Correlation of MPTP neurotoxicity in vivo with oxidation of MPTP by the brain and blood-brain barrier in vitro in five rat strains
Identifieur interne : 002A20 ( Main/Corpus ); précédent : 002A19; suivant : 002A21Correlation of MPTP neurotoxicity in vivo with oxidation of MPTP by the brain and blood-brain barrier in vitro in five rat strains
Auteurs : Naji J. Riachi ; Ramin A. Behmand ; Sami I. HarikSource :
- Brain Research [ 0006-8993 ] ; 1991.
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Abstract
We studied 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in 5 strains of rats by assessing mortality and brain monoamine changes after MPTP injections into the internal carotid artery. We then attempted to correlate the differences among rat strains in their susceptibility to MPTP neurotoxicity in vivo with MPTP oxidation by monoamine oxidase (MAO) of the cerebral cortex, striatum, and brain microvessels in vitro. Despite the fact that the carotid route delivers much higher amounts of MPTP to the ipsilateral cerebrum than can be achieved by systemic injections, no significant dopamine depletion occured in ipsilateral striata of Sprague-Dawley rats (the most resistant strain), but significant reductions of about 40% in striatal dopamine were evident in the more sensitive strains. Decreased striatal dopamine levels in these latter rat strains were associated with increased dopamine turnover. Higher doses of MPTP resulted in acute death. MPTP-induced mortality was not affected, but striatal dopamine depletion was prevented, by MAO inhibition. Differences among rat strains in their susceptibility to MPTP neurotoxicity correlated best with MAO activity in their isolated brain microvessels, but not with MAO activity in their striata or cerebral cortices. These results are consistent with the hypothesis that the rats' resistance to MPTP neurotoxicity is to some extent a property of their unique brain endothelium which has high MAO activity.
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DOI: 10.1016/0006-8993(91)90854-O
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Correlation of MPTP neurotoxicity in vivo with oxidation of MPTP by the brain and blood-brain barrier in vitro in five rat strains</title><author><name sortKey="Riachi, Naji J" sort="Riachi, Naji J" uniqKey="Riachi N" first="Naji J." last="Riachi">Naji J. Riachi</name><affiliation><mods:affiliation>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Behmand, Ramin A" sort="Behmand, Ramin A" uniqKey="Behmand R" first="Ramin A." last="Behmand">Ramin A. Behmand</name><affiliation><mods:affiliation>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Harik, Sami I" sort="Harik, Sami I" uniqKey="Harik S" first="Sami I." last="Harik">Sami I. Harik</name><affiliation><mods:affiliation>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:2286487BB13E2053453DDD0C31275B365017F2A5</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1016/0006-8993(91)90854-O</idno><idno type="url">https://api.istex.fr/document/2286487BB13E2053453DDD0C31275B365017F2A5/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002A20</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Correlation of MPTP neurotoxicity in vivo with oxidation of MPTP by the brain and blood-brain barrier in vitro in five rat strains</title><author><name sortKey="Riachi, Naji J" sort="Riachi, Naji J" uniqKey="Riachi N" first="Naji J." last="Riachi">Naji J. Riachi</name><affiliation><mods:affiliation>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Behmand, Ramin A" sort="Behmand, Ramin A" uniqKey="Behmand R" first="Ramin A." last="Behmand">Ramin A. Behmand</name><affiliation><mods:affiliation>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Harik, Sami I" sort="Harik, Sami I" uniqKey="Harik S" first="Sami I." last="Harik">Sami I. Harik</name><affiliation><mods:affiliation>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">555</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="19">19</biblScope><biblScope unit="page" to="24">24</biblScope></imprint><idno type="ISSN">0006-8993</idno></series><idno type="istex">2286487BB13E2053453DDD0C31275B365017F2A5</idno><idno type="DOI">10.1016/0006-8993(91)90854-O</idno><idno type="PII">0006-8993(91)90854-O</idno><idno type="ArticleID">9190854O</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>1-Methyl-4-phenylpyridinium cation</term><term>Blood-brain barrier</term><term>Brain capillary endothelium</term><term>Monoamine oxidase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in 5 strains of rats by assessing mortality and brain monoamine changes after MPTP injections into the internal carotid artery. We then attempted to correlate the differences among rat strains in their susceptibility to MPTP neurotoxicity in vivo with MPTP oxidation by monoamine oxidase (MAO) of the cerebral cortex, striatum, and brain microvessels in vitro. Despite the fact that the carotid route delivers much higher amounts of MPTP to the ipsilateral cerebrum than can be achieved by systemic injections, no significant dopamine depletion occured in ipsilateral striata of Sprague-Dawley rats (the most resistant strain), but significant reductions of about 40% in striatal dopamine were evident in the more sensitive strains. Decreased striatal dopamine levels in these latter rat strains were associated with increased dopamine turnover. Higher doses of MPTP resulted in acute death. MPTP-induced mortality was not affected, but striatal dopamine depletion was prevented, by MAO inhibition. Differences among rat strains in their susceptibility to MPTP neurotoxicity correlated best with MAO activity in their isolated brain microvessels, but not with MAO activity in their striata or cerebral cortices. These results are consistent with the hypothesis that the rats' resistance to MPTP neurotoxicity is to some extent a property of their unique brain endothelium which has high MAO activity.