Regional distribution of monoamine vesicular uptake sites in the mesencephalon of control subjects and patients with Parkinson's disease: a postmortem study using tritiated tetrabenazine
Identifieur interne : 001D52 ( Main/Corpus ); précédent : 001D51; suivant : 001D53Regional distribution of monoamine vesicular uptake sites in the mesencephalon of control subjects and patients with Parkinson's disease: a postmortem study using tritiated tetrabenazine
Auteurs : F. Thibaut ; B. A. Faucheux ; J. Marquez ; J. Villares ; J. F. Menard ; Y. Agid ; E. C. HirschSource :
- Brain Research [ 0006-8993 ] ; 1995.
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Abstract
The distribution of the vesicular monoamine transporter was investigated post mortem in the human ventral mesencephalon of control subjects (n = 7) and patients with Parkinson's disease (n = 4) using tritiated dihydrotetrabenazine binding and autoradiography. Tritiated dihydrotetrabenazine binding was characterized by a single class of sites with aKd of 7 nM and aBmax of 180 fmol/mg of protein in the substantia nigra. Tritiated dihydrotetrabenazine binding sites were heterogeneously distributed in the mesencephalon of control subjects: the density of tritiated dihydrotetrabenazine binding sites was high in the substantia nigra pars compacta, locus coeruleus and nucleus raphe dorsalis, moderate in the ventral tegmental area and low in the substantia nigra pars reticulata and catecholaminergic cell group A8. Within the substantia nigra, a zone with maximal density of tritiated dihydrotetrabenazine binding, two times higher than the mean estimate for the whole substantia nigra pars compacta, was detected in the medial part of the structure. The anatomical organization of the human ventral mesencephalon was analyzed on adjacent sections stained for acetylcholinesterase histochemistry and tyrosine hydroxylase immunohistochemistry. Tritiated dihydrotetrabenazine binding displayed the same characteristic regional pattern of distribution as that observed with tyrosine hydroxylase immunohistochemistry except in the nucleus raphe dorsalis, where no tyrosine hydroxylase immunoreactivity was detected. In parkinsonian brains, the level of tritiated dihydrotetrabenazine binding was dramatically decreased in all regions of the ventral mesencephalon analyzed except in the substantia nigra pars reticulata. In the substantia nigra pars compacta, the reduction was by 55% for the whole structure and by 65% in its medial zone, where binding site density was maximal. In most nigral subsectors analyzed, the decrease in density of tritiated dihydrotetrabenazine binding sites reached the level expected given the loss of tyrosine hydroxylase-positive cells observed. By contrast, the ratio of [3H]dihydrotetrabenazine binding to the number of tyrosine hydroxylase positive neurons was significantly increased in the zone of high [3H]dihydrotetrabenazine binding sites. This relative sparing of tritiated dihydrotetrabenazine binding sites may be due either to the contribution of other monoaminergic neurons such as serotoninergic neurons or more likely to hyperactivity of the still surviving dopaminergic neurons.
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DOI: 10.1016/0006-8993(95)00674-F
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Marquez</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Villares, J" sort="Villares, J" uniqKey="Villares J" first="J." last="Villares">J. Villares</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Menard, J F" sort="Menard, J F" uniqKey="Menard J" first="J. F." last="Menard">J. F. Menard</name><affiliation><mods:affiliation>Laboratoire de Biophysique, Hoˆpital Charles Nicolle, 1 rue de Germont, F-76031 Rouen ,France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. 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Fax: (33) (1) 44 24 36 58</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:06153E28A752DFC7701A70D8C2C794DE8D15B886</idno><date when="1995" year="1995">1995</date><idno type="doi">10.1016/0006-8993(95)00674-F</idno><idno type="url">https://api.istex.fr/document/06153E28A752DFC7701A70D8C2C794DE8D15B886/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001D52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Regional distribution of monoamine vesicular uptake sites in the mesencephalon of control subjects and patients with Parkinson's disease: a postmortem study using tritiated tetrabenazine</title><author><name sortKey="Thibaut, F" sort="Thibaut, F" uniqKey="Thibaut F" first="F." last="Thibaut">F. Thibaut</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Faucheux, B A" sort="Faucheux, B A" uniqKey="Faucheux B" first="B. A." last="Faucheux">B. A. Faucheux</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Marquez, J" sort="Marquez, J" uniqKey="Marquez J" first="J." last="Marquez">J. Marquez</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Villares, J" sort="Villares, J" uniqKey="Villares J" first="J." last="Villares">J. Villares</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Menard, J