Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia.
Identifieur interne : 000662 ( PubMed/Corpus ); précédent : 000661; suivant : 000663Anti-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 CartaSource :
- Neuroscience research [ 1872-8111 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Dyskinesia, Drug-Induced (drug therapy), Female, Levodopa (adverse effects), Macaca fascicularis, Parkinsonian Disorders (drug therapy), Piperidines (therapeutic use), Pyridines (therapeutic use), Rats, Rats, Sprague-Dawley, Serotonin 5-HT1 Receptor Agonists (therapeutic use).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- drug therapy : Dyskinesia, Drug-Induced, Parkinsonian Disorders.
- chemical , therapeutic use : Piperidines, Pyridines, Serotonin 5-HT1 Receptor Agonists.
- Animals, Female, Macaca fascicularis, Rats, Rats, Sprague-Dawley.
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.
DOI: 10.1016/j.neures.2013.10.002
PubMed: 24135129
Links to Exploration step
pubmed:24135129Le document en format XML
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Pioli</name></author><author><name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name></author><author><name sortKey="Porras, Gregory" sort="Porras, Gregory" uniqKey="Porras G" first="Gregory" last="Porras">Gregory Porras</name></author><author><name sortKey="Bjorklund, Anders" sort="Bjorklund, Anders" uniqKey="Bjorklund A" first="Anders" last="Björklund">Anders Björklund</name></author><author><name sortKey="Carta, Manolo" sort="Carta, Manolo" uniqKey="Carta M" first="Manolo" last="Carta">Manolo Carta</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24135129</idno><idno type="pmid">24135129</idno><idno type="doi">10.1016/j.neures.2013.10.002</idno><idno type="wicri:Area/PubMed/Corpus">000662</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000662</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia.</title><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bézard">Erwan Bézard</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China.</nlm:affiliation></affiliation></author><author><name sortKey="Mu Oz, Ana" sort="Mu Oz, Ana" uniqKey="Mu Oz A" first="Ana" last="Mu Oz">Ana Mu Oz</name></author><author><name sortKey="Tronci, Elisabetta" sort="Tronci, Elisabetta" uniqKey="Tronci E" first="Elisabetta" last="Tronci">Elisabetta Tronci</name></author><author><name sortKey="Pioli, Elsa Y" sort="Pioli, Elsa Y" uniqKey="Pioli E" first="Elsa Y" last="Pioli">Elsa Y. Pioli</name></author><author><name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name></author><author><name sortKey="Porras, Gregory" sort="Porras, Gregory" uniqKey="Porras G" first="Gregory" last="Porras">Gregory Porras</name></author><author><name sortKey="Bjorklund, Anders" sort="Bjorklund, Anders" uniqKey="Bjorklund A" first="Anders" last="Björklund">Anders Björklund</name></author><author><name sortKey="Carta, Manolo" sort="Carta, Manolo" uniqKey="Carta M" first="Manolo" last="Carta">Manolo Carta</name></author></analytic><series><title level="j">Neuroscience research</title><idno type="eISSN">1872-8111</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Female</term><term>Levodopa (adverse effects)</term><term>Macaca fascicularis</term><term>Parkinsonian Disorders (drug therapy)</term><term>Piperidines (therapeutic use)</term><term>Pyridines (therapeutic use)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Serotonin 5-HT1 Receptor Agonists (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Piperidines</term><term>Pyridines</term><term>Serotonin 5-HT1 Receptor Agonists</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Macaca fascicularis</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24135129</PMID><DateCreated><Year>2013</Year><Month>12</Month><Day>03</Day></DateCreated><DateCompleted><Year>2014</Year><Month>08</Month><Day>01</Day></DateCompleted><DateRevised><Year>2013</Year><Month>12</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8111</ISSN><JournalIssue CitedMedium="Internet"><Volume>77</Volume><Issue>4</Issue><PubDate><Year>2013</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Neuroscience research</Title><ISOAbbreviation>Neurosci. Res.</ISOAbbreviation></Journal><ArticleTitle>Anti-dyskinetic effect of anpirtoline in animal models of L-DOPA-induced dyskinesia.</ArticleTitle><Pagination><MedlinePgn>242-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neures.2013.10.002</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0168-0102(13)00223-X</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bézard</LastName><ForeName>Erwan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Muñoz</LastName><ForeName>Ana</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Tronci</LastName><ForeName>Elisabetta</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Pioli</LastName><ForeName>Elsa Y</ForeName><Initials>EY</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qin</ForeName><Initials>Q</Initials></Author><Author ValidYN="Y"><LastName>Porras</LastName><ForeName>Gregory</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Björklund</LastName><ForeName>Anders</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Carta</LastName><ForeName>Manolo</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>10</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Neurosci Res</MedlineTA><NlmUniqueID>8500749</NlmUniqueID><ISSNLinking>0168-0102</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson 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effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008252" MajorTopicYN="N">Macaca fascicularis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020734" MajorTopicYN="N">Parkinsonian Disorders</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010880" MajorTopicYN="N">Piperidines</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName 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