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Naji J. Riachi</name><affiliations><json:string>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</json:string></affiliations></json:item><json:item><name>Ramin A. Behmand</name><affiliations><json:string>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</json:string></affiliations></json:item><json:item><name>Sami I. Harik</name><affiliations><json:string>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Monoamine oxidase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Blood-brain barrier</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Brain capillary endothelium</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>1-Methyl-4-phenylpyridinium cation</value></json:item></subject><articleId><json:string>9190854O</json:string></articleId><language><json:string>eng</json:string></language><abstract>We studied 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in 5 strains of rats by assessing mortality and brain monoamine changes after MPTP injections into the internal carotid artery. We then attempted to correlate the differences among rat strains in their susceptibility to MPTP neurotoxicity in vivo with MPTP oxidation by monoamine oxidase (MAO) of the cerebral cortex, striatum, and brain microvessels in vitro. Despite the fact that the carotid route delivers much higher amounts of MPTP to the ipsilateral cerebrum than can be achieved by systemic injections, no significant dopamine depletion occured in ipsilateral striata of Sprague-Dawley rats (the most resistant strain), but significant reductions of about 40% in striatal dopamine were evident in the more sensitive strains. Decreased striatal dopamine levels in these latter rat strains were associated with increased dopamine turnover. Higher doses of MPTP resulted in acute death. MPTP-induced mortality was not affected, but striatal dopamine depletion was prevented, by MAO inhibition. Differences among rat strains in their susceptibility to MPTP neurotoxicity correlated best with MAO activity in their isolated brain microvessels, but not with MAO activity in their striata or cerebral cortices. 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I. Harik, Department of Neurology, University Hospitals of Cleveland, 2074 Abington Road, Cleveland, OH 44106, U.S.A.. Fax: (1) (216) 844-3160.</p></note><affiliation>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</affiliation></author></analytic><monogr><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="pISSN">0006-8993</idno><idno type="PII">S0006-8993(00)X0860-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991"></date><biblScope unit="volume">555</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="19">19</biblScope><biblScope unit="page" to="24">24</biblScope></imprint></monogr><idno type="istex">2286487BB13E2053453DDD0C31275B365017F2A5</idno><idno type="DOI">10.1016/0006-8993(91)90854-O</idno><idno type="PII">0006-8993(91)90854-O</idno><idno type="ArticleID">9190854O</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1991</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We studied 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in 5 strains of rats by assessing mortality and brain monoamine changes after MPTP injections into the internal carotid artery. We then attempted to correlate the differences among rat strains in their susceptibility to MPTP neurotoxicity in vivo with MPTP oxidation by monoamine oxidase (MAO) of the cerebral cortex, striatum, and brain microvessels in vitro. Despite the fact that the carotid route delivers much higher amounts of MPTP to the ipsilateral cerebrum than can be achieved by systemic injections, no significant dopamine depletion occured in ipsilateral striata of Sprague-Dawley rats (the most resistant strain), but significant reductions of about 40% in striatal dopamine were evident in the more sensitive strains. Decreased striatal dopamine levels in these latter rat strains were associated with increased dopamine turnover. Higher doses of MPTP resulted in acute death. MPTP-induced mortality was not affected, but striatal dopamine depletion was prevented, by MAO inhibition. Differences among rat strains in their susceptibility to MPTP neurotoxicity correlated best with MAO activity in their isolated brain microvessels, but not with MAO activity in their striata or cerebral cortices. These results are consistent with the hypothesis that the rats' resistance to MPTP neurotoxicity is to some extent a property of their unique brain endothelium which has high MAO activity.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Monoamine oxidase</term></item><item><term>Blood-brain barrier</term></item><item><term>Brain capillary endothelium</term></item><item><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></item><item><term>1-Methyl-4-phenylpyridinium cation</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1991-02-26">Registration</change><change when="1991">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"></istex:docType><istex:document><article version="5.0" xml:lang="en" docsubtype="fla"><item-info><jid>BRES</jid><aid>9190854O</aid><ce:pii>0006-8993(91)90854-O</ce:pii><ce:doi>10.1016/0006-8993(91)90854-O</ce:doi><ce:copyright type="unknown" year="1991">Elsevier Science Publishers B.V. All rights reserved</ce:copyright></item-info><head><ce:title>Correlation of MPTP neurotoxicity in vivo with oxidation of MPTP by the brain and blood-brain barrier in vitro in five rat strains</ce:title><ce:author-group><ce:author><ce:given-name>Naji J.</ce:given-name><ce:surname>Riachi</ce:surname></ce:author><ce:author><ce:given-name>Ramin A.</ce:given-name><ce:surname>Behmand</ce:surname></ce:author><ce:author><ce:given-name>Sami I.</ce:given-name><ce:surname>Harik</ce:surname><ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, OH 44106, U.S.A.