarrhea Enteric nervous system enteric neural pathway Fatty acids Fermentation free fatty acid receptor 3 Gastrointestinal Motility Immunoreactivity Male Motility Mucosa Muscle Contraction Myenteric plexus Myenteric Plexus - physiology Nerves Neurons Neurons - metabolism Neurons - physiology Nicotine Nicotine - administration & dosage Nicotinic Agonists - administration & dosage Nitrergic Neurons - metabolism Pertussis Pertussis toxin proximal colon Rats, Sprague-Dawley Receptors, G-Protein-Coupled - agonists Receptors, G-Protein-Coupled - metabolism Receptors, G-Protein-Coupled - physiology Rodents Serotonin Serotonin - administration & dosage Serotonin Antagonists - administration & dosage |
| title | Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon |
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