Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography
Identifieur interne : 001974 ( Main/Corpus ); précédent : 001973; suivant : 001975Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography
Auteurs : Stéphane Lehéricy ; Jean-Philippe Brandel ; Etienne C. Hirsch ; Philippe Anglade ; Joao Villares ; Daniel Scherman ; Charles Duyckaerts ; France Javoy-Agid ; Yves AgidSource :
- Brain Research [ 0006-8993 ] ; 1994.
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Abstract
The monoaminergic innervation of the caudate nucleus, putamen and ventral striatum was investigated post mortem, in patients with Parkinson's and Alzheimer's disease as compared to control subjects, by autoradiographic detection of tritiated dihydrotetrabenazine (3H-TBZOH), a specific high affinity ligand of the vesicular monoamine transporter. The binding of 3H-TBZOH was specific and saturable (Kd 5.3 nM). In control striatum, the pattern of distribution of 3H-TBZOH binding was heterogeneous, with higher binding levels in the ‘matrix’ than in the ‘striosome’ compartment. Changes in ligand binding levels were observed in the pathological brains compared to controls. In Parkinson's disease (PD), characterized by a severe damage of mesostriatal dopaminergic neurons, the density of 3H-TBZOH binding was reduced. A severe decrease in 3H-TBZOH binding was observed in all parts of the striatum (caudate nucleus: −80%, putamen: −86%, ventral striatum: −94%) in PD brains. The data corroborate the deficiency in striatal dopaminergic transmission and suggest that in PD brains dopaminergic terminals have disappeared and/or no longer contain synaptic vesicles. In Alzheimer's disease (AD), 3H-TBZOH binding was significantly reduced by 57% in the ventral striatum and not in the caudate nucleus and putamen. The specific decrease of monoaminergic transporter levels in the ventral striatum confirm that this nucleus is a target area in AD.
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DOI: 10.1016/0006-8993(94)90856-7
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The binding of 3H-TBZOH was specific and saturable (Kd 5.3 nM). In control striatum, the pattern of distribution of 3H-TBZOH binding was heterogeneous, with higher binding levels in the ‘matrix’ than in the ‘striosome’ compartment. Changes in ligand binding levels were observed in the pathological brains compared to controls. In Parkinson's disease (PD), characterized by a severe damage of mesostriatal dopaminergic neurons, the density of 3H-TBZOH binding was reduced. A severe decrease in 3H-TBZOH binding was observed in all parts of the striatum (caudate nucleus: −80%, putamen: −86%, ventral striatum: −94%) in PD brains. The data corroborate the deficiency in striatal dopaminergic transmission and suggest that in PD brains dopaminergic terminals have disappeared and/or no longer contain synaptic vesicles. In Alzheimer's disease (AD), 3H-TBZOH binding was significantly reduced by 57% in the ventral striatum and not in the caudate nucleus and putamen. The specific decrease of monoaminergic transporter levels in the ventral striatum confirm that this nucleus is a target area in AD.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Stéphane Lehéricy</name><affiliations><json:string>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</json:string></affiliations></json:item><json:item><name>Jean-Philippe Brandel</name><affiliations><json:string>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</json:string></affiliations></json:item><json:item><name>Etienne C. Hirsch</name><affiliations><json:string>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</json:string></affiliations></json:item><json:item><name>Philippe Anglade</name><affiliations><json:string>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</json:string></affiliations></json:item><json:item><name>Joao Villares</name><affiliations><json:string>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</json:string></affiliations></json:item><json:item><name>Daniel Scherman</name><affiliations><json:string>Rhône-Poulenc Rorer, 13 quai Jules Guesde, B.P. 14, 94403 Vitry sur Seine cedex, France</json:string></affiliations></json:item><json:item><name>Charles Duyckaerts</name><affiliations><json:string>Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>France Javoy-Agid</name><affiliations><json:string>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</json:string></affiliations></json:item><json:item><name>Yves Agid</name><affiliations><json:string>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Human brain</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Monoamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Caudate nucleus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Putamen</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Ventral striatum</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Striosome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Matrix</value></json:item></subject><articleId><json:string>94908567</json:string></articleId><language><json:string>eng</json:string></language><abstract>The monoaminergic innervation of the caudate nucleus, putamen