Combinations of ketamine and atropine are neuroprotective and reduce neuroinflammation after a toxic status epilepticus in mice
Epileptic seizures and status epilepticus (SE) induced by the poisoning with organophosphorus nerve agents (OP), like soman, are accompanied by neuroinflammation whose role in seizure-related brain damage (SRBD) is not clear. Antagonists of the NMDA glutamate ionotropic receptors are currently among...
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| creator | Dhote, Franck Carpentier, Pierre Barbier, Laure Peinnequin, André Baille, Valérie Pernot, Fabien Testylier, Guy Beaup, Claire Foquin, Annie Dorandeu, Fréderic |
| description | Epileptic seizures and status epilepticus (SE) induced by the poisoning with organophosphorus nerve agents (OP), like soman, are accompanied by neuroinflammation whose role in seizure-related brain damage (SRBD) is not clear. Antagonists of the NMDA glutamate ionotropic receptors are currently among the few compounds able to arrest seizures and provide neuroprotection even during refractory status epilepticus (RSE). Racemic ketamine (KET), in combination with atropine sulfate (AS), was previously shown to counteract seizures and SRBD in soman-poisoned guinea-pigs. In a mouse model of severe soman-induced SE, we assessed the potentials of KET/AS combinations as a treatment for SE/RSE-induced SRBD and neuroinflammation. When starting 30min after soman challenge, a protocol involving six injections of a sub-anesthetic dose of KET (25mg/kg) was evaluated on body weight loss, brain damage, and neuroinflammation whereas during RSE, anesthetic protocols were considered (KET 100mg/kg). After confirming that during RSE, KET injection was to be repeated despite some iatrogenic deaths, we used these proof-of-concept protocols to study the changes in mRNA and related protein contents of some inflammatory cytokines, chemokines and adhesion molecules in cortex and hippocampus 48h post-challenge. In both cases, the KET/AS combinations showed important neuroprotective effects, suppressed neutrophil granulocyte infiltration and partially suppressed glial activation. KET/AS could also reduce the increase in mRNA and related pro-inflammatory proteins provoked by the poisoning. In conclusion, the present study confirms that KET/AS treatment has a strong potential for SE/RSE management following OP poisoning. The mechanisms involved in the reduction of central neuroinflammation remain to be studied.
► During soman-induced status epilepticus, ketamine-atropine limit brain damage. ► Molecular neuroinflammatory response is strongly decreased. ► Glial activation is not fully suppressed. |
| doi_str_mv | 10.1016/j.taap.2011.12.024 |
| format | Article |
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► During soman-induced status epilepticus, ketamine-atropine limit brain damage. ► Molecular neuroinflammatory response is strongly decreased. ► Glial activation is not fully suppressed.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2011.12.024</identifier><identifier>PMID: 22245128</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; ANESTHETICS ; Animals ; Area Under Curve ; Astroglia ; ATROPINE ; Atropine - pharmacology ; Biological and medical sciences ; Brain - cytology ; Brain - drug effects ; Brain - immunology ; Brain cytokines ; Chemical and industrial products toxicology. Toxic occupational diseases ; Chemical Warfare Agents - toxicity ; Chemokine CCL5 - genetics ; Chemokine CCL5 - immunology ; Chemokine CXCL1 - genetics ; Chemokine CXCL1 - immunology ; Drug addictions ; Excitatory Amino Acid Antagonists - pharmacology ; Gas, fumes ; GUINEA PIGS ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; HIPPOCAMPUS ; INFLAMMATION ; Ketamine ; Ketamine - pharmacology ; LYMPHOKINES ; MAGNESIUM 25 ; Male ; Medical sciences ; MESSENGER-RNA ; MICE ; Microglia ; Muscarinic Antagonists - pharmacology ; Nervous system (semeiology, syndromes) ; Neuroglia - immunology ; Neurology ; Neutrophil granulocytes ; NEUTROPHILS ; Neutrophils - immunology ; Polymerase Chain Reaction ; Random Allocation ; RECEPTORS ; RNA, Messenger - chemistry ; RNA, Messenger - genetics ; Soman ; Soman - toxicity ; Status epilepticus ; Status Epilepticus - chemically induced ; Status Epilepticus - drug therapy ; Status Epilepticus - immunology ; Toxicology</subject><ispartof>Toxicology and applied pharmacology, 2012-03, Vol.259 (2), p.195-209</ispartof><rights>2012 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-b407b1a1129ae5b2034a92b0e4ccc55859822e904c233c46cc32830bbc58f2163</citedby><cites>FETCH-LOGICAL-c413t-b407b1a1129ae5b2034a92b0e4ccc55859822e904c233c46cc32830bbc58f2163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.taap.2011.12.024$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25767155$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22245128$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22215255$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Dhote, Franck</creatorcontrib><creatorcontrib>Carpentier, Pierre</creatorcontrib><creatorcontrib>Barbier, Laure</creatorcontrib><creatorcontrib>Peinnequin, André</creatorcontrib><creatorcontrib>Baille, Valérie</creatorcontrib><creatorcontrib>Pernot, Fabien</creatorcontrib><creatorcontrib>Testylier, Guy</creatorcontrib><creatorcontrib>Beaup, Claire</creatorcontrib><creatorcontrib>Foquin, Annie</creatorcontrib><creatorcontrib>Dorandeu, Fréderic</creatorcontrib><title>Combinations of ketamine and atropine are neuroprotective and reduce neuroinflammation after a toxic status epilepticus in mice</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Epileptic seizures and status epilepticus (SE) induced by the poisoning with organophosphorus nerve agents (OP), like soman, are accompanied by neuroinflammation whose role in seizure-related brain damage (SRBD) is not clear. Antagonists of the NMDA glutamate ionotropic receptors are currently among the few compounds able to arrest seizures and provide neuroprotection even during refractory status epilepticus (RSE). Racemic ketamine (KET), in combination with atropine sulfate (AS), was previously shown to counteract seizures and SRBD in soman-poisoned guinea-pigs. In a mouse model of severe soman-induced SE, we assessed the potentials of KET/AS combinations as a treatment for SE/RSE-induced SRBD and neuroinflammation. When starting 30min after soman challenge, a protocol involving six injections of a sub-anesthetic dose of KET (25mg/kg) was evaluated on body weight loss, brain damage, and neuroinflammation whereas during RSE, anesthetic protocols were considered (KET 100mg/kg). After confirming that during RSE, KET injection was to be repeated despite some iatrogenic deaths, we used these proof-of-concept protocols to study the changes in mRNA and related protein contents of some inflammatory cytokines, chemokines and adhesion molecules in cortex and hippocampus 48h post-challenge. In both cases, the KET/AS combinations showed important neuroprotective effects, suppressed neutrophil granulocyte infiltration and partially suppressed glial activation. KET/AS could also reduce the increase in mRNA and related pro-inflammatory proteins provoked by the poisoning. In conclusion, the present study confirms that KET/AS treatment has a strong potential for SE/RSE management following OP poisoning. The mechanisms involved in the reduction of central neuroinflammation remain to be studied.
► During soman-induced status epilepticus, ketamine-atropine limit brain damage. ► Molecular neuroinflammatory response is strongly decreased. ► Glial activation is not fully suppressed.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>ANESTHETICS</subject><subject>Animals</subject><subject>Area Under Curve</subject><subject>Astroglia</subject><subject>ATROPINE</subject><subject>Atropine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brain - cytology</subject><subject>Brain - drug effects</subject><subject>Brain - immunology</subject><subject>Brain cytokines</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Chemical Warfare Agents - toxicity</subject><subject>Chemokine CCL5 - genetics</subject><subject>Chemokine CCL5 - immunology</subject><subject>Chemokine CXCL1 - genetics</subject><subject>Chemokine CXCL1 - immunology</subject><subject>Drug addictions</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Gas, fumes</subject><subject>GUINEA PIGS</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>HIPPOCAMPUS</subject><subject>INFLAMMATION</subject><subject>Ketamine</subject><subject>Ketamine - pharmacology</subject><subject>LYMPHOKINES</subject><subject>MAGNESIUM 25</subject><subject>Male</subject><subject>Medical sciences</subject><subject>MESSENGER-RNA</subject><subject>MICE</subject><subject>Microglia</subject><subject>Muscarinic Antagonists - pharmacology</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neuroglia - immunology</subject><subject>Neurology</subject><subject>Neutrophil granulocytes</subject><subject>NEUTROPHILS</subject><subject>Neutrophils - immunology</subject><subject>Polymerase Chain Reaction</subject><subject>Random Allocation</subject><subject>RECEPTORS</subject><subject>RNA, Messenger - chemistry</subject><subject>RNA, Messenger - genetics</subject><subject>Soman</subject><subject>Soman - toxicity</subject><subject>Status epilepticus</subject><subject>Status Epilepticus - chemically induced</subject><subject>Status Epilepticus - drug therapy</subject><subject>Status Epilepticus - immunology</subject><subject>Toxicology</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQhi0EotvCH-CALCGOCf7MJhIXtAJaqRIXkLhZzmQivGzsyPZW7Ym_jrNZ6K0ne-TnHc88hLzhrOaMNx_2dbZ2rgXjvOaiZkI9IxvOuqZiUsrnZMOY4hVj7c8LcpnSnjHWKcVfkgshhNJctBvyZxem3nmbXfCJhpH-xmwn55FaP1CbY5hPRUTq8ViqGDJCdncrEHE4wvnJ-fFgp-nUitoxY6SW5nDvgKZs8zFRnN0B5-yg3J2nkwN8RV6M9pDw9fm8Ij--fP6-u65uv3292X26rUBxmatesW3PLeeis6h7waSynegZKgDQutVdKwR2TIGQElQDIEUrWd-DbkfBG3lF3q19Q8rOJHBli18QvC_LmKKDa6F1ocRKQQwpRRzNHN1k44PhzCzOzd4szs3i3HBhivMSeruG5mM_4fA_8k9yAd6fAZvAHsZoPbj0yOlts-Wn3z-uHBYRdw7jMid6wMHFZcwhuKfm-AudT6FW</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Dhote, Franck</creator><creator>Carpentier, Pierre</creator><creator>Barbier, Laure</creator><creator>Peinnequin, André</creator><creator>Baille, Valérie</creator><creator>Pernot, Fabien</creator><creator>Testylier, Guy</creator><creator>Beaup, Claire</creator><creator>Foquin, Annie</creator><creator>Dorandeu, Fréderic</creator><general>Elsevier Inc</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>OTOTI</scope></search><sort><creationdate>20120301</creationdate><title>Combinations of ketamine and atropine are neuroprotective and reduce neuroinflammation after a toxic status epilepticus in mice</title><author>Dhote, Franck ; Carpentier, Pierre ; Barbier, Laure ; Peinnequin, André ; Baille, Valérie ; Pernot, Fabien ; Testylier, Guy ; Beaup, Claire ; Foquin, Annie ; Dorandeu, Fréderic</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-b407b1a1129ae5b2034a92b0e4ccc55859822e904c233c46cc32830bbc58f2163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>ANESTHETICS</topic><topic>Animals</topic><topic>Area Under Curve</topic><topic>Astroglia</topic><topic>ATROPINE</topic><topic>Atropine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brain - cytology</topic><topic>Brain - drug effects</topic><topic>Brain - immunology</topic><topic>Brain cytokines</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Chemical Warfare Agents - toxicity</topic><topic>Chemokine CCL5 - genetics</topic><topic>Chemokine CCL5 - immunology</topic><topic>Chemokine CXCL1 - genetics</topic><topic>Chemokine CXCL1 - immunology</topic><topic>Drug addictions</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Gas, fumes</topic><topic>GUINEA PIGS</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>HIPPOCAMPUS</topic><topic>INFLAMMATION</topic><topic>Ketamine</topic><topic>Ketamine - pharmacology</topic><topic>LYMPHOKINES</topic><topic>MAGNESIUM 25</topic><topic>Male</topic><topic>Medical sciences</topic><topic>MESSENGER-RNA</topic><topic>MICE</topic><topic>Microglia</topic><topic>Muscarinic Antagonists - pharmacology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neuroglia - immunology</topic><topic>Neurology</topic><topic>Neutrophil granulocytes</topic><topic>NEUTROPHILS</topic><topic>Neutrophils - immunology</topic><topic>Polymerase Chain Reaction</topic><topic>Random Allocation</topic><topic>RECEPTORS</topic><topic>RNA, Messenger - chemistry</topic><topic>RNA, Messenger - genetics</topic><topic>Soman</topic><topic>Soman - toxicity</topic><topic>Status epilepticus</topic><topic>Status Epilepticus - chemically induced</topic><topic>Status Epilepticus - drug therapy</topic><topic>Status Epilepticus - immunology</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dhote, Franck</creatorcontrib><creatorcontrib>Carpentier, Pierre</creatorcontrib><creatorcontrib>Barbier, Laure</creatorcontrib><creatorcontrib>Peinnequin, André</creatorcontrib><creatorcontrib>Baille, Valérie</creatorcontrib><creatorcontrib>Pernot, Fabien</creatorcontrib><creatorcontrib>Testylier, Guy</creatorcontrib><creatorcontrib>Beaup, Claire</creatorcontrib><creatorcontrib>Foquin, Annie</creatorcontrib><creatorcontrib>Dorandeu, Fréderic</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>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dhote, Franck</au><au>Carpentier, Pierre</au><au>Barbier, Laure</au><au>Peinnequin, André</au><au>Baille, Valérie</au><au>Pernot, Fabien</au><au>Testylier, Guy</au><au>Beaup, Claire</au><au>Foquin, Annie</au><au>Dorandeu, Fréderic</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combinations