Levodopa induces a cytoplasmic localization of D1 dopamine receptors in striatal neurons in Parkinson's disease
Identifieur interne : 001396 ( Main/Corpus ); précédent : 001395; suivant : 001397Levodopa induces a cytoplasmic localization of D1 dopamine receptors in striatal neurons in Parkinson's disease
Auteurs : Marie-Paule Muriel ; Véronique Bernard ; Allan I. Levey ; Ouahiba Laribi ; D. Nora Abrous ; Yves Agid ; Bertrand Bloch ; Etienne C. HirschSource :
- Annals of Neurology [ 0364-5134 ] ; 1999-07.
Abstract
Parkinson's disease is characterized by a massive loss of nigral dopamine neurons that results in a reduction of dopamine concentrations in the striatum. The most commonly used treatment for this disease is levodopa therapy to restore striatal dopamine. This treatment is mediated by dopamine receptors, but the effect of treatment and the disease on receptor distribution is unknown. In this study, the distribution of D1 dopamine receptors was analyzed at the cellular and subcellular level in the striatum of 5 patients with Parkinson's disease (all treated with levodopa) and 4 control subjects. In the control brains, D1 dopamine receptors were mostly detected on the plasma membrane of medium‐sized spiny neurons. The quantitative analysis performed at the ultrastructural level in patients with Parkinson's disease revealed an increase in immunostaining in the cytoplasm of medium‐sized neurons. This effect was likely the result of the treatment rather than the dopaminergic denervation, as such changes were not observed in the striatum of rats with a unilateral 6‐hydroxydopamine nigrostriatal lesion, but were present in normal or lesioned rats treated with a D1 dopamine agonist. Altered localization of D1 dopamine receptors may participate in the occurrence of side effects of levodopa therapy such as dyskinesia and fluctuations in motor performances. Ann Neurol 1999;46:103–111
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DOI: 10.1002/1531-8249(199907)46:1<103::AID-ANA15>3.0.CO;2-Z
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The most commonly used treatment for this disease is levodopa therapy to restore striatal dopamine. This treatment is mediated by dopamine receptors, but the effect of treatment and the disease on receptor distribution is unknown. In this study, the distribution of D1 dopamine receptors was analyzed at the cellular and subcellular level in the striatum of 5 patients with Parkinson's disease (all treated with levodopa) and 4 control subjects. In the control brains, D1 dopamine receptors were mostly detected on the plasma membrane of medium‐sized spiny neurons. The quantitative analysis performed at the ultrastructural level in patients with Parkinson's disease revealed an increase in immunostaining in the cytoplasm of medium‐sized neurons. This effect was likely the result of the treatment rather than the dopaminergic denervation, as such changes were not observed in the striatum of rats with a unilateral 6‐hydroxydopamine nigrostriatal lesion, but were present in normal or lesioned rats treated with a D1 dopamine agonist. Altered localization of D1 dopamine receptors may participate in the occurrence of side effects of levodopa therapy such as dyskinesia and fluctuations in motor performances. 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In the control brains, D1 dopamine receptors were mostly detected on the plasma membrane of medium‐sized spiny neurons. The quantitative analysis performed at the ultrastructural level in patients with Parkinson's disease revealed an increase in immunostaining in the cytoplasm of medium‐sized neurons. This effect was likely the result of the treatment rather than the dopaminergic denervation, as such changes were not observed in the striatum of rats with a unilateral 6‐hydroxydopamine nigrostriatal lesion, but were present in normal or lesioned rats treated with a D1 dopamine agonist. Altered localization of D1 dopamine receptors may participate in the occurrence of side effects of levodopa therapy such as dyskinesia and fluctuations in motor performances. 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This effect was likely the result of the treatment rather than the dopaminergic denervation, as such changes were not observed in the striatum of rats with a unilateral 6‐hydroxydopamine nigrostriatal lesion, but were present in normal or lesioned rats treated with a D1 dopamine agonist. Altered localization of D1 dopamine receptors may participate in the occurrence of side effects of levodopa therapy such as dyskinesia and fluctuations in motor performances. 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Nora</givenNames><familyName>Abrous</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yves</givenNames><familyName>Agid</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Bertrand</givenNames><familyName>Bloch</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Etienne C.