F" sort="Menard, J F" uniqKey="Menard J" first="J. F." last="Menard">J. F. Menard</name><affiliation><mods:affiliation>Laboratoire de Biophysique, Hoˆpital Charles Nicolle, 1 rue de Germont, F-76031 Rouen ,France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. Agid</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name><affiliation><mods:affiliation>Corresponding author. Fax: (33) (1) 44 24 36 58</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</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="1995">1995</date><biblScope unit="volume">692</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="233">233</biblScope><biblScope unit="page" to="243">243</biblScope></imprint><idno type="ISSN">0006-8993</idno></series><idno type="istex">06153E28A752DFC7701A70D8C2C794DE8D15B886</idno><idno type="DOI">10.1016/0006-8993(95)00674-F</idno><idno type="PII">0006-8993(95)00674-F</idno><idno type="ArticleID">9500674F</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine</term><term>Human</term><term>Parkinson's disease</term><term>Substantia nigra</term><term>Synaptic vesicle</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The distribution of the vesicular monoamine transporter was investigated post mortem in the human ventral mesencephalon of control subjects (n = 7) and patients with Parkinson's disease (n = 4) using tritiated dihydrotetrabenazine binding and autoradiography. Tritiated dihydrotetrabenazine binding was characterized by a single class of sites with aKd of 7 nM and aBmax of 180 fmol/mg of protein in the substantia nigra. Tritiated dihydrotetrabenazine binding sites were heterogeneously distributed in the mesencephalon of control subjects: the density of tritiated dihydrotetrabenazine binding sites was high in the substantia nigra pars compacta, locus coeruleus and nucleus raphe dorsalis, moderate in the ventral tegmental area and low in the substantia nigra pars reticulata and catecholaminergic cell group A8. Within the substantia nigra, a zone with maximal density of tritiated dihydrotetrabenazine binding, two times higher than the mean estimate for the whole substantia nigra pars compacta, was detected in the medial part of the structure. The anatomical organization of the human ventral mesencephalon was analyzed on adjacent sections stained for acetylcholinesterase histochemistry and tyrosine hydroxylase immunohistochemistry. Tritiated dihydrotetrabenazine binding displayed the same characteristic regional pattern of distribution as that observed with tyrosine hydroxylase immunohistochemistry except in the nucleus raphe dorsalis, where no tyrosine hydroxylase immunoreactivity was detected. In parkinsonian brains, the level of tritiated dihydrotetrabenazine binding was dramatically decreased in all regions of the ventral mesencephalon analyzed except in the substantia nigra pars reticulata. In the substantia nigra pars compacta, the reduction was by 55% for the whole structure and by 65% in its medial zone, where binding site density was maximal. In most nigral subsectors analyzed, the decrease in density of tritiated dihydrotetrabenazine binding sites reached the level expected given the loss of tyrosine hydroxylase-positive cells observed. By contrast, the ratio of [3H]dihydrotetrabenazine binding to the number of tyrosine hydroxylase positive neurons was significantly increased in the zone of high [3H]dihydrotetrabenazine binding sites. This relative sparing of tritiated dihydrotetrabenazine binding sites may be due either to the contribution of other monoaminergic neurons such as serotoninergic neurons or more likely to hyperactivity of the still surviving dopaminergic neurons.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>F. Thibaut</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</json:string></affiliations></json:item><json:item><name>B.A. Faucheux</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</json:string></affiliations></json:item><json:item><name>J. Marquez</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</json:string></affiliations></json:item><json:item><name>J. Villares</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</json:string></affiliations></json:item><json:item><name>J.F. Menard</name><affiliations><json:string>Laboratoire de Biophysique, Hoˆpital Charles Nicolle, 1 rue de Germont, F-76031 Rouen ,France</json:string></affiliations></json:item><json:item><name>Y. Agid</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</json:string></affiliations></json:item><json:item><name>E.C. Hirsch</name><affiliations><json:string>Corresponding author. Fax: (33) (1) 44 24 36 58</json:string><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Substantia nigra</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Human</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Synaptic vesicle</value></json:item></subject><articleId><json:string>9500674F</json:string></articleId><language><json:string>eng</json:string></language><abstract>The distribution of the vesicular monoamine transporter