Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers
Identifieur interne : 003076 ( Main/Corpus ); précédent : 003075; suivant : 003077Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers
Auteurs : Masahiko Suzuki ; Timothy J. Desmond ; Roger L. Albin ; Kirk A. FreySource :
- Synapse [ 0887-4476 ] ; 2001-09-15.
English descriptors
- KwdEn :
Abstract
Markers of identified neuronal populations have previously suggested selective degeneration of projection neurons in Huntington's disease (HD) striatum. Interpretations are, however, limited by effects of compensatory regulation and atrophy. Studies of the vesicular monoamine transporter type‐2 (VMAT2) and of the vesicular acetylcholine transporter (VAChT) in experimental animals indicate that they are robust markers of presynaptic integrity and are not subject to regulation. We measured dopamine and acetylcholine vesicular transporters to characterize the selectivity of degeneration in HD striatum. Brains were obtained at autopsy from four HD patients and five controls. Autoradiography was used to quantify radioligand binding to VMAT2, VAChT, the dopamine plasmalemmal transporter (DAT), benzodiazepine (BZ) binding sites, and D2‐type dopamine receptors. The activity of choline acetyltransferase (ChAT) was determined as an additional marker of cholinergic neurons. Autoradiograms were analyzed by video‐assisted densitometry and assessment of atrophy was made from regional structural areas in the coronal projection. Striatal VMAT2, DAT, and VAChT concentrations were unchanged or increased, while D2 and BZ binding and ChAT activity were decreased in HD. After atrophy correction, all striatal binding sites were decreased. However, the decrease in ChAT activity was 3‐fold greater than that of VAChT binding. In addition to degeneration of striatal projection neurons, there are losses of extrinsic nigrostriatal projections and of striatal cholinergic interneurons in HD on the basis of vesicular transporter measures. There is also markedly reduced expression of ChAT by surviving cholinergic striatal interneurons. Synapse 41:329–336, 2001. © 2001 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/syn.1089
Links to Exploration step
ISTEX:AEE60883E6802E30CD444882D4C28F4E95650933Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title><author><name sortKey="Suzuki, Masahiko" sort="Suzuki, Masahiko" uniqKey="Suzuki M" first="Masahiko" last="Suzuki">Masahiko Suzuki</name><affiliation><mods:affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, The Jikei University, School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Desmond, Timothy J" sort="Desmond, Timothy J" uniqKey="Desmond T" first="Timothy J." last="Desmond">Timothy J. Desmond</name><affiliation><mods:affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation></author><author><name sortKey="Albin, Roger L" sort="Albin, Roger L" uniqKey="Albin R" first="Roger L." last="Albin">Roger L. Albin</name><affiliation><mods:affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>The Geriatrics Research, Education and Clinical Center, Ann Arbor Veteran's Administration Medical Center, Ann Arbor, Michigan</mods:affiliation></affiliation></author><author><name sortKey="Frey, Kirk A" sort="Frey, Kirk A" uniqKey="Frey K" first="Kirk A." last="Frey">Kirk A. Frey</name><affiliation><mods:affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:AEE60883E6802E30CD444882D4C28F4E95650933</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1002/syn.1089</idno><idno type="url">https://api.istex.fr/document/AEE60883E6802E30CD444882D4C28F4E95650933/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">003076</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title><author><name sortKey="Suzuki, Masahiko" sort="Suzuki, Masahiko" uniqKey="Suzuki M" first="Masahiko" last="Suzuki">Masahiko Suzuki</name><affiliation><mods:affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, The Jikei University, School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Desmond, Timothy J" sort="Desmond, Timothy J" uniqKey="Desmond T" first="Timothy J." last="Desmond">Timothy J. Desmond</name><affiliation><mods:affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation></author><author><name sortKey="Albin, Roger L" sort="Albin, Roger L" uniqKey="Albin R" first="Roger L." last="Albin">Roger L. Albin</name><affiliation><mods:affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>The Geriatrics Research, Education and Clinical Center, Ann Arbor Veteran's Administration Medical Center, Ann Arbor, Michigan</mods:affiliation></affiliation></author><author><name sortKey="Frey, Kirk A" sort="Frey, Kirk A" uniqKey="Frey K" first="Kirk A." last="Frey">Kirk A. Frey</name><affiliation><mods:affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation><affiliation><mods:affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="ISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-09-15">2001-09-15</date><biblScope unit="volume">41</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="329">329</biblScope><biblScope unit="page" to="336">336</biblScope></imprint><idno type="ISSN">0887-4476</idno></series><idno