and ventral striatum was investigated post mortem, in patients with Parkinson's and Alzheimer's disease as compared to control subjects, by autoradiographic detection of tritiated dihydrotetrabenazine (3H-TBZOH), a specific high affinity ligand of the vesicular monoamine transporter. The binding of 3H-TBZOH was specific and saturable (Kd 5.3 nM). In control striatum, the pattern of distribution of 3H-TBZOH binding was heterogeneous, with higher binding levels in the ‘matrix’ than in the ‘striosome’ compartment. Changes in ligand binding levels were observed in the pathological brains compared to controls. In Parkinson's disease (PD), characterized by a severe damage of mesostriatal dopaminergic neurons, the density of 3H-TBZOH binding was reduced. A severe decrease in 3H-TBZOH binding was observed in all parts of the striatum (caudate nucleus: −80%, putamen: −86%, ventral striatum: −94%) in PD brains. The data corroborate the deficiency in striatal dopaminergic transmission and suggest that in PD brains dopaminergic terminals have disappeared and/or no longer contain synaptic vesicles. In Alzheimer's disease (AD), 3H-TBZOH binding was significantly reduced by 57% in the ventral striatum and not in the caudate nucleus and putamen. The specific decrease of monoaminergic transporter levels in the ventral striatum confirm that this nucleus is a target area in AD.</abstract><qualityIndicators><score>7.484</score><pdfVersion>1.2</pdfVersion><pdfPageSize>648 x 864 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>8</keywordCount><abstractCharCount>1443</abstractCharCount><pdfWordCount>7578</pdfWordCount><pdfCharCount>33897</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>207</abstractWordCount></qualityIndicators><title>Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography</title><pii><json:string>0006-8993(94)90856-7</json:string></pii><genre><json:string>brief communication</json:string></genre><serie><volume>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>659</volume><pii><json:string>S0006-8993(00)X1087-6</json:string></pii><pages><last>9</last><first>1</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>1994</publicationDate></host><publicationDate>1994</publicationDate><copyrightDate>1994</copyrightDate><doi><json:string>10.1016/0006-8993(94)90856-7</json:string></doi><id>CC2812BB34683B8A7D4AF1FC4467460CEA86A77A</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/CC2812BB34683B8A7D4AF1FC4467460CEA86A77A/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CC2812BB34683B8A7D4AF1FC4467460CEA86A77A/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/CC2812BB34683B8A7D4AF1FC4467460CEA86A77A/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/CC2812BB34683B8A7D4AF1FC4467460CEA86A77A/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1994</date></publicationStmt><notesStmt><note type="content">Section title: Research report</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography</title><author><persName><forename type="first">Stéphane</forename><surname>Lehéricy</surname></persName><note type="correspondence"><p>Corresponding author. Fax: (33) (1) 44243658.</p></note><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation></author><author><persName><forename type="first">Jean-Philippe</forename><surname>Brandel</surname></persName><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation></author><author><persName><forename type="first">Etienne C.</forename><surname>Hirsch</surname></persName><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation></author><author><persName><forename type="first">Philippe</forename><surname>Anglade</surname></persName><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation></author><author><persName><forename type="first">Joao</forename><surname>Villares</surname></persName><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation></author><author><persName><forename type="first">Daniel</forename><surname>Scherman</surname></persName><affiliation>Rhône-Poulenc Rorer, 13 quai Jules Guesde, B.P. 14, 94403 Vitry sur Seine cedex, France</affiliation></author><author><persName><forename type="first">Charles</forename><surname>Duyckaerts</surname></persName><affiliation>Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France</affiliation></author><author><persName><forename type="first">France</forename><surname>Javoy-Agid</surname></persName><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation></author><author><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, 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)X1087-6</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1994"></date><biblScope unit="volume">659</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="9">9</biblScope></imprint></monogr><idno type="istex">CC2812BB34683B8A7D4AF1FC4467460CEA86A77A</idno><idno type="DOI">10.1016/0006-8993(94)90856-7</idno><idno type="PII">0006-8993(94)90856-7</idno><idno type="ArticleID">94908567</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The monoaminergic innervation of the caudate nucleus, putamen and ventral striatum was investigated post mortem, in patients with Parkinson's and