was investigated post mortem in the human ventral mesencephalon of control subjects (n = 7) and patients with Parkinson's disease (n = 4) using tritiated dihydrotetrabenazine binding and autoradiography. Tritiated dihydrotetrabenazine binding was characterized by a single class of sites with aKd of 7 nM and aBmax of 180 fmol/mg of protein in the substantia nigra. Tritiated dihydrotetrabenazine binding sites were heterogeneously distributed in the mesencephalon of control subjects: the density of tritiated dihydrotetrabenazine binding sites was high in the substantia nigra pars compacta, locus coeruleus and nucleus raphe dorsalis, moderate in the ventral tegmental area and low in the substantia nigra pars reticulata and catecholaminergic cell group A8. Within the substantia nigra, a zone with maximal density of tritiated dihydrotetrabenazine binding, two times higher than the mean estimate for the whole substantia nigra pars compacta, was detected in the medial part of the structure. The anatomical organization of the human ventral mesencephalon was analyzed on adjacent sections stained for acetylcholinesterase histochemistry and tyrosine hydroxylase immunohistochemistry. Tritiated dihydrotetrabenazine binding displayed the same characteristic regional pattern of distribution as that observed with tyrosine hydroxylase immunohistochemistry except in the nucleus raphe dorsalis, where no tyrosine hydroxylase immunoreactivity was detected. In parkinsonian brains, the level of tritiated dihydrotetrabenazine binding was dramatically decreased in all regions of the ventral mesencephalon analyzed except in the substantia nigra pars reticulata. In the substantia nigra pars compacta, the reduction was by 55% for the whole structure and by 65% in its medial zone, where binding site density was maximal. In most nigral subsectors analyzed, the decrease in density of tritiated dihydrotetrabenazine binding sites reached the level expected given the loss of tyrosine hydroxylase-positive cells observed. By contrast, the ratio of [3H]dihydrotetrabenazine binding to the number of tyrosine hydroxylase positive neurons was significantly increased in the zone of high [3H]dihydrotetrabenazine binding sites. This relative sparing of tritiated dihydrotetrabenazine binding sites may be due either to the contribution of other monoaminergic neurons such as serotoninergic neurons or more likely to hyperactivity of the still surviving dopaminergic neurons.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>605 x 814 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>2525</abstractCharCount><pdfWordCount>6146</pdfWordCount><pdfCharCount>38775</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>345</abstractWordCount></qualityIndicators><title>Regional distribution of monoamine vesicular uptake sites in the mesencephalon of control subjects and patients with Parkinson's disease: a postmortem study using tritiated tetrabenazine</title><pii><json:string>0006-8993(95)00674-F</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>Vol. 2</volume><pages><last>230</last><first>166</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title></serie><host><volume>692</volume><pii><json:string>S0006-8993(00)X0042-X</json:string></pii><pages><last>243</last><first>233</first></pages><issn><json:string>0006-8993</json:string></issn><issue>1–2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Brain Research</title><publicationDate>1995</publicationDate></host><categories><wos><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1016/0006-8993(95)00674-F</json:string></doi><id>06153E28A752DFC7701A70D8C2C794DE8D15B886</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/06153E28A752DFC7701A70D8C2C794DE8D15B886/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/06153E28A752DFC7701A70D8C2C794DE8D15B886/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/06153E28A752DFC7701A70D8C2C794DE8D15B886/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/06153E28A752DFC7701A70D8C2C794DE8D15B886/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Regional distribution of monoamine vesicular uptake sites in the mesencephalon of control subjects and patients with Parkinson's disease: a postmortem study using tritiated tetrabenazine</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1995</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Regional distribution of monoamine vesicular uptake sites in the mesencephalon of control subjects and patients with Parkinson's disease: a postmortem study using tritiated tetrabenazine</title><author><persName><forename type="first">F.</forename><surname>Thibaut</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation></author><author><persName><forename type="first">B.A.</forename><surname>Faucheux</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation></author><author><persName><forename type="first">J.</forename><surname>Marquez</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation></author><author><persName><forename type="first">J.