type="istex">AEE60883E6802E30CD444882D4C28F4E95650933</idno><idno type="DOI">10.1002/syn.1089</idno><idno type="ArticleID">SYN1089</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0887-4476</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>VAChT</term><term>VMAT2</term><term>choline acetyltransferase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Markers of identified neuronal populations have previously suggested selective degeneration of projection neurons in Huntington's disease (HD) striatum. Interpretations are, however, limited by effects of compensatory regulation and atrophy. Studies of the vesicular monoamine transporter type‐2 (VMAT2) and of the vesicular acetylcholine transporter (VAChT) in experimental animals indicate that they are robust markers of presynaptic integrity and are not subject to regulation. We measured dopamine and acetylcholine vesicular transporters to characterize the selectivity of degeneration in HD striatum. Brains were obtained at autopsy from four HD patients and five controls. Autoradiography was used to quantify radioligand binding to VMAT2, VAChT, the dopamine plasmalemmal transporter (DAT), benzodiazepine (BZ) binding sites, and D2‐type dopamine receptors. The activity of choline acetyltransferase (ChAT) was determined as an additional marker of cholinergic neurons. Autoradiograms were analyzed by video‐assisted densitometry and assessment of atrophy was made from regional structural areas in the coronal projection. Striatal VMAT2, DAT, and VAChT concentrations were unchanged or increased, while D2 and BZ binding and ChAT activity were decreased in HD. After atrophy correction, all striatal binding sites were decreased. However, the decrease in ChAT activity was 3‐fold greater than that of VAChT binding. In addition to degeneration of striatal projection neurons, there are losses of extrinsic nigrostriatal projections and of striatal cholinergic interneurons in HD on the basis of vesicular transporter measures. There is also markedly reduced expression of ChAT by surviving cholinergic striatal interneurons. Synapse 41:329–336, 2001. © 2001 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Masahiko Suzuki</name><affiliations><json:string>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</json:string><json:string>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</json:string><json:string>Department of Neurology, The Jikei University, School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Timothy J. Desmond</name><affiliations><json:string>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</json:string></affiliations></json:item><json:item><name>Roger L. Albin</name><affiliations><json:string>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</json:string><json:string>The Geriatrics Research, Education and Clinical Center, Ann Arbor Veteran's Administration Medical Center, Ann Arbor, Michigan</json:string></affiliations></json:item><json:item><name>Kirk A. Frey</name><affiliations><json:string>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</json:string><json:string>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</json:string><json:string>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>VAChT</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>VMAT2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>choline acetyltransferase</value></json:item></subject><articleId><json:string>SYN1089</json:string></articleId><language><json:string>eng</json:string></language><abstract>Markers of identified neuronal populations have previously suggested selective degeneration of projection neurons in Huntington's disease (HD) striatum. Interpretations are, however, limited by effects of compensatory regulation and atrophy. Studies of the vesicular monoamine transporter type‐2 (VMAT2) and of the vesicular acetylcholine transporter (VAChT) in experimental animals indicate that they are robust markers of presynaptic integrity and are not subject to regulation. We measured dopamine and acetylcholine vesicular transporters to characterize the selectivity of degeneration in HD striatum. Brains were obtained at autopsy from four HD patients and five controls. Autoradiography was used to quantify radioligand binding to VMAT2, VAChT, the dopamine plasmalemmal transporter (DAT), benzodiazepine (BZ) binding sites, and D2‐type dopamine receptors. The activity of choline acetyltransferase (ChAT) was determined as an additional marker of cholinergic neurons. Autoradiograms were analyzed by video‐assisted densitometry and assessment of atrophy was made from regional structural areas in the coronal projection. Striatal VMAT2, DAT, and VAChT concentrations were unchanged or increased, while D2 and BZ binding and ChAT activity were decreased in HD. After atrophy correction, all striatal binding sites were decreased. However, the decrease in ChAT activity was 3‐fold greater than that of VAChT binding. In addition to degeneration of striatal projection neurons, there are losses of extrinsic nigrostriatal projections and of striatal cholinergic interneurons in HD on the basis of vesicular transporter measures. There is also markedly