Lack of change in striatal DARPP-32 levels following nigrostriatal dopaminergic lesions in animals and in parkinsonian syndromes in man
Identifieur interne : 002F80 ( Main/Corpus ); précédent : 002F79; suivant : 002F81Lack of change in striatal DARPP-32 levels following nigrostriatal dopaminergic lesions in animals and in parkinsonian syndromes in man
Auteurs : R. Raisman-Vozari ; J.-A. Girault ; S. Moussaoui ; C. Feuerstein ; P. Jenner ; C. D. Marsden ; Y. AgidSource :
- Brain Research [ 0006-8993 ] ; 1989.
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Abstract
The present study was performed to determine the effect of a nearly complete nigrostriatal dopaminergic denervation on DARPP-32 levels in the striatum from animals and parkinsonian patients. DARPP-32 levels were estimated by in vitro phosphorylation in the presence of cAMP, or after inactivation of endogenous kinases and phosphatases, in the presence of the catalytic subunit of cAMP-dependent protein kinase. Intranigral 6-hydroxydopamine (6-OHDA) infusion in rats, or peripheral administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets, did not change striatal DARPP-32 levels. Postmortem studies, carried out on brains obtained shortly after death, from patients with Parkinson disease, or from patients with progressive supranuclear palsy, showed that the levels of striatal DARPP-32 were not different from controls. These results indicate that dopaminergic striatal denervation did not modify the amount of DARPP-32 in the striatum, suggesting that the expression of DARPP-32, a protein which mediates some of the effects of dopamine in striatal neurons, is independent from the dopaminergic innervation.
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DOI: 10.1016/0006-8993(90)90520-L
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Moussaoui</name><affiliation><mods:affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</mods:affiliation></affiliation></author><author><name sortKey="Feuerstein, C" sort="Feuerstein, C" uniqKey="Feuerstein C" first="C." last="Feuerstein">C. Feuerstein</name><affiliation><mods:affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</mods:affiliation></affiliation></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P." last="Jenner">P. 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Agid</name><affiliation><mods:affiliation>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:FE34E2B9547A365626A3AD65A8E4BEAA74087A3B</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1016/0006-8993(90)90520-L</idno><idno type="url">https://api.istex.fr/document/FE34E2B9547A365626A3AD65A8E4BEAA74087A3B/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002F80</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Lack of change in striatal DARPP-32 levels following nigrostriatal dopaminergic lesions in animals and in parkinsonian syndromes in man</title><author><name sortKey="Raisman Vozari, R" sort="Raisman Vozari, R" uniqKey="Raisman Vozari R" first="R." last="Raisman-Vozari">R. Raisman-Vozari</name><affiliation><mods:affiliation>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</mods:affiliation></affiliation></author><author><name sortKey="Girault, J A" sort="Girault, J A" uniqKey="Girault J" first="J.-A." last="Girault">J.-A. Girault</name><affiliation><mods:affiliation>Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021 U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Moussaoui, S" sort="Moussaoui, S" uniqKey="Moussaoui S" first="S." last="Moussaoui">S. Moussaoui</name><affiliation><mods:affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</mods:affiliation></affiliation></author><author><name sortKey="Feuerstein, C" sort="Feuerstein, C" uniqKey="Feuerstein C" first="C." last="Feuerstein">C. Feuerstein</name><affiliation><mods:affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</mods:affiliation></affiliation></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P." last="Jenner">P. Jenner</name><affiliation><mods:affiliation>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</mods:affiliation></affiliation></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><affiliation><mods:affiliation>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. Agid</name><affiliation><mods:affiliation>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989">1989</date><biblScope unit="volume">507</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="45">45</biblScope><biblScope unit="page" to="50">50</biblScope></imprint><idno type="ISSN">0006-8993</idno></series><idno type="istex">FE34E2B9547A365626A3AD65A8E4BEAA74087A3B</idno><idno type="DOI">10.1016/0006-8993(90)90520-L</idno><idno type="PII">0006-8993(90)90520-L</idno><idno type="ArticleID">9090520L</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>DARPP-32</term><term>Dopaminergic lesion</term><term>Parkinson</term><term>Phosphoprotein</term><term>Striatum</term><term>Tyrosine hydroxylase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The present study was performed to determine the effect of a nearly complete nigrostriatal dopaminergic denervation on DARPP-32 levels in the striatum from animals and parkinsonian patients. DARPP-32 levels were estimated by in vitro phosphorylation in the presence of cAMP, or after inactivation of endogenous kinases and phosphatases, in the presence of the catalytic subunit of cAMP-dependent protein kinase. Intranigral 6-hydroxydopamine (6-OHDA) infusion in rats, or peripheral administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets, did not change striatal DARPP-32 levels. Postmortem studies, carried out on brains obtained shortly after death, from patients with Parkinson disease, or from patients with progressive supranuclear palsy, showed that the levels of striatal DARPP-32 were not different from controls. These results indicate that dopaminergic striatal denervation did not modify the amount of DARPP-32 in the striatum, suggesting that the expression of DARPP-32, a protein which mediates some of the effects of dopamine in striatal neurons, is independent from the dopaminergic innervation.