Alzheimer's disease as compared to control subjects, by autoradiographic detection of tritiated dihydrotetrabenazine (3H-TBZOH), a specific high affinity ligand of the vesicular monoamine transporter. The binding of 3H-TBZOH was specific and saturable (Kd 5.3 nM). In control striatum, the pattern of distribution of 3H-TBZOH binding was heterogeneous, with higher binding levels in the ‘matrix’ than in the ‘striosome’ compartment. Changes in ligand binding levels were observed in the pathological brains compared to controls. In Parkinson's disease (PD), characterized by a severe damage of mesostriatal dopaminergic neurons, the density of 3H-TBZOH binding was reduced. A severe decrease in 3H-TBZOH binding was observed in all parts of the striatum (caudate nucleus: −80%, putamen: −86%, ventral striatum: −94%) in PD brains. The data corroborate the deficiency in striatal dopaminergic transmission and suggest that in PD brains dopaminergic terminals have disappeared and/or no longer contain synaptic vesicles. In Alzheimer's disease (AD), 3H-TBZOH binding was significantly reduced by 57% in the ventral striatum and not in the caudate nucleus and putamen. The specific decrease of monoaminergic transporter levels in the ventral striatum confirm that this nucleus is a target area in AD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Human brain</term></item><item><term>Dopamine</term></item><item><term>Monoamine</term></item><item><term>Caudate nucleus</term></item><item><term>Putamen</term></item><item><term>Ventral striatum</term></item><item><term>Striosome</term></item><item><term>Matrix</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-06-14">Registration</change><change when="1994">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="sco" xml:lang="en"><item-info><jid>BRES</jid><aid>94908567</aid><ce:pii>0006-8993(94)90856-7</ce:pii><ce:doi>10.1016/0006-8993(94)90856-7</ce:doi><ce:copyright type="unknown" year="1994"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Research report</ce:textfn></ce:dochead><ce:title>Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography</ce:title><ce:author-group><ce:author><ce:given-name>Stéphane</ce:given-name><ce:surname>Lehéricy</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:author><ce:given-name>Jean-Philippe</ce:given-name><ce:surname>Brandel</ce:surname><ce:cross-ref refid="AFF1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Etienne C.</ce:given-name><ce:surname>Hirsch</ce:surname><ce:cross-ref refid="AFF1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Philippe</ce:given-name><ce:surname>Anglade</ce:surname><ce:cross-ref refid="AFF1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Joao</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>Daniel</ce:given-name><ce:surname>Scherman</ce:surname><ce:cross-ref refid="AFF2"><ce:sup loc="post">b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Charles</ce:given-name><ce:surname>Duyckaerts</ce:surname><ce:cross-ref refid="AFF3"><ce:sup loc="post">c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>France</ce:given-name><ce:surname>Javoy-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>Yves</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:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Rhône-Poulenc Rorer, 13 quai Jules Guesde, B.P. 14, 94403 Vitry sur Seine cedex, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Fax: (33) (1) 44243658.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="14" month="6" year="1994"></ce:date-accepted><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">The monoaminergic innervation of the caudate nucleus, putamen and ventral striatum was investigated post mortem, in patients with Parkinson's and Alzheimer's disease as compared to control subjects, by autoradiographic detection of tritiated dihydrotetrabenazine (<ce:sup loc="pre">3</ce:sup>H-TBZOH), a specific high affinity ligand of the vesicular monoamine transporter. The binding of <ce:sup loc="post">3</ce:sup>H-TBZOH was specific and saturable (<ce:italic>K</ce:italic><ce:inf loc="post">d</ce:inf> 5.3 nM). In control striatum, the pattern of distribution of <ce:sup loc="pre">3</ce:sup>H-TBZOH binding was heterogeneous, with higher binding levels in the ‘matrix’ than in the ‘striosome’ compartment. Changes in ligand binding levels were observed in the pathological brains compared to controls. In Parkinson's disease (PD), characterized by a severe damage of mesostriatal dopaminergic neurons, the density of <ce:sup loc="pre">3</ce:sup>H-TBZOH binding was reduced. A severe decrease in <ce:sup loc="pre">3</ce:sup>H-TBZOH binding was observed in all parts of the striatum (caudate nucleus: −80%, putamen: −86%, ventral striatum: −94%) in PD brains. The data corroborate the deficiency in striatal dopaminergic transmission and suggest that in PD brains dopaminergic terminals have disappeared and/or no longer contain synaptic vesicles. In Alzheimer's disease (AD), <ce:sup loc="pre">3</ce:sup>H-TBZOH binding was significantly reduced by 57% in the ventral striatum and not in the caudate nucleus and putamen. The specific decrease of monoaminergic transporter levels in the ventral striatum confirm that this nucleus is a target area in AD.