reduced expression of ChAT by surviving cholinergic striatal interneurons. Synapse 41:329–336, 2001. © 2001 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.904</score><pdfVersion>1.2</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1783</abstractCharCount><pdfWordCount>5102</pdfWordCount><pdfCharCount>33577</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>242</abstractWordCount></qualityIndicators><title>Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title><genre><json:string>article</json:string></genre><host><volume>41</volume><publisherId><json:string>SYN</json:string></publisherId><pages><total>8</total><last>336</last><first>329</first></pages><issn><json:string>0887-4476</json:string></issn><issue>4</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1098-2396</json:string></eissn><title>Synapse</title><doi><json:string>10.1002/(ISSN)1098-2396</json:string></doi></host><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1002/syn.1089</json:string></doi><id>AEE60883E6802E30CD444882D4C28F4E95650933</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/AEE60883E6802E30CD444882D4C28F4E95650933/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/AEE60883E6802E30CD444882D4C28F4E95650933/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/AEE60883E6802E30CD444882D4C28F4E95650933/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><availability><p>WILEY</p></availability><date>2001</date></publicationStmt><notesStmt><note>National Institute of Aging - No. USPHS AG08671;</note><note>National Institute of Neurological Disorders and Stroke - No. AG08671; No. NS38166;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title><author><persName><forename type="first">Masahiko</forename><surname>Suzuki</surname></persName><affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>Department of Neurology, The Jikei University, School of Medicine, Tokyo, Japan</affiliation></author><author><persName><forename type="first">Timothy J.</forename><surname>Desmond</surname></persName><affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</affiliation></author><author><persName><forename type="first">Roger L.</forename><surname>Albin</surname></persName><affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>The Geriatrics Research, Education and Clinical Center, Ann Arbor Veteran's Administration Medical Center, Ann Arbor, Michigan</affiliation></author><author><persName><forename type="first">Kirk A.</forename><surname>Frey</surname></persName><note type="correspondence"><p>Correspondence: The University of Michigan Hospitals, Room B1G 412/0028 AGH 1500 East Medical Center Drive, Ann Arbor, MI 48109‐0028</p></note><affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</affiliation></author></analytic><monogr><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="pISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><idno type="DOI">10.1002/(ISSN)1098-2396</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-09-15"></date><biblScope unit="volume">41</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="329">329</biblScope><biblScope unit="page" to="336">336</biblScope></imprint></monogr><idno type="istex">AEE60883E6802E30CD444882D4C28F4E95650933</idno><idno type="DOI">10.1002/syn.1089</idno><idno type="ArticleID">SYN1089</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Markers of identified neuronal populations have previously suggested selective degeneration of projection neurons in Huntington's disease (HD) striatum. Interpretations are, however, limited by effects of compensatory regulation and atrophy. Studies of the vesicular monoamine transporter type‐2 (VMAT2) and of the vesicular acetylcholine transporter (VAChT) in experimental animals indicate that they are robust markers of presynaptic integrity and are not subject to regulation. We measured dopamine and acetylcholine vesicular transporters to characterize the selectivity of degeneration in HD striatum. Brains were obtained at autopsy from four HD patients and five controls. Autoradiography was used to quantify radioligand binding to VMAT2, VAChT, the dopamine plasmalemmal transporter (DAT), benzodiazepine (BZ) binding sites, and D2‐type dopamine receptors. The activity of choline acetyltransferase (ChAT) was determined as an additional marker of cholinergic neurons. Autoradiograms were analyzed by video‐assisted densitometry and assessment of atrophy was made from regional structural areas in the coronal projection. Striatal VMAT2, DAT, and VAChT concentrations were unchanged or increased, while D2 and BZ binding and ChAT activity were decreased in HD. After atrophy correction, all striatal binding sites were decreased. However, the decrease in ChAT activity was 3‐fold greater than that of VAChT binding. In addition to degeneration of striatal projection neurons, there are losses of extrinsic nigrostriatal projections and of striatal cholinergic interneurons in HD on the basis of vesicular transporter measures. There is also markedly reduced expression of ChAT by surviving cholinergic striatal interneurons. Synapse 41:329–336, 2001. © 2001 