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>R. Raisman-Vozari</name><affiliations><json:string>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</json:string></affiliations></json:item><json:item><name>J.-A. Girault</name><affiliations><json:string>Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021 U.S.A.</json:string></affiliations></json:item><json:item><name>S. Moussaoui</name><affiliations><json:string>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</json:string></affiliations></json:item><json:item><name>C. Feuerstein</name><affiliations><json:string>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</json:string></affiliations></json:item><json:item><name>P. Jenner</name><affiliations><json:string>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</json:string></affiliations></json:item><json:item><name>C.D. Marsden</name><affiliations><json:string>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</json:string></affiliations></json:item><json:item><name>Y. Agid</name><affiliations><json:string>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>DARPP-32</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Tyrosine hydroxylase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Phosphoprotein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Striatum</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopaminergic lesion</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</value></json:item></subject><articleId><json:string>9090520L</json:string></articleId><language><json:string>eng</json:string></language><abstract>The present study was performed to determine the effect of a nearly complete nigrostriatal dopaminergic denervation on DARPP-32 levels in the striatum from animals and parkinsonian patients. DARPP-32 levels were estimated by in vitro phosphorylation in the presence of cAMP, or after inactivation of endogenous kinases and phosphatases, in the presence of the catalytic subunit of cAMP-dependent protein kinase. Intranigral 6-hydroxydopamine (6-OHDA) infusion in rats, or peripheral administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets, did not change striatal DARPP-32 levels. Postmortem studies, carried out on brains obtained shortly after death, from patients with Parkinson disease, or from patients with progressive supranuclear palsy, showed that the levels of striatal DARPP-32 were not different from controls. These results indicate that dopaminergic striatal denervation did not modify the amount of DARPP-32 in the striatum, suggesting that the expression of DARPP-32, a protein which mediates some of the effects of dopamine in striatal neurons, is independent from the dopaminergic innervation.</abstract><qualityIndicators><score>6.896</score><pdfVersion>1.3</pdfVersion><pdfPageSize>591 x 814 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1160</abstractCharCount><pdfWordCount>6093</pdfWordCount><pdfCharCount>25394</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>158</abstractWordCount></qualityIndicators><title>Lack of change in striatal DARPP-32 levels following nigrostriatal dopaminergic lesions in animals and in parkinsonian syndromes in man</title><pii><json:string>0006-8993(90)90520-L</json:string></pii><genre><json:string>brief communication</json:string></genre><serie><volume>89</volume><pages><last>2497</last><first>2493</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Proc. 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Raisman, Laboratoire de Me´decine Expe´rimentale, INSERM U 289, Hoˆpital de la Salpeˆtrie`re, 47 boulevard de l'Hoˆpital, 75651 Paris Cedex 13, France.</p></note><affiliation>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</affiliation></author><author><persName><forename type="first">J.-A.</forename><surname>Girault</surname></persName><affiliation>Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021 U.S.A.</affiliation></author><author><persName><forename type="first">S.</forename><surname>Moussaoui</surname></persName><affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</affiliation></author><author><persName><forename type="first">C.</forename><surname>Feuerstein</surname></persName><affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</affiliation></author><author><persName><forename type="first">P.</forename><surname>Jenner</surname></persName><affiliation>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</affiliation></author><author><persName><forename type="first">C.D.</forename><surname>Marsden</surname></persName><affiliation>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</affiliation></author><author><persName><forename type="first">Y.