</forename><surname>Villares</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation></author><author><persName><forename type="first">J.F.</forename><surname>Menard</surname></persName><affiliation>Laboratoire de Biophysique, Hoˆpital Charles Nicolle, 1 rue de Germont, F-76031 Rouen ,France</affiliation></author><author><persName><forename type="first">Y.</forename><surname>Agid</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation></author><author><persName><forename type="first">E.C.</forename><surname>Hirsch</surname></persName><affiliation>Corresponding author. Fax: (33) (1) 44 24 36 58</affiliation><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</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)X0042-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">692</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="233">233</biblScope><biblScope unit="page" to="243">243</biblScope></imprint></monogr><idno type="istex">06153E28A752DFC7701A70D8C2C794DE8D15B886</idno><idno type="DOI">10.1016/0006-8993(95)00674-F</idno><idno type="PII">0006-8993(95)00674-F</idno><idno type="ArticleID">9500674F</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The distribution of the vesicular monoamine transporter was investigated post mortem in the human ventral mesencephalon of control subjects (n = 7) and patients with Parkinson's disease (n = 4) using tritiated dihydrotetrabenazine binding and autoradiography. Tritiated dihydrotetrabenazine binding was characterized by a single class of sites with aKd of 7 nM and aBmax of 180 fmol/mg of protein in the substantia nigra. Tritiated dihydrotetrabenazine binding sites were heterogeneously distributed in the mesencephalon of control subjects: the density of tritiated dihydrotetrabenazine binding sites was high in the substantia nigra pars compacta, locus coeruleus and nucleus raphe dorsalis, moderate in the ventral tegmental area and low in the substantia nigra pars reticulata and catecholaminergic cell group A8. Within the substantia nigra, a zone with maximal density of tritiated dihydrotetrabenazine binding, two times higher than the mean estimate for the whole substantia nigra pars compacta, was detected in the medial part of the structure. The anatomical organization of the human ventral mesencephalon was analyzed on adjacent sections stained for acetylcholinesterase histochemistry and tyrosine hydroxylase immunohistochemistry. Tritiated dihydrotetrabenazine binding displayed the same characteristic regional pattern of distribution as that observed with tyrosine hydroxylase immunohistochemistry except in the nucleus raphe dorsalis, where no tyrosine hydroxylase immunoreactivity was detected. In parkinsonian brains, the level of tritiated dihydrotetrabenazine binding was dramatically decreased in all regions of the ventral mesencephalon analyzed except in the substantia nigra pars reticulata. In the substantia nigra pars compacta, the reduction was by 55% for the whole structure and by 65% in its medial zone, where binding site density was maximal. In most nigral subsectors analyzed, the decrease in density of tritiated dihydrotetrabenazine binding sites reached the level expected given the loss of tyrosine hydroxylase-positive cells observed. By contrast, the ratio of [3H]dihydrotetrabenazine binding to the number of tyrosine hydroxylase positive neurons was significantly increased in the zone of high [3H]dihydrotetrabenazine binding sites. This relative sparing of tritiated dihydrotetrabenazine binding sites may be due either to the contribution of other monoaminergic neurons such as serotoninergic neurons or more likely to hyperactivity of the still surviving dopaminergic neurons.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Dopamine</term></item><item><term>Parkinson's disease</term></item><item><term>Substantia nigra</term></item><item><term>Human</term></item><item><term>Synaptic vesicle</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-05-16">Registration</change><change when="1995">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>9500674F</aid><ce:pii>0006-8993(95)00674-F</ce:pii><ce:doi>10.1016/0006-8993(95)00674-F</ce:doi><ce:copyright type="unknown" year="1995">Elsevier Science B.V. All rights reserved</ce:copyright></item-info><head><ce:title>Regional distribution of monoamine vesicular uptake sites in the mesencephalon of control subjects and patients with Parkinson's disease: a postmortem study using tritiated tetrabenazine</ce:title><ce:author-group><ce:author><ce:given-name>F.</ce:given-name><ce:surname>Thibaut</ce:surname><ce:cross-ref refid="aff1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>B.A.</ce:given-name><ce:surname>Faucheux</ce:surname><ce:cross-ref refid="aff1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.</ce:given-name><ce:surname>Marquez</ce:surname><ce:cross-ref refid="aff1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.</ce:given-name><ce:surname>Villares</ce:surname><ce:cross-ref refid="aff1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.F.