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>VAChT</term></item><item><term>VMAT2</term></item><item><term>choline acetyltransferase</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-02-14">Received</change><change when="2001-04-09">Registration</change><change when="2001-09-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/AEE60883E6802E30CD444882D4C28F4E95650933/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1098-2396</doi><issn type="print">0887-4476</issn><issn type="electronic">1098-2396</issn><idGroup><id type="product" value="SYN"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="SYNAPSE">Synapse</title><title type="short">Synapse</title></titleGroup></publicationMeta><publicationMeta level="part" position="40"><doi origin="wiley" registered="yes">10.1002/syn.v41:4</doi><numberingGroup><numbering type="journalVolume" number="41">41</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="2001-09-15">15 September 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="60" status="forIssue"><doi origin="wiley" registered="yes">10.1002/syn.1089</doi><idGroup><id type="unit" value="SYN1089"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><copyright ownership="publisher">Copyright © 2001 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2001-02-14"></event><event type="manuscriptAccepted" date="2001-04-09"></event><event type="firstOnline" date="2001-06-27"></event><event type="publishedOnlineFinalForm" date="2001-06-27"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-04"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-10"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst">329</numbering><numbering type="pageLast">336</numbering></numberingGroup><correspondenceTo>The University of Michigan Hospitals, Room B1G 412/0028 AGH 1500 East Medical Center Drive, Ann Arbor, MI 48109‐0028</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:SYN.SYN1089.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="4"></count><count type="referenceTotal" number="52"></count><count type="wordTotal" number="6302"></count></countGroup><titleGroup><title type="main" xml:lang="en">Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title><title type="short" xml:lang="en">Transporters in HD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af3 #af5"><personName><givenNames>Masahiko</givenNames><familyName>Suzuki</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Timothy J.</givenNames><familyName>Desmond</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2 #af4"><personName><givenNames>Roger L.</givenNames><familyName>Albin</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2 #af3" corresponding="yes"><personName><givenNames>Kirk A.</givenNames><familyName>Frey</familyName></personName><contactDetails><email>kfrey@umich.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>The Geriatrics Research, Education and Clinical Center, Ann Arbor Veteran's Administration Medical Center, Ann Arbor, Michigan</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurology, The Jikei University, School of Medicine, Tokyo, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">VAChT</keyword><keyword xml:id="kwd2">VMAT2</keyword><keyword xml:id="kwd3">choline acetyltransferase</keyword></keywordGroup><fundingInfo><fundingAgency>National Institute of Aging</fundingAgency><fundingNumber>USPHS AG08671</fundingNumber></fundingInfo><fundingInfo><fundingAgency>National Institute of Neurological Disorders and Stroke</fundingAgency><fundingNumber>AG08671</fundingNumber><fundingNumber>NS38166</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Markers of identified neuronal populations have previously suggested selective degeneration of projection neurons in Huntington's disease (HD) striatum. Interpretations are, however, limited by effects of compensatory regulation and atrophy. Studies of the vesicular monoamine transporter type‐2 (VMAT2) and of the vesicular acetylcholine transporter (VAChT) in experimental animals indicate that they are robust markers of presynaptic integrity and are not subject to regulation. We measured dopamine and acetylcholine vesicular transporters to characterize the selectivity of degeneration in HD striatum. Brains were obtained at autopsy from four HD patients and five controls. Autoradiography was used to quantify radioligand binding to VMAT2, VAChT, the dopamine plasmalemmal transporter (DAT), benzodiazepine (BZ) binding sites, and D2‐type dopamine receptors. The activity of choline acetyltransferase (ChAT) was determined as an additional marker of cholinergic neurons. Autoradiograms were analyzed by video‐assisted densitometry and assessment of atrophy was made from regional structural areas in the coronal projection. Striatal VMAT2, DAT, and VAChT concentrations were unchanged or increased, while D2 and BZ binding and ChAT activity were decreased in HD. After atrophy correction, all striatal binding sites were decreased. However, the decrease in ChAT activity was 3‐fold greater than that of VAChT binding. In addition to degeneration of striatal projection neurons, there are losses of extrinsic nigrostriatal projections and of striatal cholinergic interneurons in HD on the basis of vesicular transporter measures. There is also markedly reduced expression of ChAT by surviving cholinergic striatal interneurons. Synapse 41:329–336, 2001. © 2001 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Transporters in HD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers</title></titleInfo><name type="personal"><namePart type="given">Masahiko</namePart><namePart type="family">Suzuki</namePart><affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>Department of Neurology, The Jikei University, School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Timothy J.