An investigation into the early stages of the inflammatory response following ibotenic acid-induced neuronal degeneration
Injection of the excitatory neurotoxin ibotenic acid into the septum produces rapid destruction of neuronal cell bodies and accompanying gliosis. We have previously shown that following ibotenate-induced cell death this may also result in damage to healthy axons en passage (Coffey et al., Neurosci....
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| Veröffentlicht in: | Neuroscience 1990, Vol.35 (1), p.121-132 |
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| creator | Coffey, P.J. Perry, V.H. Rawlins, J.N.P. |
| description | Injection of the excitatory neurotoxin ibotenic acid into the septum produces rapid destruction of neuronal cell bodies and accompanying gliosis. We have previously shown that following ibotenate-induced cell death this may also result in damage to healthy axons
en passage (Coffey
et al., Neurosci. Lett.
84, 178–184, 1988). We suggested that the axonal damage resulted from non-specific damage by recruited inflammatory cells. In this study we have further examined the phenotype of the cells involved in the inflammatory response in the rat. Immunocytochemical identification of cells in the region of the lesion site identifies them as being of haematopoitic origin and most of them have the phenotype of macrophages. The dramatic increase in their number following an ibotenate lesion is sensitive to irradiation of the body providing evidence that the majority are blood derived.
The inflammatory response is accompanied by a loss of myelin and a breakdown of the blood-brain barrier in the region of the lesion site. We have shown that these two effects are consequences of the inflammatory response since reduction in the inflammatory response by prior irradiation will abrogate these two effects. |
| doi_str_mv | 10.1016/0306-4522(90)90126-O |
| format | Article |
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en passage (Coffey
et al., Neurosci. Lett.
84, 178–184, 1988). We suggested that the axonal damage resulted from non-specific damage by recruited inflammatory cells. In this study we have further examined the phenotype of the cells involved in the inflammatory response in the rat. Immunocytochemical identification of cells in the region of the lesion site identifies them as being of haematopoitic origin and most of them have the phenotype of macrophages. The dramatic increase in their number following an ibotenate lesion is sensitive to irradiation of the body providing evidence that the majority are blood derived.
The inflammatory response is accompanied by a loss of myelin and a breakdown of the blood-brain barrier in the region of the lesion site. We have shown that these two effects are consequences of the inflammatory response since reduction in the inflammatory response by prior irradiation will abrogate these two effects.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/0306-4522(90)90126-O</identifier><identifier>PMID: 2359491</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Biochemistry and metabolism ; Biological and medical sciences ; Blood-Brain Barrier - drug effects ; Central nervous system ; Encephalitis - chemically induced ; Encephalitis - immunology ; Encephalitis - pathology ; Fundamental and applied biological sciences. Psychology ; Gliosis - chemically induced ; Gliosis - pathology ; horseradish peroxidase ; HRP ; Ibotenic Acid - toxicity ; LCA ; leucocyte common antigen ; Macrophage Activation - immunology ; Macrophage Activation - radiation effects ; N-methyl- d-aspartate ; Nerve Degeneration ; Neurotoxins - pharmacology ; NMDA ; Oxazoles - toxicity ; PBS ; phosphate-buffered saline ; Rats ; Rats, Inbred Strains ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 1990, Vol.35 (1), p.121-132</ispartof><rights>1990 IBRO</rights><rights>1990 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-5ae139de8c17ad05e89226bbc0de087c0f548f838ccff4f50efd4870b0139e703</citedby><cites>FETCH-LOGICAL-c417t-5ae139de8c17ad05e89226bbc0de087c0f548f838ccff4f50efd4870b0139e703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0306-4522(90)90126-O$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=6864284$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2359491$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Coffey, P.J.</creatorcontrib><creatorcontrib>Perry, V.H.</creatorcontrib><creatorcontrib>Rawlins, J.N.P.</creatorcontrib><title>An investigation into the early stages of the inflammatory response following ibotenic acid-induced neuronal degeneration</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Injection of the excitatory neurotoxin ibotenic acid into the septum produces rapid destruction of neuronal cell bodies and accompanying gliosis. We have previously shown that following ibotenate-induced cell death this may also result in damage to healthy axons
en passage (Coffey
et al., Neurosci. Lett.
84, 178–184, 1988). We suggested that the axonal damage resulted from non-specific damage by recruited inflammatory cells. In this study we have further examined the phenotype of the cells involved in the inflammatory response in the rat. Immunocytochemical identification of cells in the region of the lesion site identifies them as being of haematopoitic origin and most of them have the phenotype of macrophages. The dramatic increase in their number following an ibotenate lesion is sensitive to irradiation of the body providing evidence that the majority are blood derived.