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Human brain</ce:text></ce:keyword><ce:keyword><ce:text>Dopamine</ce:text></ce:keyword><ce:keyword><ce:text>Monoamine</ce:text></ce:keyword><ce:keyword><ce:text>Caudate nucleus</ce:text></ce:keyword><ce:keyword><ce:text>Putamen</ce:text></ce:keyword><ce:keyword><ce:text>Ventral striatum</ce:text></ce:keyword><ce:keyword><ce:text>Striosome</ce:text></ce:keyword><ce:keyword><ce:text>Matrix</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography</title></titleInfo><name type="personal"><namePart type="given">Stéphane</namePart><namePart type="family">Lehéricy</namePart><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation><description>Corresponding author. Fax: (33) (1) 44243658.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean-Philippe</namePart><namePart type="family">Brandel</namePart><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Etienne C.</namePart><namePart type="family">Hirsch</namePart><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Anglade</namePart><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joao</namePart><namePart type="family">Villares</namePart><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniel</namePart><namePart type="family">Scherman</namePart><affiliation>Rhône-Poulenc Rorer, 13 quai Jules Guesde, B.P. 14, 94403 Vitry sur Seine cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Charles</namePart><namePart type="family">Duyckaerts</namePart><affiliation>Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">France</namePart><namePart type="family">Javoy-Agid</namePart><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Agid</namePart><affiliation>Laboratoire de Médecine Expérimentale, INSERM U 289, Hôpital de la Salpêtrière, 47 Bd de l'Hôpital, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief communication" displayLabel="Short communication"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1994</dateIssued><dateValid encoding="w3cdtf">1994-06-14</dateValid><copyrightDate encoding="w3cdtf">1994</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 monoaminergic innervation of the caudate nucleus, putamen and ventral striatum was investigated post mortem, in patients with Parkinson's and Alzheimer's disease as compared to control subjects, by autoradiographic detection of tritiated dihydrotetrabenazine (3H-TBZOH), a specific high affinity ligand of the vesicular monoamine transporter. The binding of 3H-TBZOH was specific and saturable (Kd 5.3 nM). In control striatum, the pattern of distribution of 3H-TBZOH binding was heterogeneous, with higher binding levels in the ‘matrix’ than in the ‘striosome’ compartment. Changes in ligand binding levels were observed in the pathological brains compared to controls. In Parkinson's disease (PD), characterized by a severe damage of mesostriatal dopaminergic neurons, the density of 3H-TBZOH binding was reduced. A severe decrease in 3H-TBZOH binding was observed in all parts of the striatum (caudate nucleus: −80%, putamen: −86%, ventral striatum: −94%) in PD brains. The data corroborate the deficiency in striatal dopaminergic transmission and suggest that in PD brains dopaminergic terminals have disappeared and/or no longer contain synaptic vesicles. In Alzheimer's disease (AD), 3H-TBZOH binding was significantly reduced by 57% in the ventral striatum and not in the caudate nucleus and putamen. The specific decrease of monoaminergic transporter levels in the ventral striatum confirm that this nucleus is a target area in AD.</abstract><note type="content">Section title: Research report</note><subject lang="en"><genre>Keywords</genre><topic>Human brain</topic><topic>Dopamine</topic><topic>Monoamine</topic><topic>Caudate nucleus</topic><topic>Putamen</topic><topic>Ventral striatum</topic><topic>Striosome</topic><topic>Matrix</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">19941003</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X1087-6</identifier><part><date>19941003</date><detail type="volume"><number>659</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>300</end></extent><extent unit="pages"><start>1</start><end>9</end></extent></part></relatedItem><identifier type="istex">CC2812BB34683B8A7D4AF1FC4467460CEA86A77A</identifier><identifier type="DOI">10.1016/0006-8993(94)90856-7</identifier><identifier type="PII">0006-8993(94)90856-7</identifier><identifier type="ArticleID">94908567</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/CC2812BB34683B8A7D4AF1FC4467460CEA86A77A/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct><analytic><title level="a" type="main">Biochemistry of neurotransminers in Parkinson's disease</title><author><persName><forename type="first">Y</forename><surname>Agid</surname></persName></author><author><persName><forename type="first">F</forename><surname>Javoy-Agid</surname></persName></author><author><persName><forename type="first">M</forename><surname>And Ruberg</surname></persName></author></analytic><monogr><title level="m">Mo~,ement Disorders</title><editor>C.D. 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