Markers of dopamine depletion and compensatory response in striatum and cerebrospinal fluid
Identifieur interne : 000791 ( Main/Corpus ); précédent : 000790; suivant : 000792Markers of dopamine depletion and compensatory response in striatum and cerebrospinal fluid
Auteurs : A. Loeffler ; A. Lewitt ; J. Demaggio ; L. Juneau ; E. Milbury ; R. MatsonSource :
- Journal of Neural Transmission - Parkinson's Disease and Dementia Section [ 0936-3076 ] ; 1995-02-01.
Abstract
Summary: Though depletion of CSF homovanillic acid (HVA) concentration has often been regarded as a direct indicator of dopamine (DA) deficiency in Parkinson's Disease (PD), CSF HVA is normal in mildly affected patients. To explore why, we measured DA and its metabolites in striatum and CSF in rabbits receiving reserpine for 5 days. Reserpine, which depletes striatal DA by disrupting vesicular storage of the neurotransmitter, results in a compensatory increase of DA turnover. In response to a 96% depletion of striatal DA, its catabolic intermediates 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) decreased 64% and 92% in striatum, although the endproduct, HVA, was unchanged. In contrast, CSF concentrations of HVA and DOPAC increased significantly, though 3-MT and levodopa (LD) were unaltered. A 5-fold rise in striatal LD concentration after reserpine-induced DA depletion provided evidence for enhanced DA synthesis. As in PD, the compensatory increase of DA synthesis after reserpine administration confounds the ability of CSF HVA to reflect DA depletion.
Url:
DOI: 10.1007/BF02252962
Links to Exploration step
ISTEX:580E8356C3EC4678951DC05A1BD774683BB6EE3BLe document en format XML
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Lewitt</name><affiliation><mods:affiliation>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</mods:affiliation></affiliation><affiliation><mods:affiliation>Departments of Neurology and Psychiatry, Wayne State University School of Medicine, Detroit, Michigan, U.S.A.</mods:affiliation></affiliation><affiliation><mods:affiliation>Cellular and Clinical Neuroscience Program, Wayne State University School of Medicine, Detroit, Michigan, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Demaggio, J" sort="Demaggio, J" uniqKey="Demaggio J" first="J." last="Demaggio">J. Demaggio</name><affiliation><mods:affiliation>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Juneau, L" sort="Juneau, L" uniqKey="Juneau L" first="L." last="Juneau">L. 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Matson</name><affiliation><mods:affiliation>ESA, Incorporated, Chelmsford, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title><title level="j" type="abbrev">J Neural Transm Gen Sect</title><idno type="ISSN">0936-3076</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1995-02-01">1995-02-01</date><biblScope unit="volume">9</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="45">45</biblScope><biblScope unit="page" to="53">53</biblScope></imprint><idno type="ISSN">0936-3076</idno></series><idno type="istex">580E8356C3EC4678951DC05A1BD774683BB6EE3B</idno><idno type="DOI">10.1007/BF02252962</idno><idno type="ArticleID">Art4</idno><idno type="ArticleID">BF02252962</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0936-3076</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Though depletion of CSF homovanillic acid (HVA) concentration has often been regarded as a direct indicator of dopamine (DA) deficiency in Parkinson's Disease (PD), CSF HVA is normal in mildly affected patients. To explore why, we measured DA and its metabolites in striatum and CSF in rabbits receiving reserpine for 5 days. Reserpine, which depletes striatal DA by disrupting vesicular storage of the neurotransmitter, results in a compensatory increase of DA turnover. In response to a 96% depletion of striatal DA, its catabolic intermediates 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) decreased 64% and 92% in striatum, although the endproduct, HVA, was unchanged. In contrast, CSF concentrations of HVA and DOPAC increased significantly, though 3-MT and levodopa (LD) were unaltered. A 5-fold rise in striatal LD concentration after reserpine-induced DA depletion provided evidence for enhanced DA synthesis. As in PD, the compensatory increase of DA synthesis after reserpine administration confounds the ability of CSF HVA to reflect DA depletion.