The inflammatory response is accompanied by a loss of myelin and a breakdown of the blood-brain barrier in the region of the lesion site. We have shown that these two effects are consequences of the inflammatory response since reduction in the inflammatory response by prior irradiation will abrogate these two effects.</description><subject>Animals</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Central nervous system</subject><subject>Encephalitis - chemically induced</subject><subject>Encephalitis - immunology</subject><subject>Encephalitis - pathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gliosis - chemically induced</subject><subject>Gliosis - pathology</subject><subject>horseradish peroxidase</subject><subject>HRP</subject><subject>Ibotenic Acid - toxicity</subject><subject>LCA</subject><subject>leucocyte common antigen</subject><subject>Macrophage Activation - immunology</subject><subject>Macrophage Activation - radiation effects</subject><subject>N-methyl- d-aspartate</subject><subject>Nerve Degeneration</subject><subject>Neurotoxins - pharmacology</subject><subject>NMDA</subject><subject>Oxazoles - toxicity</subject><subject>PBS</subject><subject>phosphate-buffered saline</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEuPFCEURolxMrat_0ATFsbookaogipqM8lk4mOSSXozrgkFlxZDQQvUmP730o_0UjYE7vnuhYPQO0puKKH9F9KRvmG8bT-N5PNIaNs3mxdoRcXQNQNn7CVaXZBX6HXOv0ldnHXX6Lrt-MhGukL7u4BdeIZc3FYVFw-nEnH5BRhU8nuci9pCxtEe71ywXs2zKjHtcYK8iyEDttH7-NeFLXZTLBCcxko707hgFg0GB1hSDMpjA1sIkI6D3qArq3yGt-d9jX5--_p0_6N53Hx_uL97bDSjQ2m4AtqNBoSmgzKEgxjbtp8mTQwQMWhiORNWdEJra5nlBKxhYiATqTEYSLdGH099dyn-WepH5eyyBu9VgLhkSXlPBan0GrETqFPMOYGVu-RmlfaSEnkwLg865UGnHIk8GpebGnt_7r9MM5hL6Ky41j-c6ypr5W1SQbt8wXrRs1awit2eMKgunh0kmbWDUPW5BLpIE93_3_EPpqqfiw</recordid><startdate>1990</startdate><enddate>1990</enddate><creator>Coffey, P.J.</creator><creator>Perry, V.H.</creator><creator>Rawlins, J.N.P.</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></search><sort><creationdate>1990</creationdate><title>An investigation into the early stages of the inflammatory response following ibotenic acid-induced neuronal degeneration</title><author>Coffey, P.J. ; Perry, V.H. ; Rawlins, J.N.P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-5ae139de8c17ad05e89226bbc0de087c0f548f838ccff4f50efd4870b0139e703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Animals</topic><topic>Biochemistry and metabolism</topic><topic>Biological and medical sciences</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Central nervous system</topic><topic>Encephalitis - chemically induced</topic><topic>Encephalitis - immunology</topic><topic>Encephalitis - pathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gliosis - chemically induced</topic><topic>Gliosis - pathology</topic><topic>horseradish peroxidase</topic><topic>HRP</topic><topic>Ibotenic Acid - toxicity</topic><topic>LCA</topic><topic>leucocyte common antigen</topic><topic>Macrophage Activation - immunology</topic><topic>Macrophage Activation - radiation effects</topic><topic>N-methyl- d-aspartate</topic><topic>Nerve Degeneration</topic><topic>Neurotoxins - pharmacology</topic><topic>NMDA</topic><topic>Oxazoles - toxicity</topic><topic>PBS</topic><topic>phosphate-buffered saline</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Coffey, P.J.</creatorcontrib><creatorcontrib>Perry, V.H.</creatorcontrib><creatorcontrib>Rawlins, J.N.P.</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><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Coffey, P.J.</au><au>Perry, V.H.</au><au>Rawlins, J.N.P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An investigation into the early stages of the inflammatory response following ibotenic acid-induced neuronal degeneration</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>1990</date><risdate>1990</risdate><volume>35</volume><issue>1</issue><spage>121</spage><epage>132</epage><pages>121-132</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Injection of the excitatory neurotoxin ibotenic acid into the septum produces rapid destruction of neuronal cell bodies and accompanying gliosis. We have previously shown that following ibotenate-induced cell death this may also result in damage to healthy axons
en passage (Coffey
et al., Neurosci. Lett.
84, 178–184, 1988). We suggested that the axonal damage resulted from non-specific damage by recruited inflammatory cells. In this study we have further examined the phenotype of the cells involved in the inflammatory response in the rat. Immunocytochemical identification of cells in the region of the lesion site identifies them as being of haematopoitic origin and most of them have the phenotype of macrophages. The dramatic increase in their number following an ibotenate lesion is sensitive to irradiation of the body providing evidence that the majority are blood derived.
The inflammatory response is accompanied by a loss of myelin and a breakdown of the blood-brain barrier in the region of the lesion site. We have shown that these two effects are consequences of the inflammatory response since reduction in the inflammatory response by prior irradiation will abrogate these two effects.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>2359491</pmid><doi>10.1016/0306-4522(90)90126-O</doi><tpages>12</tpages></addata></record> |
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| subjects | Animals Biochemistry and metabolism Biological and medical sciences Blood-Brain Barrier - drug effects Central nervous system Encephalitis - chemically induced Encephalitis - immunology Encephalitis - pathology Fundamental and applied biological sciences. Psychology Gliosis - chemically induced Gliosis - pathology horseradish peroxidase HRP Ibotenic Acid - toxicity LCA leucocyte common antigen Macrophage Activation - immunology Macrophage Activation - radiation effects N-methyl- d-aspartate Nerve Degeneration Neurotoxins - pharmacology NMDA Oxazoles - toxicity PBS phosphate-buffered saline Rats Rats, Inbred Strains Vertebrates: nervous system and sense organs |
| title | An investigation into the early stages of the inflammatory response following ibotenic acid-induced neuronal degeneration |
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