</ce:given-name><ce:surname>Menard</ce:surname><ce:cross-ref refid="aff2"><ce:sup loc="post">b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Y.</ce:given-name><ce:surname>Agid</ce:surname><ce:cross-ref refid="aff1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>E.C.</ce:given-name><ce:surname>Hirsch</ce:surname><ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup></ce:cross-ref><ce:cross-ref refid="aff1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="aff1"><ce:label>a</ce:label><ce:textfn>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</ce:textfn></ce:affiliation><ce:affiliation id="aff2"><ce:label>b</ce:label><ce:textfn>Laboratoire de Biophysique, Hoˆpital Charles Nicolle, 1 rue de Germont, F-76031 Rouen ,France</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text>Corresponding author. Fax: (33) (1) 44 24 36 58</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="16" month="5" year="1995"></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">The distribution of the vesicular monoamine transporter was investigated post mortem in the human ventral mesencephalon of control subjects (<ce:italic>n = 7</ce:italic>) and patients with Parkinson's disease (<ce:italic>n = 4</ce:italic>) using tritiated dihydrotetrabenazine binding and autoradiography. Tritiated dihydrotetrabenazine binding was characterized by a single class of sites with a<ce:italic>K<ce:inf loc="post">d</ce:inf></ce:italic> of 7 nM and a<ce:italic>B<ce:inf loc="post">max</ce:inf></ce:italic> of 180 fmol/mg of protein in the substantia nigra. Tritiated dihydrotetrabenazine binding sites were heterogeneously distributed in the mesencephalon of control subjects: the density of tritiated dihydrotetrabenazine binding sites was high in the substantia nigra pars compacta, locus coeruleus and nucleus raphe dorsalis, moderate in the ventral tegmental area and low in the substantia nigra pars reticulata and catecholaminergic cell group A8. Within the substantia nigra, a zone with maximal density of tritiated dihydrotetrabenazine binding, two times higher than the mean estimate for the whole substantia nigra pars compacta, was detected in the medial part of the structure. The anatomical organization of the human ventral mesencephalon was analyzed on adjacent sections stained for acetylcholinesterase histochemistry and tyrosine hydroxylase immunohistochemistry. Tritiated dihydrotetrabenazine binding displayed the same characteristic regional pattern of distribution as that observed with tyrosine hydroxylase immunohistochemistry except in the nucleus raphe dorsalis, where no tyrosine hydroxylase immunoreactivity was detected. In parkinsonian brains, the level of tritiated dihydrotetrabenazine binding was dramatically decreased in all regions of the ventral mesencephalon analyzed except in the substantia nigra pars reticulata. In the substantia nigra pars compacta, the reduction was by 55% for the whole structure and by 65% in its medial zone, where binding site density was maximal. In most nigral subsectors analyzed, the decrease in density of tritiated dihydrotetrabenazine binding sites reached the level expected given the loss of tyrosine hydroxylase-positive cells observed. By contrast, the ratio of [<ce:sup loc="pre">3</ce:sup>H]dihydrotetrabenazine binding to the number of tyrosine hydroxylase positive neurons was significantly increased in the zone of high [<ce:sup loc="pre">3</ce:sup>H]dihydrotetrabenazine binding sites. This relative sparing of tritiated dihydrotetrabenazine binding sites may be due either to the contribution of other monoaminergic neurons such as serotoninergic neurons or more likely to hyperactivity of the still surviving dopaminergic neurons.</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>Dopamine</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Substantia nigra</ce:text></ce:keyword><ce:keyword><ce:text>Human</ce:text></ce:keyword><ce:keyword><ce:text>Synaptic vesicle</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>Agid</ce:surname><ce:given-name>Y.</ce:given-name></sb:author><sb:author><ce:surname>Javoy-Agid</ce:surname><ce:given-name>F.</ce:given-name></sb:author><sb:author><ce:surname>Ruberg</ce:surname><ce:given-name>M.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Biochemistry of neurotransmitters in Parkinson's disease</sb:maintitle></sb:title></sb:contribution><sb:host><sb:edited-book><sb:edition>2nd edn.</sb:edition><sb:book-series><sb:editors><sb:editor><ce:surname>Marsden</ce:surname><ce:given-name>C.D.</ce:given-name></sb:editor><sb:editor><ce:surname>Fahn</ce:surname><ce:given-name>S.</ce:given-name></sb:editor></sb:editors><sb:series><sb:title><sb:maintitle>Movement Disorders</sb:maintitle></sb:title><sb:volume-nr>Vol. 2</sb:volume-nr></sb:series></sb:book-series><sb:date>1987</sb:date><sb:publisher><sb:name>Butterworths</sb:name><sb:location>London</sb:location></sb:publisher></sb:edited-book><sb:pages><sb:first-page>166</sb:first-page><sb:last-page>230</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference><ce:bib-reference id="bib2"><ce:label>[2]</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Arai</ce:surname><ce:given-name>H.