ParkinsonFranceV1, Hal, Corpus, bibRecord, 000091

Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia

Identifieur interne : 000091 ( Hal/Corpus ); précédent : 000090; suivant : 000092

Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia

Auteurs : Erwan Bézard ; Ana Mu Oz ; Elisabetta Tronci ; Elsa Y. Pioli ; Qin Li ; Gregory Porras ; Anders Björklund ; Manolo Carta

Source :

Clinical Neuroscience Research [ 1566-2772 ] ; 2013-12.

RBID : Hal:hal-01289966

Abstract

The serotonin system has emerged as a potential target for anti-dyskinetic therapy in Parkinson's disease. In fact, serotonin neurons can convert L-DOPA into dopamine, and mediate its synaptic release. However, they lack a feedback control mechanism able to regulate synaptic dopamine levels, which leads to un-physiological stimulation of post-synaptic striatal dopamine receptors. Accordingly, drugs able to dampen the activity of serotonin neurons can suppress L-DOPA-induced dyskinesia in animal models of Parkinson's disease. Here, we investigated the ability of the 5-HT1A/1B receptor agonist anpirtoline to counteract L-DOPA-induced dyskinesia in L-DOPA-primed 6-OHDA-lesioned rats and MPTP-treated macaques. Results suggest that anpirtoline dose-dependently reduced dyskinesia both in rats and monkeys; however, the effect in MPTP-treated macaques was accompanied by a worsening of the Parkinson's disease score at significantly effective doses (1.5 and 2.0mg/kg). At a lower dose (0.75mg/kg), anpirtoline markedly reduced dyskinesia in 4 out of 5 subjects, but statistical significance was prevented by the presence of a non-responsive subject. These results provide further evidence that the serotonin neurons contribute both to the pro-dyskinetic effect of L-DOPA and to its therapeutic efficacy in the rat and monkey models of Parkinson's disease.

Url:

