Antagonism of ionotropic glutamate receptors attenuates chemical ischemia-induced injury in rat primary cultured myenteric ganglia
Alterations of the enteric glutamatergic transmission may underlay changes in the function of myenteric neurons following intestinal ischemia and reperfusion (I/R) contributing to impairment of gastrointestinal motility occurring in these pathological conditions. The aim of the present study was to...
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| Veröffentlicht in: | PloS one 2014-11, Vol.9 (11), p.e113613-e113613 |
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| creator | Carpanese, Elisa Moretto, Paola Filpa, Viviana Marchet, Silvia Moro, Elisabetta Crema, Francesca Frigo, Gianmario Giaroni, Cristina |
| description | Alterations of the enteric glutamatergic transmission may underlay changes in the function of myenteric neurons following intestinal ischemia and reperfusion (I/R) contributing to impairment of gastrointestinal motility occurring in these pathological conditions. The aim of the present study was to evaluate whether glutamate receptors of the NMDA and AMPA/kainate type are involved in myenteric neuron cell damage induced by I/R. Primary cultured rat myenteric ganglia were exposed to sodium azide and glucose deprivation (in vitro chemical ischemia). After 6 days of culture, immunoreactivity for NMDA, AMPA and kainate receptors subunits, GluN(1) and GluA(1-3), GluK(1-3) respectively, was found in myenteric neurons. In myenteric cultured ganglia, in normal metabolic conditions, -AP5, an NMDA antagonist, decreased myenteric neuron number and viability, determined by calcein AM/ethidium homodimer-1 assay, and increased reactive oxygen species (ROS) levels, measured with hydroxyphenyl fluorescein. CNQX, an AMPA/kainate antagonist exerted an opposite action on the same parameters. The total number and viability of myenteric neurons significantly decreased after I/R. In these conditions, the number of neurons staining for GluN1 and GluA(1-3) subunits remained unchanged, while, the number of GluK(1-3)-immunopositive neurons increased. After I/R, -AP5 and CNQX, concentration-dependently increased myenteric neuron number and significantly increased the number of living neurons. Both -AP5 and CNQX (100-500 µM) decreased I/R-induced increase of ROS levels in myenteric ganglia. On the whole, the present data provide evidence that, under normal metabolic conditions, the enteric glutamatergic system exerts a dualistic effect on cultured myenteric ganglia, either by improving or reducing neuron survival via NMDA or AMPA/kainate receptor activation, respectively. However, blockade of both receptor pathways may exert a protective role on myenteric neurons following and I/R damage. The neuroprotective effect may depend, at least in part, on the ability of both receptors to increase intraneuronal ROS production. |
| doi_str_mv | 10.1371/journal.pone.0113613 |
| format | Article |
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The aim of the present study was to evaluate whether glutamate receptors of the NMDA and AMPA/kainate type are involved in myenteric neuron cell damage induced by I/R. Primary cultured rat myenteric ganglia were exposed to sodium azide and glucose deprivation (in vitro chemical ischemia). After 6 days of culture, immunoreactivity for NMDA, AMPA and kainate receptors subunits, GluN(1) and GluA(1-3), GluK(1-3) respectively, was found in myenteric neurons. In myenteric cultured ganglia, in normal metabolic conditions, -AP5, an NMDA antagonist, decreased myenteric neuron number and viability, determined by calcein AM/ethidium homodimer-1 assay, and increased reactive oxygen species (ROS) levels, measured with hydroxyphenyl fluorescein. CNQX, an AMPA/kainate antagonist exerted an opposite action on the same parameters. The total number and viability of myenteric neurons significantly decreased after I/R. In these conditions, the number of neurons staining for GluN1 and GluA(1-3) subunits remained unchanged, while, the number of GluK(1-3)-immunopositive neurons increased. After I/R, -AP5 and CNQX, concentration-dependently increased myenteric neuron number and significantly increased the number of living neurons. Both -AP5 and CNQX (100-500 µM) decreased I/R-induced increase of ROS levels in myenteric ganglia. On the whole, the present data provide evidence that, under normal metabolic conditions, the enteric glutamatergic system exerts a dualistic effect on cultured myenteric ganglia, either by improving or reducing neuron survival via NMDA or AMPA/kainate receptor activation, respectively. However, blockade of both receptor pathways may exert a protective role on myenteric neurons following and I/R damage. The neuroprotective effect may depend, at least in part, on the ability of both receptors to increase intraneuronal ROS production.