Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease
Identifieur interne : 002626 ( Main/Corpus ); précédent : 002625; suivant : 002627Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease
Auteurs : Cristina M. B Ckman ; Lufei Shan ; Yajun Zhang ; Barry J. Hoffer ; Andreas C. TomacSource :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2007-03.
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Abstract
A real‐time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67‐kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA‐specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes‐3‐phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, β‐peptide 2‐like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging. © 2007 Wiley‐Liss, Inc.
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DOI: 10.1002/jnr.21164
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B Ckman</name><affiliation><mods:affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Shan, Lufei" sort="Shan, Lufei" uniqKey="Shan L" first="Lufei" last="Shan">Lufei Shan</name><affiliation><mods:affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Zhang, Yajun" sort="Zhang, Yajun" uniqKey="Zhang Y" first="Yajun" last="Zhang">Yajun Zhang</name><affiliation><mods:affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Hoffer, Barry J" sort="Hoffer, Barry J" uniqKey="Hoffer B" first="Barry J." last="Hoffer">Barry J. 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Hoffer</name><affiliation><mods:affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Tomac, Andreas C" sort="Tomac, Andreas C" uniqKey="Tomac A" first="Andreas C." last="Tomac">Andreas C. Tomac</name><affiliation><mods:affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-03">2007-03</date><biblScope unit="volume">85</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="798">798</biblScope><biblScope unit="page" to="804">804</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">3EBA8EF86DE410CDCBD926C7A23C6A36C970F290</idno><idno type="DOI">10.1002/jnr.21164</idno><idno type="ArticleID">JNR21164</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>dynorphin</term><term>enkephalin</term><term>human</term><term>midbrain</term><term>post‐mortem</term><term>striatum</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A real‐time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67‐kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA‐specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes‐3‐phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, β‐peptide 2‐like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging. © 2007 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Cristina M. Bäckman</name><affiliations><json:string>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</json:string></affiliations></json:item><json:item><name>Lufei Shan</name><affiliations><json:string>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</json:string></affiliations></json:item><json:item><name>YaJun Zhang</name><affiliations><json:string>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</json:string></affiliations></json:item><json:item><name>Barry J. Hoffer</name><affiliations><json:string>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</json:string></affiliations></json:item><json:item><name>Andreas C. Tomac</name><affiliations><json:string>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>enkephalin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dynorphin</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>post‐mortem</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>midbrain</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>striatum</value></json:item></subject><articleId><json:string>JNR21164</json:string></articleId><language><json:string>eng</json:string></language><abstract>A real‐time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67‐kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA‐specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes‐3‐phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, β‐peptide 2‐like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging. © 2007 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.591</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1679</abstractCharCount><pdfWordCount>4639</pdfWordCount><pdfCharCount>29567</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>246</abstractWordCount></qualityIndicators><title>Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>85</volume><publisherId><json:string>JNR</json:string></publisherId><pages><total>7</total><last>804</last><first>798</first></pages><issn><json:string>0360-4012</json:string></issn><issue>4</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1097-4547</json:string></eissn><title>Journal of Neuroscience Research</title><doi><json:string>10.1002/(ISSN)1097-4547</json:string></doi></host><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1002/jnr.21164</json:string></doi><id>3EBA8EF86DE410CDCBD926C7A23C6A36C970F290</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/3EBA8EF86DE410CDCBD926C7A23C6A36C970F290/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/3EBA8EF86DE410CDCBD926C7A23C6A36C970F290/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3EBA8EF86DE410CDCBD926C7A23C6A36C970F290/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2007</date></publicationStmt><notesStmt><note type="content">*This article is a US Government work and, as such, is in the public domain in the United States of America.</note><note>Intramural Research Program of the NIDA, NIH</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease</title><author><persName><forename type="first">Cristina M.</forename><surname>Bäckman</surname></persName><note type="correspondence"><p>Correspondence: Cellular Neurobiology Section, National Institute on Drug Abuse, 5500 Nathan Shock Drive, Baltimore, MD 21224</p></note><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation></author><author><persName><forename type="first">Lufei</forename><surname>Shan</surname></persName><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation></author><author><persName><forename type="first">YaJun</forename><surname>Zhang</surname></persName><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation></author><author><persName><forename type="first">Barry J.</forename><surname>Hoffer</surname></persName><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation></author><author><persName><forename type="first">Andreas C.</forename><surname>Tomac</surname></persName><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation></author></analytic><monogr><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. Res.