https://hal.archives-ouvertes.fr/hal-01289966

DOI: 10.1016/j.neures.2013.10.002

Links to Exploration step

Hal:hal-01289966

Le document en format XML

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<front><div type="abstract" xml:lang="en">The serotonin system has emerged as a potential target for anti-dyskinetic therapy in Parkinson's disease. In fact, serotonin neurons can convert L-DOPA into dopamine, and mediate its synaptic release. However, they lack a feedback control mechanism able to regulate synaptic dopamine levels, which leads to un-physiological stimulation of post-synaptic striatal dopamine receptors. Accordingly, drugs able to dampen the activity of serotonin neurons can suppress L-DOPA-induced dyskinesia in animal models of Parkinson's disease. Here, we investigated the ability of the 5-HT1A/1B receptor agonist anpirtoline to counteract L-DOPA-induced dyskinesia in L-DOPA-primed 6-OHDA-lesioned rats and MPTP-treated macaques. Results suggest that anpirtoline dose-dependently reduced dyskinesia both in rats and monkeys; however, the effect in MPTP-treated macaques was accompanied by a worsening of the Parkinson's disease score at significantly effective doses (1.5 and 2.0mg/kg). At a lower dose (0.75mg/kg), anpirtoline markedly reduced dyskinesia in 4 out of 5 subjects, but statistical significance was prevented by the presence of a non-responsive subject. These results provide further evidence that the serotonin neurons contribute both to the pro-dyskinetic effect of L-DOPA and to its therapeutic efficacy in the rat and monkey models of Parkinson's disease. </div>
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            <author role="aut">              <persName>                <forename type="first">Gregory</forename>
                <surname>Porras</surname>
              </persName>
              <idno type="halauthorid">1061378</idno>
              <affiliation ref="#struct-244085"></affiliation>
            </author>
            <author role="aut">              <persName>                <forename type="first">Anders</forename>
                <surname>Björklund</surname>
              </persName>
              <idno type="halauthorid">1059979</idno>
              <affiliation ref="#struct-262353"></affiliation>
            </author>
            <author role="aut">              <persName>                <forename type="first">Manolo</forename>
                <surname>Carta</surname>
              </persName>
              <idno type="halauthorid">1190816</idno>
              <affiliation ref="#struct-452954"></affiliation>
            </author>
            <editor role="depositor">              <persName>                <forename>Chantal</forename>
                <surname>GUERIN</surname>
              </persName>
              <email type="md5">eb4bde61f74652335183b0bd05630b2c</email>
              <email type="domain">u-bordeaux.fr</email>
            </editor>
          </titleStmt>
          <editionStmt>            <edition n="v1" type="current">              <date type="whenSubmitted">2016-03-17 14:32:01</date>
              <date type="whenModified">2016-03-18 01:00:36</date>
              <date type="whenReleased">2016-03-17 14:32:01</date>
              <date type="whenProduced">2013-12</date>
            </edition>
            <respStmt>              <resp>contributor</resp>
              <name key="321070">                <persName>                  <forename>Chantal</forename>
                  <surname>GUERIN</surname>
                </persName>
                <email type="md5">eb4bde61f74652335183b0bd05630b2c</email>
                <email type="domain">u-bordeaux.fr</email>
              </name>
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            <idno type="halId">hal-01289966</idno>
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            <idno type="halBibtex">bezard:hal-01289966</idno>
            <idno type="halRefHtml">Clinical Neuroscience Research, Elsevier, 2013, 77 (4), <10.1016/j.neures.2013.10.002></idno>
            <idno type="halRef">Clinical Neuroscience Research, Elsevier, 2013, 77 (4), <10.1016/j.neures.2013.10.002></idno>
          </publicationStmt>
          <seriesStmt>            <idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno>
          </seriesStmt>
          <notesStmt>            <note type="audience" n="2">International</note>
            <note type="popular" n="0">No</note>
            <note type="peer" n="1">Yes</note>
          </notesStmt>
          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia</title>
                <author role="aut">                  <persName>                    <forename type="first">Erwan</forename>
                    <surname>Bézard</surname>
                  </persName>
                  <idno type="halauthorid">1063976</idno>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Ana</forename>
                    <surname>Muñoz</surname>
                  </persName>
                  <idno type="halauthorid">921866</idno>
                  <affiliation ref="#struct-452605"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Elisabetta</forename>
                    <surname>Tronci</surname>
                  </persName>
                  <idno type="halauthorid">1059977</idno>
                  <affiliation ref="#struct-452954"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Elsa Y.</forename>
                    <surname>Pioli</surname>
                  </persName>
                  <idno type="halauthorid">1059978</idno>
                  <affiliation ref="#struct-262347"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Qin</forename>
                    <surname>Li</surname>
                  </persName>
                  <idno type="halauthorid">224848</idno>
                  <affiliation ref="#struct-439125"></affiliation>
                  <affiliation ref="#struct-439190"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Gregory</forename>
                    <surname>Porras</surname>
                  </persName>
                  <idno type="halauthorid">1061378</idno>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Anders</forename>
                    <surname>Björklund</surname>
                  </persName>
                  <idno type="halauthorid">1059979</idno>
                  <affiliation ref="#struct-262353"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Manolo</forename>
                    <surname>Carta</surname>
                  </persName>
                  <idno type="halauthorid">1190816</idno>
                  <affiliation ref="#struct-452954"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">11803</idno>
                <idno type="issn">1566-2772</idno>
                <title level="j">Clinical Neuroscience Research</title>
                <imprint>                  <publisher>Elsevier</publisher>
                  <biblScope unit="volume">77</biblScope>
                  <biblScope unit="issue">4</biblScope>
                  <date type="datePub">2013-12</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1016/j.neures.2013.10.002</idno>
              <idno type="pubmed">24135129</idno>
            </biblStruct>
          </sourceDesc>
          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <classCode scheme="halDomain" n="sdv">Life Sciences [q-bio]</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">The serotonin system has emerged as a potential target for anti-dyskinetic therapy in Parkinson's disease. In fact, serotonin neurons can convert L-DOPA into dopamine, and mediate its synaptic release. However, they lack a feedback control mechanism able to regulate synaptic dopamine levels, which leads to un-physiological stimulation of post-synaptic striatal dopamine receptors. Accordingly, drugs able to dampen the activity of serotonin neurons can suppress L-DOPA-induced dyskinesia in animal models of Parkinson's disease. Here, we investigated the ability of the 5-HT1A/1B receptor agonist anpirtoline to counteract L-DOPA-induced dyskinesia in L-DOPA-primed 6-OHDA-lesioned rats and MPTP-treated macaques. Results suggest that anpirtoline dose-dependently reduced dyskinesia both in rats and monkeys; however, the effect in MPTP-treated macaques was accompanied by a worsening of the Parkinson's disease score at significantly effective doses (1.5 and 2.0mg/kg). At a lower dose (0.75mg/kg), anpirtoline markedly reduced dyskinesia in 4 out of 5 subjects, but statistical significance was prevented by the presence of a non-responsive subject. These results provide further evidence that the serotonin neurons contribute both to the pro-dyskinetic effect of L-DOPA and to its therapeutic efficacy in the rat and monkey models of Parkinson's disease. </abstract>
          </profileDesc>
        </hal>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia

Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia

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