</givenNames><familyName>Hirsch</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>Unité Mixte de Recherche Centre National de la Recherche Scientifique 5541, Laboratoire d'Histologie Embryologie, Université Victor Ségalen‐Bordeaux 2, Bordeaux, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Institut National de la Santé et de la Recherche Médicale U279 Institut Fédératif de Recherche en Neurosciences Cliniques et Expérimentales, Université Victor Ségalen‐Bordeaux 2, Bordeaux, France</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>INSERM</fundingAgency></fundingInfo><fundingInfo><fundingAgency>CNRS</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Parkinson Foundation, Miami, FL</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson's disease is characterized by a massive loss of nigral dopamine neurons that results in a reduction of dopamine concentrations in the striatum. The most commonly used treatment for this disease is levodopa therapy to restore striatal dopamine. This treatment is mediated by dopamine receptors, but the effect of treatment and the disease on receptor distribution is unknown. In this study, the distribution of D1 dopamine receptors was analyzed at the cellular and subcellular level in the striatum of 5 patients with Parkinson's disease (all treated with levodopa) and 4 control subjects. In the control brains, D1 dopamine receptors were mostly detected on the plasma membrane of medium‐sized spiny neurons. The quantitative analysis performed at the ultrastructural level in patients with Parkinson's disease revealed an increase in immunostaining in the cytoplasm of medium‐sized neurons. This effect was likely the result of the treatment rather than the dopaminergic denervation, as such changes were not observed in the striatum of rats with a unilateral 6‐hydroxydopamine nigrostriatal lesion, but were present in normal or lesioned rats treated with a D1 dopamine agonist. Altered localization of D1 dopamine receptors may participate in the occurrence of side effects of levodopa therapy such as dyskinesia and fluctuations in motor performances. Ann Neurol 1999;46:103–111</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Levodopa induces a cytoplasmic localization of D1 dopamine receptors in striatal neurons in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>D1 Receptors in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa induces a cytoplasmic localization of D1 dopamine receptors in striatal neurons in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Marie‐Paule</namePart><namePart type="family">Muriel</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Véronique</namePart><namePart type="family">Bernard</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Unité Mixte de Recherche Centre National de la Recherche Scientifique 5541, Laboratoire d'Histologie Embryologie, Université Victor Ségalen‐Bordeaux 2, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Allan I.</namePart><namePart type="family">Levey</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ouahiba</namePart><namePart type="family">Laribi</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Unité Mixte de Recherche Centre National de la Recherche Scientifique 5541, Laboratoire d'Histologie Embryologie, Université Victor Ségalen‐Bordeaux 2, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. Nora</namePart><namePart type="family">Abrous</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U279 Institut Fédératif de Recherche en Neurosciences Cliniques et Expérimentales, Université Victor Ségalen‐Bordeaux 2, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Agid</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bertrand</namePart><namePart type="family">Bloch</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Unité Mixte de Recherche Centre National de la Recherche Scientifique 5541, Laboratoire d'Histologie Embryologie, Université Victor Ségalen‐Bordeaux 2, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Etienne C.</namePart><namePart type="family">Hirsch</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, Paris, France</affiliation><description>Correspondence: INSERM U289, Höpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75631 Paris Cedex 13, France</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">1999-07</dateIssued><dateCaptured encoding="w3cdtf">1998-07-29</dateCaptured><dateValid encoding="w3cdtf">1999-02-26</dateValid><copyrightDate encoding="w3cdtf">1999</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">5</extent><extent unit="tables">2</extent><extent unit="references">35</extent><extent unit="words">5879</extent></physicalDescription><abstract lang="en">Parkinson's disease is characterized by a massive loss of nigral dopamine neurons that results in a reduction of dopamine concentrations in the striatum. The most commonly used treatment for this disease is levodopa therapy to restore striatal dopamine. This treatment is mediated by dopamine receptors, but the effect of treatment and the disease on receptor distribution is unknown. In this study, the distribution of D1 dopamine receptors was analyzed at the cellular and subcellular level in the striatum of 5 patients with Parkinson's disease (all treated with levodopa) and 4 control subjects. In the control brains, D1 dopamine receptors were mostly detected on the plasma membrane of medium‐sized spiny neurons. The quantitative analysis performed at the ultrastructural level in patients with Parkinson's disease revealed an increase in immunostaining in the cytoplasm of medium‐sized neurons. This effect was likely the result of the treatment rather than the dopaminergic denervation, as such changes were not observed in the striatum of rats with a unilateral 6‐hydroxydopamine nigrostriatal lesion, but were present in normal or lesioned rats treated with a D1 dopamine agonist. Altered localization of D1 dopamine receptors may participate in the occurrence of side effects of levodopa therapy such as dyskinesia and fluctuations in motor performances. 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