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>D. A. Loeffler DVM, PhD</name><affiliations><json:string>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</json:string></affiliations></json:item><json:item><name>P. A. LeWitt</name><affiliations><json:string>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</json:string><json:string>Departments of Neurology and Psychiatry, Wayne State University School of Medicine, Detroit, Michigan, U.S.A.</json:string><json:string>Cellular and Clinical Neuroscience Program, Wayne State University School of Medicine, Detroit, Michigan, U.S.A.</json:string></affiliations></json:item><json:item><name>A. J. DeMaggio</name><affiliations><json:string>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</json:string></affiliations></json:item><json:item><name>P. L. Juneau</name><affiliations><json:string>Preclinical Biometrics, Warner Lambert Company, Ann Arbor, Michigan, U.S.A.</json:string></affiliations></json:item><json:item><name>P. E. Milbury</name><affiliations><json:string>ESA, Incorporated, Chelmsford, U.S.A.</json:string></affiliations></json:item><json:item><name>W. R. Matson</name><affiliations><json:string>ESA, Incorporated, Chelmsford, U.S.A.</json:string></affiliations></json:item></author><articleId><json:string>Art4</json:string><json:string>BF02252962</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: Though depletion of CSF homovanillic acid (HVA) concentration has often been regarded as a direct indicator of dopamine (DA) deficiency in Parkinson's Disease (PD), CSF HVA is normal in mildly affected patients. To explore why, we measured DA and its metabolites in striatum and CSF in rabbits receiving reserpine for 5 days. Reserpine, which depletes striatal DA by disrupting vesicular storage of the neurotransmitter, results in a compensatory increase of DA turnover. In response to a 96% depletion of striatal DA, its catabolic intermediates 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) decreased 64% and 92% in striatum, although the endproduct, HVA, was unchanged. In contrast, CSF concentrations of HVA and DOPAC increased significantly, though 3-MT and levodopa (LD) were unaltered. A 5-fold rise in striatal LD concentration after reserpine-induced DA depletion provided evidence for enhanced DA synthesis. As in PD, the compensatory increase of DA synthesis after reserpine administration confounds the ability of CSF HVA to reflect DA depletion.</abstract><qualityIndicators><score>5.911</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 774 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1089</abstractCharCount><pdfWordCount>4003</pdfWordCount><pdfCharCount>21644</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>159</abstractWordCount></qualityIndicators><title>Markers of dopamine depletion and compensatory response in striatum and cerebrospinal fluid</title><genre><json:string>research-article</json:string></genre><host><volume>9</volume><pages><last>53</last><first>45</first></pages><issn><json:string>0936-3076</json:string></issn><issue>1</issue><subject><json:item><value>Pharmacology/Toxicology</value></json:item><json:item><value>Psychiatry</value></json:item><json:item><value>Neurology</value></json:item></subject><journalId><json:string>722</json:string></journalId><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1435-1463</json:string></eissn><title>Journal of Neural Transmission - 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Parkinson's Disease and Dementia Section</title><title level="j" type="abbrev">J Neural Transm Gen Sect</title><idno type="JournalID">722</idno><idno type="pISSN">0936-3076</idno><idno type="eISSN">1435-1463</idno><idno type="IssueArticleCount">8</idno><idno type="VolumeIssueCount">3</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1995-02-01"></date><biblScope unit="volume">9</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="45">45</biblScope><biblScope unit="page" to="53">53</biblScope></imprint></monogr><idno type="istex">580E8356C3EC4678951DC05A1BD774683BB6EE3B</idno><idno type="DOI">10.1007/BF02252962</idno><idno type="ArticleID">Art4</idno><idno type="ArticleID">BF02252962</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994-09-12</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Though depletion of CSF homovanillic acid (HVA) concentration has often been regarded as a direct indicator of dopamine (DA) deficiency in Parkinson's Disease (PD), CSF HVA is normal in mildly affected patients. To explore why, we measured DA and its metabolites in striatum and CSF in rabbits receiving reserpine for 5 days. Reserpine, which depletes striatal DA by disrupting vesicular storage of the neurotransmitter, results in a compensatory increase of DA turnover. In response to a 96% depletion of striatal DA, its catabolic intermediates 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) decreased 64% and 92% in striatum, although the endproduct, HVA, was unchanged. In contrast, CSF concentrations of HVA and DOPAC increased significantly, though 3-MT and levodopa (LD) were unaltered. A 5-fold rise in striatal LD concentration after reserpine-induced DA depletion provided evidence for enhanced DA synthesis. As in PD, the compensatory increase of DA synthesis after reserpine administration confounds the ability of CSF HVA to reflect DA depletion.