</forename><surname>Agid</surname></persName><affiliation>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, 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)X0534-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989"></date><biblScope unit="volume">507</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="45">45</biblScope><biblScope unit="page" to="50">50</biblScope></imprint></monogr><idno type="istex">FE34E2B9547A365626A3AD65A8E4BEAA74087A3B</idno><idno type="DOI">10.1016/0006-8993(90)90520-L</idno><idno type="PII">0006-8993(90)90520-L</idno><idno type="ArticleID">9090520L</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1990</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The present study was performed to determine the effect of a nearly complete nigrostriatal dopaminergic denervation on DARPP-32 levels in the striatum from animals and parkinsonian patients. DARPP-32 levels were estimated by in vitro phosphorylation in the presence of cAMP, or after inactivation of endogenous kinases and phosphatases, in the presence of the catalytic subunit of cAMP-dependent protein kinase. Intranigral 6-hydroxydopamine (6-OHDA) infusion in rats, or peripheral administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets, did not change striatal DARPP-32 levels. Postmortem studies, carried out on brains obtained shortly after death, from patients with Parkinson disease, or from patients with progressive supranuclear palsy, showed that the levels of striatal DARPP-32 were not different from controls. These results indicate that dopaminergic striatal denervation did not modify the amount of DARPP-32 in the striatum, suggesting that the expression of DARPP-32, a protein which mediates some of the effects of dopamine in striatal neurons, is independent from the dopaminergic innervation.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>DARPP-32</term></item><item><term>Tyrosine hydroxylase</term></item><item><term>Phosphoprotein</term></item><item><term>Parkinson</term></item><item><term>Striatum</term></item><item><term>Dopaminergic lesion</term></item><item><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1989-06-13">Registration</change><change when="1989">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"></istex:docType><istex:document><article version="5.0" xml:lang="en" docsubtype="sco"><item-info><jid>BRES</jid><aid>9090520L</aid><ce:pii>0006-8993(90)90520-L</ce:pii><ce:doi>10.1016/0006-8993(90)90520-L</ce:doi><ce:copyright type="unknown" year="1990">Elsevier Science Publishers B.V.</ce:copyright></item-info><head><ce:title>Lack of change in striatal DARPP-32 levels following nigrostriatal dopaminergic lesions in animals and in parkinsonian syndromes in man</ce:title><ce:author-group><ce:author><ce:given-name>R.</ce:given-name><ce:surname>Raisman-Vozari</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">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.-A.</ce:given-name><ce:surname>Girault</ce:surname><ce:cross-ref refid="aff2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>S.</ce:given-name><ce:surname>Moussaoui</ce:surname><ce:cross-ref refid="aff3"><ce:sup loc="post">3</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>C.</ce:given-name><ce:surname>Feuerstein</ce:surname><ce:cross-ref refid="aff3"><ce:sup loc="post">3</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.</ce:given-name><ce:surname>Jenner</ce:surname><ce:cross-ref refid="aff4"><ce:sup loc="post">4</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>C.D.</ce:given-name><ce:surname>Marsden</ce:surname><ce:cross-ref refid="aff4"><ce:sup loc="post">4</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Y.</ce:given-name><ce:surname>Agid</ce:surname><ce:cross-ref refid="aff1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="aff1"><ce:label>a</ce:label><ce:textfn>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</ce:textfn></ce:affiliation><ce:affiliation id="aff2"><ce:label>b</ce:label><ce:textfn>Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021 U.S.A.</ce:textfn></ce:affiliation><ce:affiliation id="aff3"><ce:label>c</ce:label><ce:textfn>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</ce:textfn></ce:affiliation><ce:affiliation id="aff4"><ce:label>d</ce:label><ce:textfn>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text><ce:italic>Correspondence:</ce:italic> R. Raisman, Laboratoire de Me´decine Expe´rimentale, INSERM U 289, Hoˆpital de la Salpeˆtrie`re, 47 boulevard de l'Hoˆpital, 75651 Paris Cedex 13, France.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="13" month="6" year="1989"></ce:date-accepted><ce:abstract id="ab1" class="author" xml:lang="en"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">The present study was performed to determine the effect of a nearly complete nigrostriatal dopaminergic denervation on DARPP-32 levels in the striatum from animals and parkinsonian patients. DARPP-32 levels were estimated by in vitro phosphorylation in the presence of cAMP, or after inactivation of endogenous kinases and phosphatases, in the presence of the catalytic subunit of cAMP-dependent protein kinase. Intranigral 6-hydroxydopamine (6-OHDA) infusion in rats, or peripheral administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets, did not change striatal DARPP-32 levels. Postmortem studies, carried out on brains obtained shortly after death, from patients with Parkinson disease, or from patients with progressive supranuclear palsy, showed that the levels of striatal DARPP-32 were not different from controls. These results indicate that dopaminergic striatal denervation did not modify the amount of DARPP-32 in the striatum, suggesting that the expression of DARPP-32, a protein which mediates some of the effects of dopamine in striatal neurons, is independent from the dopaminergic innervation.