</title><idno type="pISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><idno type="DOI">10.1002/(ISSN)1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-03"></date><biblScope unit="volume">85</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="798">798</biblScope><biblScope unit="page" to="804">804</biblScope></imprint></monogr><idno type="istex">3EBA8EF86DE410CDCBD926C7A23C6A36C970F290</idno><idno type="DOI">10.1002/jnr.21164</idno><idno type="ArticleID">JNR21164</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>A real‐time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67‐kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA‐specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes‐3‐phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, β‐peptide 2‐like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging. © 2007 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>enkephalin</term></item><item><term>dynorphin</term></item><item><term>human</term></item><item><term>post‐mortem</term></item><item><term>midbrain</term></item><item><term>striatum</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-09-19">Received</change><change when="2006-11-01">Registration</change><change when="2007-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3EBA8EF86DE410CDCBD926C7A23C6A36C970F290/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4547</doi><issn type="print">0360-4012</issn><issn type="electronic">1097-4547</issn><idGroup><id type="product" value="JNR"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF NEUROSCIENCE RESEARCH">Journal of Neuroscience Research</title><title type="short">J. 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Res.</title></titleGroup></publicationMeta><publicationMeta level="part" position="40"><doi origin="wiley" registered="yes">10.1002/jnr.v85:4</doi><numberingGroup><numbering type="journalVolume" number="85">85</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="2007-03">March 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jnr.21164</doi><idGroup><id type="unit" value="JNR21164"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="restricted">Copyright © 2007 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2006-09-19"></event><event type="manuscriptRevised" date="2006-11-01"></event><event type="manuscriptAccepted" date="2006-11-01"></event><event type="publishedOnlineEarlyUnpaginated" date="2007-01-03"></event><event type="firstOnline" date="2007-01-03"></event><event type="publishedOnlineFinalForm" date="2007-02-14"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-15"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-31"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst">798</numbering><numbering type="pageLast">804</numbering></numberingGroup><correspondenceTo>Cellular Neurobiology Section, National Institute on Drug Abuse, 5500 Nathan Shock Drive, Baltimore, MD 21224</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JNR.JNR21164.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="32"></count><count type="wordTotal" number="6061"></count></countGroup><titleGroup><title type="main" xml:lang="en">Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease<link href="#fn3"></link></title><title type="short" xml:lang="en">Neuropeptide mRNA Levels in the Aged Human Putamen</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Cristina M.</givenNames><familyName>Bäckman</familyName></personName><contactDetails><email>cbackman@mail.nih.gov</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Lufei</givenNames><familyName>Shan</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>YaJun</givenNames><familyName>Zhang</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Barry J.</givenNames><familyName>Hoffer</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Andreas C.</givenNames><familyName>Tomac</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">enkephalin</keyword><keyword xml:id="kwd2">dynorphin</keyword><keyword xml:id="kwd3">human</keyword><keyword xml:id="kwd4">post‐mortem</keyword><keyword xml:id="kwd5">midbrain</keyword><keyword xml:id="kwd6">striatum</keyword></keywordGroup><fundingInfo><fundingAgency>Intramural Research Program of the NIDA, NIH</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>A real‐time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67‐kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA‐specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes‐3‐phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, β‐peptide 2‐like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging. © 2007 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn3"><p>This article is a US Government work and, as such, is in the public domain in the United States of America.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Neuropeptide mRNA Levels in the Aged Human Putamen</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Cristina M.</namePart><namePart type="family">Bäckman</namePart><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation><description>Correspondence: Cellular Neurobiology Section, National Institute on Drug Abuse, 5500 Nathan Shock Drive, Baltimore, MD 21224</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lufei</namePart><namePart type="family">Shan</namePart><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YaJun</namePart><namePart type="family">Zhang</namePart><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Barry J.</namePart><namePart type="family">Hoffer</namePart><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andreas C.</namePart><namePart type="family">Tomac</namePart><affiliation>Cellular Neurobiology Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-03</dateIssued><dateCaptured encoding="w3cdtf">2006-09-19</dateCaptured><dateValid encoding="w3cdtf">2006-11-01</dateValid><copyrightDate encoding="w3cdtf">2007</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">4</extent><extent unit="tables">2</extent><extent unit="references">32</extent><extent unit="words">6061</extent></physicalDescription><abstract lang="en">A real‐time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67‐kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA‐specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes‐3‐phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, β‐peptide 2‐like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging. © 2007 Wiley‐Liss, Inc.</abstract><note type="content">*This article is a US Government work and, as such, is in the public domain in the United States of America.</note><note type="funding">Intramural Research Program of the NIDA, NIH</note><subject lang="en"><genre>Keywords</genre><topic>enkephalin</topic><topic>dynorphin</topic><topic>human</topic><topic>post‐mortem</topic><topic>midbrain</topic><topic>striatum</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroscience Research</title></titleInfo><titleInfo type="abbreviated"><title>J. Neurosci. Res.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0360-4012</identifier><identifier type="eISSN">1097-4547</identifier><identifier type="DOI">10.1002/(ISSN)1097-4547</identifier><identifier type="PublisherID">JNR</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>85</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>798</start><end>804</end><total>7</total></extent></part></relatedItem><identifier type="istex">3EBA8EF86DE410CDCBD926C7A23C6A36C970F290</identifier><identifier type="DOI">10.1002/jnr.21164</identifier><identifier type="ArticleID">JNR21164</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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