</namePart><namePart type="family">Desmond</namePart><affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roger L.</namePart><namePart type="family">Albin</namePart><affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>The Geriatrics Research, Education and Clinical Center, Ann Arbor Veteran's Administration Medical Center, Ann Arbor, Michigan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kirk A.</namePart><namePart type="family">Frey</namePart><affiliation>Department of Radiology (Division of Nuclear Medicine), The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>Department of Neurology, The University of Michigan, Ann Arbor, Michigan</affiliation><affiliation>The Mental Health Research Institute, The University of Michigan, Ann Arbor, Michigan</affiliation><description>Correspondence: The University of Michigan Hospitals, Room B1G 412/0028 AGH 1500 East Medical Center Drive, Ann Arbor, MI 48109‐0028</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2001-09-15</dateIssued><dateCaptured encoding="w3cdtf">2001-02-14</dateCaptured><dateValid encoding="w3cdtf">2001-04-09</dateValid><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">4</extent><extent unit="references">52</extent><extent unit="words">6302</extent></physicalDescription><abstract lang="en">Markers of identified neuronal populations have previously suggested selective degeneration of projection neurons in Huntington's disease (HD) striatum. Interpretations are, however, limited by effects of compensatory regulation and atrophy. Studies of the vesicular monoamine transporter type‐2 (VMAT2) and of the vesicular acetylcholine transporter (VAChT) in experimental animals indicate that they are robust markers of presynaptic integrity and are not subject to regulation. We measured dopamine and acetylcholine vesicular transporters to characterize the selectivity of degeneration in HD striatum. Brains were obtained at autopsy from four HD patients and five controls. Autoradiography was used to quantify radioligand binding to VMAT2, VAChT, the dopamine plasmalemmal transporter (DAT), benzodiazepine (BZ) binding sites, and D2‐type dopamine receptors. The activity of choline acetyltransferase (ChAT) was determined as an additional marker of cholinergic neurons. Autoradiograms were analyzed by video‐assisted densitometry and assessment of atrophy was made from regional structural areas in the coronal projection. Striatal VMAT2, DAT, and VAChT concentrations were unchanged or increased, while D2 and BZ binding and ChAT activity were decreased in HD. After atrophy correction, all striatal binding sites were decreased. However, the decrease in ChAT activity was 3‐fold greater than that of VAChT binding. In addition to degeneration of striatal projection neurons, there are losses of extrinsic nigrostriatal projections and of striatal cholinergic interneurons in HD on the basis of vesicular transporter measures. There is also markedly reduced expression of ChAT by surviving cholinergic striatal interneurons. Synapse 41:329–336, 2001. © 2001 Wiley‐Liss, Inc.</abstract><note type="funding">National Institute of Aging - No. USPHS AG08671; </note><note type="funding">National Institute of Neurological Disorders and Stroke - No. AG08671; No. NS38166; </note><subject lang="en"><genre>Keywords</genre><topic>VAChT</topic><topic>VMAT2</topic><topic>choline acetyltransferase</topic></subject><relatedItem type="host"><titleInfo><title>Synapse</title></titleInfo><titleInfo type="abbreviated"><title>Synapse</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0887-4476</identifier><identifier type="eISSN">1098-2396</identifier><identifier type="DOI">10.1002/(ISSN)1098-2396</identifier><identifier type="PublisherID">SYN</identifier><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>41</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>329</start><end>336</end><total>8</total></extent></part></relatedItem><identifier type="istex">AEE60883E6802E30CD444882D4C28F4E95650933</identifier><identifier type="DOI">10.1002/syn.1089</identifier><identifier type="ArticleID">SYN1089</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Inc.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003076 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 003076 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:AEE60883E6802E30CD444882D4C28F4E95650933
|texte= Vesicular neurotransmitter transporters in Huntington's disease: Initial observations and comparison with traditional synaptic markers
}}
| This area was generated with Dilib version V0.6.23. |  |