</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text><ce:italic>Correspondence:</ce:italic> S. I. Harik, Department of Neurology, University Hospitals of Cleveland, 2074 Abington Road, Cleveland, OH 44106, U.S.A.. Fax: (1) (216) 844-3160.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="26" month="2" year="1991"></ce:date-accepted><ce:abstract id="ab1" class="author" xml:lang="en"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">We studied 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in 5 strains of rats by assessing mortality and brain monoamine changes after MPTP injections into the internal carotid artery. We then attempted to correlate the differences among rat strains in their susceptibility to MPTP neurotoxicity in vivo with MPTP oxidation by monoamine oxidase (MAO) of the cerebral cortex, striatum, and brain microvessels in vitro. Despite the fact that the carotid route delivers much higher amounts of MPTP to the ipsilateral cerebrum than can be achieved by systemic injections, no significant dopamine depletion occured in ipsilateral striata of Sprague-Dawley rats (the most resistant strain), but significant reductions of about 40% in striatal dopamine were evident in the more sensitive strains. Decreased striatal dopamine levels in these latter rat strains were associated with increased dopamine turnover. Higher doses of MPTP resulted in acute death. MPTP-induced mortality was not affected, but striatal dopamine depletion was prevented, by MAO inhibition. Differences among rat strains in their susceptibility to MPTP neurotoxicity correlated best with MAO activity in their isolated brain microvessels, but not with MAO activity in their striata or cerebral cortices. These results are consistent with the hypothesis that the rats' resistance to MPTP neurotoxicity is to some extent a property of their unique brain endothelium which has high MAO activity.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Monoamine oxidase</ce:text></ce:keyword><ce:keyword><ce:text>Blood-brain barrier</ce:text></ce:keyword><ce:keyword><ce:text>Brain capillary endothelium</ce:text></ce:keyword><ce:keyword><ce:text>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</ce:text></ce:keyword><ce:keyword><ce:text>1-Methyl-4-phenylpyridinium cation</ce:text></ce:keyword></ce:keywords></head><tail view="all"><ce:bibliography view="all" id="bibliography.0010"><ce:section-title>References</ce:section-title><ce:bibliography-sec id="bibliography-sec.0010"><ce:bib-reference id="bib1"><ce:label>1</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Amsden</ce:surname><ce:given-name>A.F.</ce:given-name></sb:author><sb:author><ce:surname>Smith</ce:surname><ce:given-name>R.N.</ce:given-name></sb:author><sb:author><ce:surname>Chiralkawasan</ce:surname><ce:given-name>N.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>The alloantibody response in the allogeneically pregnant rat. 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I. Harik, Department of Neurology, University Hospitals of Cleveland, 2074 Abington Road, Cleveland, OH 44106, U.S.A.. Fax: (1) (216) 844-3160.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1991</dateIssued><dateValid encoding="w3cdtf">1991-02-26</dateValid><copyrightDate encoding="w3cdtf">1991</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">We studied 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in 5 strains of rats by assessing mortality and brain monoamine changes after MPTP injections into the internal carotid artery. We then attempted to correlate the differences among rat strains in their susceptibility to MPTP neurotoxicity in vivo with MPTP oxidation by monoamine oxidase (MAO) of the cerebral cortex, striatum, and brain microvessels in vitro. Despite the fact that the carotid route delivers much higher amounts of MPTP to the ipsilateral cerebrum than can be achieved by systemic injections, no significant dopamine depletion occured in ipsilateral striata of Sprague-Dawley rats (the most resistant strain), but significant reductions of about 40% in striatal dopamine were evident in the more sensitive strains. Decreased striatal dopamine levels in these latter rat strains were associated with increased dopamine turnover. Higher doses of MPTP resulted in acute death. MPTP-induced mortality was not affected, but striatal dopamine depletion was prevented, by MAO inhibition. Differences among rat strains in their susceptibility to MPTP neurotoxicity correlated best with MAO activity in their isolated brain microvessels, but not with MAO activity in their striata or cerebral cortices. These results are consistent with the hypothesis that the rats' resistance to MPTP neurotoxicity is to some extent a property of their unique brain endothelium which has high MAO activity.</abstract><subject lang="en"><genre>Keywords</genre><topic>Monoamine oxidase</topic><topic>Blood-brain barrier</topic><topic>Brain capillary endothelium</topic><topic>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</topic><topic>1-Methyl-4-phenylpyridinium cation</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research</title></titleInfo><titleInfo type="abbreviated"><title>BRES</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19910726</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X0860-8</identifier><part><detail type="volume"><number>555</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>180</end></extent><extent unit="pages"><start>19</start><end>24</end></extent></part></relatedItem><identifier type="istex">2286487BB13E2053453DDD0C31275B365017F2A5</identifier><identifier type="DOI">10.1016/0006-8993(91)90854-O</identifier><identifier type="PII">0006-8993(91)90854-O</identifier><identifier type="ArticleID">9190854O</identifier><accessCondition type="use and reproduction" contentType="">© 1991Elsevier Science Publishers B.V. 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