of ketamine and atropine are neuroprotective and reduce neuroinflammation after a toxic status epilepticus in mice</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>259</volume><issue>2</issue><spage>195</spage><epage>209</epage><pages>195-209</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Epileptic seizures and status epilepticus (SE) induced by the poisoning with organophosphorus nerve agents (OP), like soman, are accompanied by neuroinflammation whose role in seizure-related brain damage (SRBD) is not clear. Antagonists of the NMDA glutamate ionotropic receptors are currently among the few compounds able to arrest seizures and provide neuroprotection even during refractory status epilepticus (RSE). Racemic ketamine (KET), in combination with atropine sulfate (AS), was previously shown to counteract seizures and SRBD in soman-poisoned guinea-pigs. In a mouse model of severe soman-induced SE, we assessed the potentials of KET/AS combinations as a treatment for SE/RSE-induced SRBD and neuroinflammation. When starting 30min after soman challenge, a protocol involving six injections of a sub-anesthetic dose of KET (25mg/kg) was evaluated on body weight loss, brain damage, and neuroinflammation whereas during RSE, anesthetic protocols were considered (KET 100mg/kg). After confirming that during RSE, KET injection was to be repeated despite some iatrogenic deaths, we used these proof-of-concept protocols to study the changes in mRNA and related protein contents of some inflammatory cytokines, chemokines and adhesion molecules in cortex and hippocampus 48h post-challenge. In both cases, the KET/AS combinations showed important neuroprotective effects, suppressed neutrophil granulocyte infiltration and partially suppressed glial activation. KET/AS could also reduce the increase in mRNA and related pro-inflammatory proteins provoked by the poisoning. In conclusion, the present study confirms that KET/AS treatment has a strong potential for SE/RSE management following OP poisoning. The mechanisms involved in the reduction of central neuroinflammation remain to be studied.
► During soman-induced status epilepticus, ketamine-atropine limit brain damage. ► Molecular neuroinflammatory response is strongly decreased. ► Glial activation is not fully suppressed.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>22245128</pmid><doi>10.1016/j.taap.2011.12.024</doi><tpages>15</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0041-008X |
| ispartof | Toxicology and applied pharmacology, 2012-03, Vol.259 (2), p.195-209 |
| issn | 0041-008X 1096-0333 |
| language | eng |
| recordid | cdi_osti_scitechconnect_22215255 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | 60 APPLIED LIFE SCIENCES ANESTHETICS Animals Area Under Curve Astroglia ATROPINE Atropine - pharmacology Biological and medical sciences Brain - cytology Brain - drug effects Brain - immunology Brain cytokines Chemical and industrial products toxicology. Toxic occupational diseases Chemical Warfare Agents - toxicity Chemokine CCL5 - genetics Chemokine CCL5 - immunology Chemokine CXCL1 - genetics Chemokine CXCL1 - immunology Drug addictions Excitatory Amino Acid Antagonists - pharmacology Gas, fumes GUINEA PIGS Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy HIPPOCAMPUS INFLAMMATION Ketamine Ketamine - pharmacology LYMPHOKINES MAGNESIUM 25 Male Medical sciences MESSENGER-RNA MICE Microglia Muscarinic Antagonists - pharmacology Nervous system (semeiology, syndromes) Neuroglia - immunology Neurology Neutrophil granulocytes NEUTROPHILS Neutrophils - immunology Polymerase Chain Reaction Random Allocation RECEPTORS RNA, Messenger - chemistry RNA, Messenger - genetics Soman Soman - toxicity Status epilepticus Status Epilepticus - chemically induced Status Epilepticus - drug therapy Status Epilepticus - immunology Toxicology |
| title | Combinations of ketamine and atropine are neuroprotective and reduce neuroinflammation after a toxic status epilepticus in mice |
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