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Psychiatry</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-09-12">Created</change><change when="1995-02-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/580E8356C3EC4678951DC05A1BD774683BB6EE3B/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" 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and cerebrospinal fluid</ArticleTitle><ArticleCategory>Full Papers</ArticleCategory><ArticleFirstPage>45</ArticleFirstPage><ArticleLastPage>53</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>10</Month><Day>25</Day></RegistrationDate><Received><Year>1994</Year><Month>9</Month><Day>12</Day></Received><Accepted><Year>1994</Year><Month>10</Month><Day>21</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1995</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>722</JournalID><VolumeIDStart>9</VolumeIDStart><VolumeIDEnd>9</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>D.</GivenName><GivenName>A.</GivenName><FamilyName>Loeffler</FamilyName><Degrees>DVM, PhD</Degrees></AuthorName></Author><Author AffiliationIDS="Aff1 Aff2 Aff3"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><GivenName>A.</GivenName><FamilyName>LeWitt</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>A.</GivenName><GivenName>J.</GivenName><FamilyName>DeMaggio</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><GivenName>L.</GivenName><FamilyName>Juneau</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff5"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><GivenName>E.</GivenName><FamilyName>Milbury</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff5"><AuthorName DisplayOrder="Western"><GivenName>W.</GivenName><GivenName>R.</GivenName><FamilyName>Matson</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Clinical Neuroscience Laboratory, Research Building, Room 209</OrgDivision><OrgName>Sinai Hospital</OrgName><OrgAddress><Street>6767 West Outer Drive</Street><Postcode>48235</Postcode><City>Detroit</City><State>Michigan</State><Country>U.S.A.</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Departments of Neurology and Psychiatry</OrgDivision><OrgName>Wayne State University School of Medicine</OrgName><OrgAddress><City>Detroit</City><State>Michigan</State><Country>U.S.A.</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Cellular and Clinical Neuroscience Program</OrgDivision><OrgName>Wayne State University School of Medicine</OrgName><OrgAddress><City>Detroit</City><State>Michigan</State><Country>U.S.A.</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Preclinical Biometrics</OrgDivision><OrgName>Warner Lambert Company</OrgName><OrgAddress><City>Ann Arbor</City><State>Michigan</State><Country>U.S.A.</Country></OrgAddress></Affiliation><Affiliation ID="Aff5"><OrgName>ESA, Incorporated</OrgName><OrgAddress><City>Chelmsford</City><City>Massachusetts</City><Country>U.S.A.</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Though depletion of CSF homovanillic acid (HVA) concentration has often been regarded as a direct indicator of dopamine (DA) deficiency in Parkinson's Disease (PD), CSF HVA is normal in mildly affected patients. To explore why, we measured DA and its metabolites in striatum and CSF in rabbits receiving reserpine for 5 days. Reserpine, which depletes striatal DA by disrupting vesicular storage of the neurotransmitter, results in a compensatory increase of DA turnover. In response to a 96% depletion of striatal DA, its catabolic intermediates 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) decreased 64% and 92% in striatum, although the endproduct, HVA, was unchanged. In contrast, CSF concentrations of HVA and DOPAC increased significantly, though 3-MT and levodopa (LD) were unaltered. A 5-fold rise in striatal LD concentration after reserpine-induced DA depletion provided evidence for enhanced DA synthesis. As in PD, the compensatory increase of DA synthesis after reserpine administration confounds the ability of CSF HVA to reflect DA depletion.