ParkinsonFranceV1, Hal, Corpus, bibRecord, 000A48

Study of the antidyskinetic effect of eltoprazine in animal models of levodopa-induced dyskinesia.

Identifieur interne : 000A48 ( Hal/Corpus ); précédent : 000A47; suivant : 000A49

Study of the antidyskinetic effect of eltoprazine in animal models of levodopa-induced dyskinesia.

Auteurs : Erwan Bezard ; Elisabetta Tronci ; Elsa Y. Pioli ; Qin Li ; Gregory Porras ; Anders Björklund ; Manolo Carta

Source :

Movement Disorders [ 0885-3185 ] ; 2013-06-30.

RBID : Hal:hal-01290025

Abstract

The serotonin (5-hydroxytryptamine [5HT]) system has recently emerged as an important player in the appearance of l-3,4-dihydroxyphenylalanine (levodopa [l-dopa])-induced dyskinesia in animal models of Parkinson's disease. In fact, dopamine released as a false transmitter from serotonin neurons appears to contribute to the pulsatile stimulation of dopamine receptors, leading to the appearance of the abnormal involuntary movements. Thus, drugs able to dampen the activity of serotonin neurons hold promise for the treatment of dyskinesia. The authors investigated the ability of the mixed 5-HT 1A/1B receptor agonist eltoprazine to counteract l-dopa-induced dyskinesia in 6-hydroxydopamine-lesioned rats and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaques. The data demonstrated that eltoprazine is extremely effective in suppressing dyskinesia in experimental models, although this effect was accompanied by a partial worsening of the therapeutic effect of l-dopa. Interestingly, eltoprazine was found to (synergistically) potentiate the antidyskinetic effect of amantadine. The current data indicated that eltoprazine is highly effective in counteracting dyskinesia in preclinical models. However, the partial worsening of the l-dopa effect observed after eltoprazine administration represents a concern; whether this side effect is due to a limitation of the animal models or to an intrinsic property of eltoprazine needs to be addressed in ongoing clinical trials. The data also suggest that the combination of low doses of eltoprazine with amantadine may represent a valid strategy to increase the antidyskinetic effect and reduce the eltoprazine-induced worsening of l-dopa therapeutic effects.

Url:

https://hal.archives-ouvertes.fr/hal-01290025

DOI: 10.1002/mds.25366

Links to Exploration step

Hal:hal-01290025

Le document en format XML

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<front><div type="abstract" xml:lang="en">The serotonin (5-hydroxytryptamine [5HT]) system has recently emerged as an important player in the appearance of l-3,4-dihydroxyphenylalanine (levodopa [l-dopa])-induced dyskinesia in animal models of Parkinson's disease. In fact, dopamine released as a false transmitter from serotonin neurons appears to contribute to the pulsatile stimulation of dopamine receptors, leading to the appearance of the abnormal involuntary movements. Thus, drugs able to dampen the activity of serotonin neurons hold promise for the treatment of dyskinesia. The authors investigated the ability of the mixed 5-HT 1A/1B receptor agonist eltoprazine to counteract l-dopa-induced dyskinesia in 6-hydroxydopamine-lesioned rats and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaques. The data demonstrated that eltoprazine is extremely effective in suppressing dyskinesia in experimental models, although this effect was accompanied by a partial worsening of the therapeutic effect of l-dopa. Interestingly, eltoprazine was found to (synergistically) potentiate the antidyskinetic effect of amantadine. The current data indicated that eltoprazine is highly effective in counteracting dyskinesia in preclinical models. However, the partial worsening of the l-dopa effect observed after eltoprazine administration represents a concern; whether this side effect is due to a limitation of the animal models or to an intrinsic property of eltoprazine needs to be addressed in ongoing clinical trials. The data also suggest that the combination of low doses of eltoprazine with amantadine may represent a valid strategy to increase the antidyskinetic effect and reduce the eltoprazine-induced worsening of l-dopa therapeutic effects.</div>
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              <name key="321070">                <persName>                  <forename>Chantal</forename>
                  <surname>GUERIN</surname>
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                <email type="domain">u-bordeaux.fr</email>
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            <idno type="halId">hal-01290025</idno>
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            <idno type="halBibtex">bezard:hal-01290025</idno>
            <idno type="halRefHtml">Movement Disorders, Wiley, 2013, 28 (8), pp.1088-96. <10.1002/mds.25366></idno>
            <idno type="halRef">Movement Disorders, Wiley, 2013, 28 (8), pp.1088-96. <10.1002/mds.25366></idno>
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          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">Study of the antidyskinetic effect of eltoprazine in animal models of levodopa-induced dyskinesia.</title>
                <author role="aut">                  <persName>                    <forename type="first">Erwan</forename>
                    <surname>Bezard</surname>
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                  <idno type="halauthorid">537314</idno>
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                </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>
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                </author>
                <author role="aut">                  <persName>                    <forename type="first">Qin</forename>
                    <surname>Li</surname>
                  </persName>
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                  <affiliation ref="#struct-439190"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Gregory</forename>
                    <surname>Porras</surname>
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                  <idno type="halauthorid">1061378</idno>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Anders</forename>
                    <surname>Björklund</surname>
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                  <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>
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                <idno type="issn">0885-3185</idno>
                <idno type="eissn">1531-8257</idno>
                <title level="j">Movement Disorders</title>
                <imprint>                  <publisher>Wiley</publisher>
                  <biblScope unit="volume">28</biblScope>
                  <biblScope unit="issue">8</biblScope>
                  <biblScope unit="pp">1088-96</biblScope>
                  <date type="datePub">2013-06-30</date>
                </imprint>
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              <idno type="doi">10.1002/mds.25366</idno>
              <idno type="pubmed">23389842</idno>
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            <abstract xml:lang="en">The serotonin (5-hydroxytryptamine [5HT]) system has recently emerged as an important player in the appearance of l-3,4-dihydroxyphenylalanine (levodopa [l-dopa])-induced dyskinesia in animal models of Parkinson's disease. In fact, dopamine released as a false transmitter from serotonin neurons appears to contribute to the pulsatile stimulation of dopamine receptors, leading to the appearance of the abnormal involuntary movements. Thus, drugs able to dampen the activity of serotonin neurons hold promise for the treatment of dyskinesia. The authors investigated the ability of the mixed 5-HT 1A/1B receptor agonist eltoprazine to counteract l-dopa-induced dyskinesia in 6-hydroxydopamine-lesioned rats and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaques. The data demonstrated that eltoprazine is extremely effective in suppressing dyskinesia in experimental models, although this effect was accompanied by a partial worsening of the therapeutic effect of l-dopa. Interestingly, eltoprazine was found to (synergistically) potentiate the antidyskinetic effect of amantadine. The current data indicated that eltoprazine is highly effective in counteracting dyskinesia in preclinical models. However, the partial worsening of the l-dopa effect observed after eltoprazine administration represents a concern; whether this side effect is due to a limitation of the animal models or to an intrinsic property of eltoprazine needs to be addressed in ongoing clinical trials. The data also suggest that the combination of low doses of eltoprazine with amantadine may represent a valid strategy to increase the antidyskinetic effect and reduce the eltoprazine-induced worsening of l-dopa therapeutic effects.</abstract>
          </profileDesc>
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	La maladie de Parkinson en France (serveur d'exploration)
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Study of the antidyskinetic effect of eltoprazine in animal models of levodopa-induced dyskinesia.

Study of the antidyskinetic effect of eltoprazine in animal models of levodopa-induced dyskinesia.

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