</ce:given-name></sb:author><sb:author><ce:surname>Kosaka</ce:surname><ce:given-name>K.</ce:given-name></sb:author><sb:author><ce:surname>Iizuka</ce:surname><ce:given-name>R.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Changes of biogenic amines and their metabolites in postmortem brains from patients with Alzheimer-type dementia</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>J. 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type="personal"><namePart type="given">F.</namePart><namePart type="family">Thibaut</namePart><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.A.</namePart><namePart type="family">Faucheux</namePart><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Marquez</namePart><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Villares</namePart><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.F.</namePart><namePart type="family">Menard</namePart><affiliation>Laboratoire de Biophysique, Hoˆpital Charles Nicolle, 1 rue de Germont, F-76031 Rouen ,France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Agid</namePart><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.C.</namePart><namePart type="family">Hirsch</namePart><affiliation>Corresponding author. Fax: (33) (1) 44 24 36 58</affiliation><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 Blvd de l'Hoˆpital, F-75013 Paris ,France</affiliation><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">1995</dateIssued><dateValid encoding="w3cdtf">1995-05-16</dateValid><copyrightDate encoding="w3cdtf">1995</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">The distribution of the vesicular monoamine transporter was investigated post mortem in the human ventral mesencephalon of control subjects (n = 7) and patients with Parkinson's disease (n = 4) using tritiated dihydrotetrabenazine binding and autoradiography. Tritiated dihydrotetrabenazine binding was characterized by a single class of sites with aKd of 7 nM and aBmax of 180 fmol/mg of protein in the substantia nigra. Tritiated dihydrotetrabenazine binding sites were heterogeneously distributed in the mesencephalon of control subjects: the density of tritiated dihydrotetrabenazine binding sites was high in the substantia nigra pars compacta, locus coeruleus and nucleus raphe dorsalis, moderate in the ventral tegmental area and low in the substantia nigra pars reticulata and catecholaminergic cell group A8. Within the substantia nigra, a zone with maximal density of tritiated dihydrotetrabenazine binding, two times higher than the mean estimate for the whole substantia nigra pars compacta, was detected in the medial part of the structure. The anatomical organization of the human ventral mesencephalon was analyzed on adjacent sections stained for acetylcholinesterase histochemistry and tyrosine hydroxylase immunohistochemistry. Tritiated dihydrotetrabenazine binding displayed the same characteristic regional pattern of distribution as that observed with tyrosine hydroxylase immunohistochemistry except in the nucleus raphe dorsalis, where no tyrosine hydroxylase immunoreactivity was detected. In parkinsonian brains, the level of tritiated dihydrotetrabenazine binding was dramatically decreased in all regions of the ventral mesencephalon analyzed except in the substantia nigra pars reticulata. In the substantia nigra pars compacta, the reduction was by 55% for the whole structure and by 65% in its medial zone, where binding site density was maximal. In most nigral subsectors analyzed, the decrease in density of tritiated dihydrotetrabenazine binding sites reached the level expected given the loss of tyrosine hydroxylase-positive cells observed. By contrast, the ratio of [3H]dihydrotetrabenazine binding to the number of tyrosine hydroxylase positive neurons was significantly increased in the zone of high [3H]dihydrotetrabenazine binding sites. This relative sparing of tritiated dihydrotetrabenazine binding sites may be due either to the contribution of other monoaminergic neurons such as serotoninergic neurons or more likely to hyperactivity of the still surviving dopaminergic neurons.</abstract><subject lang="en"><genre>Keywords</genre><topic>Dopamine</topic><topic>Parkinson's disease</topic><topic>Substantia nigra</topic><topic>Human</topic><topic>Synaptic vesicle</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">19950918</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X0042-X</identifier><part><detail type="volume"><number>692</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>289</end></extent><extent unit="pages"><start>233</start><end>243</end></extent></part></relatedItem><identifier type="istex">06153E28A752DFC7701A70D8C2C794DE8D15B886</identifier><identifier type="DOI">10.1016/0006-8993(95)00674-F</identifier><identifier type="PII">0006-8993(95)00674-F</identifier><identifier type="ArticleID">9500674F</identifier><accessCondition type="use and reproduction" contentType="">© 1995Elsevier Science B.V. 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