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>DARPP-32</ce:text></ce:keyword><ce:keyword><ce:text>Tyrosine hydroxylase</ce:text></ce:keyword><ce:keyword><ce:text>Phosphoprotein</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson</ce:text></ce:keyword><ce:keyword><ce:text>Striatum</ce:text></ce:keyword><ce:keyword><ce:text>Dopaminergic lesion</ce:text></ce:keyword><ce:keyword><ce:text>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</ce:text></ce:keyword></ce:keywords></head><tail view="all"><ce:bibliography view="all" id="bibliography.0010"><ce:section-title>Reference</ce:section-title><ce:bibliography-sec id="bibliography-sec.0010"><ce:bib-reference id="bib1"><ce:label>1</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Cash</ce:surname><ce:given-name>R.</ce:given-name></sb:author><sb:author><ce:surname>Raisman</ce:surname><ce:given-name>R.</ce:given-name></sb:author><sb:author><ce:surname>Cervera</ce:surname><ce:given-name>P.</ce:given-name></sb:author><sb:author><ce:surname>Javoy-Agid</ce:surname><ce:given-name>F.</ce:given-name></sb:author><sb:author><ce:surname>Agid</ce:surname><ce:given-name>Y.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Pitfalls in membrane binding sites studies in postmortem human brain</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>J. 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Pharmacol.</sb:maintitle></sb:title><sb:volume-nr>10</sb:volume-nr></sb:series><sb:date>1974</sb:date></sb:issue><sb:pages><sb:first-page>725</sb:first-page><sb:last-page>735</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference></ce:bibliography-sec></ce:bibliography></tail></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Lack of change in striatal DARPP-32 levels following nigrostriatal dopaminergic lesions in animals and in parkinsonian syndromes in man</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Lack of change in striatal DARPP-32 levels following nigrostriatal dopaminergic lesions in animals and in parkinsonian syndromes in man</title></titleInfo><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Raisman-Vozari</namePart><affiliation>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, Paris France</affiliation><description>Correspondence: R. Raisman, Laboratoire de Me´decine Expe´rimentale, INSERM U 289, Hoˆpital de la Salpeˆtrie`re, 47 boulevard de l'Hoˆpital, 75651 Paris Cedex 13, France.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.-A.</namePart><namePart type="family">Girault</namePart><affiliation>Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021 U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Moussaoui</namePart><affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Feuerstein</namePart><affiliation>INSERM U 318, Laboratoire de Physiologie, Section Neurophysiologie, De´partement des Neurosciences Cliniques et Biologiques, CHU de Grenoble, Grenoble France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Jenner</namePart><affiliation>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.D.</namePart><namePart type="family">Marsden</namePart><affiliation>Parkinson's Disease Society Research Center, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, London U.K.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Agid</namePart><affiliation>INSERM U 289, CHU Pitie´-Salpeˆtrie`re, 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">1989</dateIssued><dateValid encoding="w3cdtf">1989-06-13</dateValid><copyrightDate encoding="w3cdtf">1990</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 present study was performed to determine the effect of a nearly complete nigrostriatal dopaminergic denervation on DARPP-32 levels in the striatum from animals and parkinsonian patients. DARPP-32 levels were estimated by in vitro phosphorylation in the presence of cAMP, or after inactivation of endogenous kinases and phosphatases, in the presence of the catalytic subunit of cAMP-dependent protein kinase. Intranigral 6-hydroxydopamine (6-OHDA) infusion in rats, or peripheral administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets, did not change striatal DARPP-32 levels. Postmortem studies, carried out on brains obtained shortly after death, from patients with Parkinson disease, or from patients with progressive supranuclear palsy, showed that the levels of striatal DARPP-32 were not different from controls. These results indicate that dopaminergic striatal denervation did not modify the amount of DARPP-32 in the striatum, suggesting that the expression of DARPP-32, a protein which mediates some of the effects of dopamine in striatal neurons, is independent from the dopaminergic innervation.</abstract><subject lang="en"><genre>Keywords</genre><topic>DARPP-32</topic><topic>Tyrosine hydroxylase</topic><topic>Phosphoprotein</topic><topic>Parkinson</topic><topic>Striatum</topic><topic>Dopaminergic lesion</topic><topic>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</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">19900115</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X0534-3</identifier><part><detail type="volume"><number>507</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>180</end></extent><extent unit="pages"><start>45</start><end>50</end></extent></part></relatedItem><identifier type="istex">FE34E2B9547A365626A3AD65A8E4BEAA74087A3B</identifier><identifier type="DOI">10.1016/0006-8993(90)90520-L</identifier><identifier type="PII">0006-8993(90)90520-L</identifier><identifier type="ArticleID">9090520L</identifier><accessCondition type="use and reproduction" contentType="">© 1990Elsevier Science Publishers B.V.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science Publishers B.V., ©1990</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/FE34E2B9547A365626A3AD65A8E4BEAA74087A3B/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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