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0113613</identifier><identifier>PMID: 25419700</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>2-Amino-5-phosphonovalerate - pharmacology ; 6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology ; Animals ; Apoptosis ; Biology and Life Sciences ; Calcein ; Cell Count ; Cell culture ; Cell survival ; Cell Survival - drug effects ; Cells, Cultured ; Deprivation ; Excitatory Amino Acid Antagonists - pharmacology ; Fluorescein ; Ganglia ; Ganglia - blood supply ; Ganglia - cytology ; Ganglia - metabolism ; Gastric motility ; Glucose ; Glucose - metabolism ; Glutamate ; Glutamatergic transmission ; Glutamic acid receptors (ionotropic) ; Immunohistochemistry ; Immunoreactivity ; Internal medicine ; Intestine ; Ischemia ; Ischemia - chemically induced ; Ischemia - physiopathology ; Kainic acid receptors ; Laboratory animals ; Male ; Medicine ; Medicine and Health Sciences ; Motility ; Myenteric ganglia ; Myenteric plexus ; Myenteric Plexus - blood supply ; Myenteric Plexus - metabolism ; N-methyl-D-aspartate ; N-Methyl-D-aspartic acid receptors ; Nervous system ; Neurons ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotection ; Neurotoxicity ; Oxygen ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptor mechanisms ; Receptors ; Receptors, AMPA - antagonists & inhibitors ; Receptors, AMPA - metabolism ; Receptors, Ionotropic Glutamate - antagonists & inhibitors ; Receptors, Ionotropic Glutamate - metabolism ; Receptors, Kainic Acid - antagonists & inhibitors ; Receptors, Kainic Acid - metabolism ; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors ; Receptors, N-Methyl-D-Aspartate - metabolism ; Reperfusion ; Reperfusion Injury - physiopathology ; Rodents ; Small intestine ; Sodium ; Sodium azide ; Sodium Azide - pharmacology ; Studies ; Viability ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</subject><ispartof>PloS one, 2014-11, Vol.9 (11), p.e113613-e113613</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Carpanese et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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The aim of the present study was to evaluate whether glutamate receptors of the NMDA and AMPA/kainate type are involved in myenteric neuron cell damage induced by I/R. Primary cultured rat myenteric ganglia were exposed to sodium azide and glucose deprivation (in vitro chemical ischemia). After 6 days of culture, immunoreactivity for NMDA, AMPA and kainate receptors subunits, GluN(1) and GluA(1-3), GluK(1-3) respectively, was found in myenteric neurons. In myenteric cultured ganglia, in normal metabolic conditions, -AP5, an NMDA antagonist, decreased myenteric neuron number and viability, determined by calcein AM/ethidium homodimer-1 assay, and increased reactive oxygen species (ROS) levels, measured with hydroxyphenyl fluorescein. CNQX, an AMPA/kainate antagonist exerted an opposite action on the same parameters. The total number and viability of myenteric neurons significantly decreased after I/R. In these conditions, the number of neurons staining for GluN1 and GluA(1-3) subunits remained unchanged, while, the number of GluK(1-3)-immunopositive neurons increased. After I/R, -AP5 and CNQX, concentration-dependently increased myenteric neuron number and significantly increased the number of living neurons. Both -AP5 and CNQX (100-500 µM) decreased I/R-induced increase of ROS levels in myenteric ganglia. On the whole, the present data provide evidence that, under normal metabolic conditions, the enteric glutamatergic system exerts a dualistic effect on cultured myenteric ganglia, either by improving or reducing neuron survival via NMDA or AMPA/kainate receptor activation, respectively. However, blockade of both receptor pathways may exert a protective role on myenteric neurons following and I/R damage. The neuroprotective effect may depend, at least in part, on the ability of both receptors to increase intraneuronal ROS production.</description><subject>2-Amino-5-phosphonovalerate - pharmacology</subject><subject>6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biology and Life Sciences</subject><subject>Calcein</subject><subject>Cell Count</subject><subject>Cell culture</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Deprivation</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Fluorescein</subject><subject>Ganglia</subject><subject>Ganglia - blood supply</subject><subject>Ganglia - cytology</subject><subject>Ganglia - metabolism</subject><subject>Gastric motility</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glutamate</subject><subject>Glutamatergic transmission</subject><subject>Glutamic acid receptors (ionotropic)</subject><subject>Immunohistochemistry</subject><subject>Immunoreactivity</subject><subject>Internal medicine</subject><subject>Intestine</subject><subject>Ischemia</subject><subject>Ischemia - 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physiopathology</topic><topic>Kainic acid receptors</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Motility</topic><topic>Myenteric ganglia</topic><topic>Myenteric plexus</topic><topic>Myenteric Plexus - blood supply</topic><topic>Myenteric Plexus - metabolism</topic><topic>N-methyl-D-aspartate</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Nervous system</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotection</topic><topic>Neurotoxicity</topic><topic>Oxygen</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptor mechanisms</topic><topic>Receptors</topic><topic>Receptors, AMPA - antagonists & inhibitors</topic><topic>Receptors, AMPA - metabolism</topic><topic>Receptors, Ionotropic Glutamate - antagonists & inhibitors</topic><topic>Receptors, Ionotropic Glutamate - metabolism</topic><topic>Receptors, Kainic Acid - antagonists & inhibitors</topic><topic>Receptors, Kainic Acid - metabolism</topic><topic>Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Rodents</topic><topic>Small intestine</topic><topic>Sodium</topic><topic>Sodium azide</topic><topic>Sodium Azide - pharmacology</topic><topic>Studies</topic><topic>Viability</topic><topic>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carpanese, Elisa</creatorcontrib><creatorcontrib>Moretto, Paola</creatorcontrib><creatorcontrib>Filpa, Viviana</creatorcontrib><creatorcontrib>Marchet, Silvia</creatorcontrib><creatorcontrib>Moro, Elisabetta</creatorcontrib><creatorcontrib>Crema, Francesca</creatorcontrib><creatorcontrib>Frigo, Gianmario</creatorcontrib><creatorcontrib>Giaroni, Cristina</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 (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</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 - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - 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>Carpanese, Elisa</au><au>Moretto, Paola</au><au>Filpa, Viviana</au><au>Marchet, Silvia</au><au>Moro, Elisabetta</au><au>Crema, Francesca</au><au>Frigo, Gianmario</au><au>Giaroni, Cristina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antagonism of ionotropic glutamate receptors attenuates chemical ischemia-induced injury in rat primary cultured myenteric ganglia</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-11-24</date><risdate>2014</risdate><volume>9</volume><issue>11</issue><spage>e113613</spage><epage>e113613</epage><pages>e113613-e113613</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Alterations of the enteric glutamatergic transmission may underlay changes in the function of myenteric neurons following intestinal ischemia and reperfusion (I/R) contributing to impairment of gastrointestinal motility occurring in these pathological conditions. The aim of the present study was to evaluate whether glutamate receptors of the NMDA and AMPA/kainate type are involved in myenteric neuron cell damage induced by I/R. Primary cultured rat myenteric ganglia were exposed to sodium azide and glucose deprivation (in vitro chemical ischemia). After 6 days of culture, immunoreactivity for NMDA, AMPA and kainate receptors subunits, GluN(1) and GluA(1-3), GluK(1-3) respectively, was found in myenteric neurons. In myenteric cultured ganglia, in normal metabolic conditions, -AP5, an NMDA antagonist, decreased myenteric neuron number and viability, determined by calcein AM/ethidium homodimer-1 assay, and increased reactive oxygen species (ROS) levels, measured with hydroxyphenyl fluorescein. CNQX, an AMPA/kainate antagonist exerted an opposite action on the same parameters. The total number and viability of myenteric neurons significantly decreased after I/R. In these conditions, the number of neurons staining for GluN1 and GluA(1-3) subunits remained unchanged, while, the number of GluK(1-3)-immunopositive neurons increased. After I/R, -AP5 and CNQX, concentration-dependently increased myenteric neuron number and significantly increased the number of living neurons. Both -AP5 and CNQX (100-500 µM) decreased I/R-induced increase of ROS levels in myenteric ganglia. On the whole, the present data provide evidence that, under normal metabolic conditions, the enteric glutamatergic system exerts a dualistic effect on cultured myenteric ganglia, either by improving or reducing neuron survival via NMDA or AMPA/kainate receptor activation, respectively. However, blockade of both receptor pathways may exert a protective role on myenteric neurons following and I/R damage. The neuroprotective effect may depend, at least in part, on the ability of both receptors to increase intraneuronal ROS production.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25419700</pmid><doi>10.1371/journal.pone.0113613</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-11, Vol.9 (11), p.e113613-e113613 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1627711306 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 2-Amino-5-phosphonovalerate - pharmacology 6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology Animals Apoptosis Biology and Life Sciences Calcein Cell Count Cell culture Cell survival Cell Survival - drug effects Cells, Cultured Deprivation Excitatory Amino Acid Antagonists - pharmacology Fluorescein Ganglia Ganglia - blood supply Ganglia - cytology Ganglia - metabolism Gastric motility Glucose Glucose - metabolism Glutamate Glutamatergic transmission Glutamic acid receptors (ionotropic) Immunohistochemistry Immunoreactivity Internal medicine Intestine Ischemia Ischemia - chemically induced Ischemia - physiopathology Kainic acid receptors Laboratory animals Male Medicine Medicine and Health Sciences Motility Myenteric ganglia Myenteric plexus Myenteric Plexus - blood supply Myenteric Plexus - metabolism N-methyl-D-aspartate N-Methyl-D-aspartic acid receptors Nervous system Neurons Neurons - drug effects Neurons - metabolism Neuroprotection Neurotoxicity Oxygen Rats Reactive oxygen species Reactive Oxygen Species - metabolism Receptor mechanisms Receptors Receptors, AMPA - antagonists & inhibitors Receptors, AMPA - metabolism Receptors, Ionotropic Glutamate - antagonists & inhibitors Receptors, Ionotropic Glutamate - metabolism Receptors, Kainic Acid - antagonists & inhibitors Receptors, Kainic Acid - metabolism Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors Receptors, N-Methyl-D-Aspartate - metabolism Reperfusion Reperfusion Injury - physiopathology Rodents Small intestine Sodium Sodium azide Sodium Azide - pharmacology Studies Viability α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid |
| title | Antagonism of ionotropic glutamate receptors attenuates chemical ischemia-induced injury in rat primary cultured myenteric ganglia |
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