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Parkinson's disease</Keyword><Keyword>cerebrospinal fluid</Keyword><Keyword>dopamine</Keyword><Keyword>reserpine</Keyword><Keyword>homovanillic acid</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Markers of dopamine depletion and compensatory response in striatum and cerebrospinal fluid</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Markers of dopamine depletion and compensatory response in striatum and cerebrospinal fluid</title></titleInfo><name type="personal"><namePart type="given">D.</namePart><namePart type="given">A.</namePart><namePart type="family">Loeffler</namePart><namePart type="termsOfAddress">DVM, PhD</namePart><affiliation>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="given">A.</namePart><namePart type="family">LeWitt</namePart><affiliation>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</affiliation><affiliation>Departments of Neurology and Psychiatry, Wayne State University School of Medicine, Detroit, Michigan, U.S.A.</affiliation><affiliation>Cellular and Clinical Neuroscience Program, Wayne State University School of Medicine, Detroit, Michigan, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="given">J.</namePart><namePart type="family">DeMaggio</namePart><affiliation>Clinical Neuroscience Laboratory, Research Building, Room 209, Sinai Hospital, 6767 West Outer Drive, 48235, Detroit, Michigan, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="given">L.</namePart><namePart type="family">Juneau</namePart><affiliation>Preclinical Biometrics, Warner Lambert Company, Ann Arbor, Michigan, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="given">E.</namePart><namePart type="family">Milbury</namePart><affiliation>ESA, Incorporated, Chelmsford, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="given">R.</namePart><namePart type="family">Matson</namePart><affiliation>ESA, Incorporated, Chelmsford, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1994-09-12</dateCreated><dateIssued encoding="w3cdtf">1995-02-01</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Though depletion of CSF homovanillic acid (HVA) concentration has often been regarded as a direct indicator of dopamine (DA) deficiency in Parkinson's Disease (PD), CSF HVA is normal in mildly affected patients. To explore why, we measured DA and its metabolites in striatum and CSF in rabbits receiving reserpine for 5 days. Reserpine, which depletes striatal DA by disrupting vesicular storage of the neurotransmitter, results in a compensatory increase of DA turnover. In response to a 96% depletion of striatal DA, its catabolic intermediates 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) decreased 64% and 92% in striatum, although the endproduct, HVA, was unchanged. In contrast, CSF concentrations of HVA and DOPAC increased significantly, though 3-MT and levodopa (LD) were unaltered. A 5-fold rise in striatal LD concentration after reserpine-induced DA depletion provided evidence for enhanced DA synthesis. As in PD, the compensatory increase of DA synthesis after reserpine administration confounds the ability of CSF HVA to reflect DA depletion.</abstract><note>Full Papers</note><relatedItem type="host"><titleInfo><title>Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title></titleInfo><titleInfo type="abbreviated"><title>J Neural Transm Gen Sect</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1995-02-01</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pharmacology/Toxicology</topic><topic>Psychiatry</topic><topic>Neurology</topic></subject><identifier type="ISSN">0936-3076</identifier><identifier type="eISSN">1435-1463</identifier><identifier type="JournalID">722</identifier><identifier type="IssueArticleCount">8</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>1995</date><detail type="volume"><number>9</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="pages"><start>45</start><end>53</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1995</recordOrigin></recordInfo></relatedItem><identifier type="istex">580E8356C3EC4678951DC05A1BD774683BB6EE3B</identifier><identifier type="DOI">10.1007/BF02252962</identifier><identifier type="ArticleID">Art4</identifier><identifier type="ArticleID">BF02252962</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1995</recordOrigin></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/580E8356C3EC4678951DC05A1BD774683BB6EE3B/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct 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