De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset
Identifieur interne : 007F46 ( Main/Merge ); précédent : 007F45; suivant : 007F47De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset
Auteurs : Ronald K. B. Pearce [Royaume-Uni] ; Tara Banerji [Royaume-Uni] ; Jenner [Royaume-Uni] ; C. David Marsden [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1998-03.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Antiparkinson Agents (pharmacology), Bromocriptine (pharmacology), Callithrix, Dose-Response Relationship, Drug, Drug Administration Schedule, Dyskinesia, Dyskinesia, Drug-Induced (physiopathology), Female, Indoles (pharmacology), Levodopa (pharmacology), Male, Motor Skills (drug effects), Motor Skills (physiology), Neurologic Examination (drug effects), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Parkinson's disease, Receptors, Dopamine D2 (agonists), Receptors, Dopamine D2 (physiology), Ropinirole.
- MESH :
- chemical , agonists : Receptors, Dopamine D2.
- chemical , pharmacology : Antiparkinson Agents, Bromocriptine, Indoles, Levodopa.
- chemical , physiology : Receptors, Dopamine D2.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Motor Skills, Neurologic Examination.
- physiology : Motor Skills.
- physiopathology : Dyskinesia, Drug-Induced, Parkinson Disease, Secondary.
- Animals, Callithrix, Dose-Response Relationship, Drug, Drug Administration Schedule, Female, Male.
Abstract
In contrast to levodopa (L‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.
Url:
DOI: 10.1002/mds.870130207
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B." last="Pearce">Ronald K. B. Pearce</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="Banerji, Tara" sort="Banerji, Tara" uniqKey="Banerji T" first="Tara" last="Banerji">Tara Banerji</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>National Hospital for Neurology and Neurosurgery, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="David Marsden, C" sort="David Marsden, C" uniqKey="David Marsden C" first="C." last="David Marsden">C. David Marsden</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-03">1998-03</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="234">234</biblScope><biblScope unit="page" to="241">241</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">982D4676EE3271FE1ABC9DB732BA6A99D80145F1</idno><idno type="DOI">10.1002/mds.870130207</idno><idno type="ArticleID">MDS870130207</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Bromocriptine (pharmacology)</term><term>Callithrix</term><term>Dose-Response Relationship, Drug</term><term>Drug Administration Schedule</term><term>Dyskinesia</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Female</term><term>Indoles (pharmacology)</term><term>Levodopa (pharmacology)</term><term>Male</term><term>Motor Skills (drug effects)</term><term>Motor Skills (physiology)</term><term>Neurologic Examination (drug effects)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Parkinson's disease</term><term>Receptors, Dopamine D2 (agonists)</term><term>Receptors, Dopamine D2 (physiology)</term><term>Ropinirole</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Bromocriptine</term><term>Indoles</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Skills</term><term>Neurologic Examination</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Skills</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callithrix</term><term>Dose-Response Relationship, Drug</term><term>Drug Administration Schedule</term><term>Female</term><term>Male</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In contrast to levodopa (L‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.</div></front></TEI><double doi="10.1002/mds.870130207"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset</title><author><name sortKey="Pearce, Ronald K B" sort="Pearce, Ronald K B" uniqKey="Pearce R" first="Ronald K. B." last="Pearce">Ronald K. B. Pearce</name></author><author><name sortKey="Banerji, Tara" sort="Banerji, Tara" uniqKey="Banerji T" first="Tara" last="Banerji">Tara Banerji</name></author><author><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name></author><author><name sortKey="David Marsden, C" sort="David Marsden, C" uniqKey="David Marsden C" first="C." last="David Marsden">C. David Marsden</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:982D4676EE3271FE1ABC9DB732BA6A99D80145F1</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1002/mds.870130207</idno><idno type="url">https://api.istex.fr/document/982D4676EE3271FE1ABC9DB732BA6A99D80145F1/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000890</idno><idno type="wicri:Area/Istex/Curation">000890</idno><idno type="wicri:Area/Istex/Checkpoint">003769</idno><idno type="wicri:doubleKey">0885-3185:1998:Pearce R:de:novo:administration</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset</title><author><name sortKey="Pearce, Ronald K B" sort="Pearce, Ronald K B" uniqKey="Pearce R" first="Ronald K. B." last="Pearce">Ronald K. B. Pearce</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="Banerji, Tara" sort="Banerji, Tara" uniqKey="Banerji T" first="Tara" last="Banerji">Tara Banerji</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>National Hospital for Neurology and Neurosurgery, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="David Marsden, C" sort="David Marsden, C" uniqKey="David Marsden C" first="C." last="David Marsden">C. David Marsden</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-03">1998-03</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="234">234</biblScope><biblScope unit="page" to="241">241</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">982D4676EE3271FE1ABC9DB732BA6A99D80145F1</idno><idno type="DOI">10.1002/mds.870130207</idno><idno type="ArticleID">MDS870130207</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dyskinesia</term><term>Parkinson's disease</term><term>Ropinirole</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In contrast to levodopa (L‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">De novo administration of ropinirole and bromocriptine induces less dyskinesia than L-dopa in the MPTP-treated marmoset.</title><author><name sortKey="Pearce, R K" sort="Pearce, R K" uniqKey="Pearce R" first="R K" last="Pearce">R K Pearce</name><affiliation wicri:level="2"><nlm:affiliation>Neurodegenerative Diseases Research Centre, Biomedical Sciences Division, King's College , London, England.</nlm:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Biomedical Sciences Division, King's College , London</wicri:cityArea></affiliation></author><author><name sortKey="Banerji, T" sort="Banerji, T" uniqKey="Banerji T" first="T" last="Banerji">T. Banerji</name></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P" last="Jenner">P. Jenner</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9539335</idno><idno type="pmid">9539335</idno><idno type="doi">10.1002/mds.870130207</idno><idno type="wicri:Area/PubMed/Corpus">004477</idno><idno type="wicri:Area/PubMed/Curation">004477</idno><idno type="wicri:Area/PubMed/Checkpoint">004464</idno><idno type="wicri:Area/Ncbi/Merge">004F06</idno><idno type="wicri:Area/Ncbi/Curation">004F06</idno><idno type="wicri:Area/Ncbi/Checkpoint">004F06</idno><idno type="wicri:doubleKey">0885-3185:1998:Pearce R:de:novo:administration</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">De novo administration of ropinirole and bromocriptine induces less dyskinesia than L-dopa in the MPTP-treated marmoset.</title><author><name sortKey="Pearce, R K" sort="Pearce, R K" uniqKey="Pearce R" first="R K" last="Pearce">R K Pearce</name><affiliation wicri:level="2"><nlm:affiliation>Neurodegenerative Diseases Research Centre, Biomedical Sciences Division, King's College , London, England.</nlm:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Diseases Research Centre, Biomedical Sciences Division, King's College , London</wicri:cityArea></affiliation></author><author><name sortKey="Banerji, T" sort="Banerji, T" uniqKey="Banerji T" first="T" last="Banerji">T. Banerji</name></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P" last="Jenner">P. Jenner</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Bromocriptine (pharmacology)</term><term>Callithrix</term><term>Dose-Response Relationship, Drug</term><term>Drug Administration Schedule</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Female</term><term>Indoles (pharmacology)</term><term>Levodopa (pharmacology)</term><term>Male</term><term>Motor Skills (drug effects)</term><term>Motor Skills (physiology)</term><term>Neurologic Examination (drug effects)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Receptors, Dopamine D2 (agonists)</term><term>Receptors, Dopamine D2 (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Bromocriptine</term><term>Indoles</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Skills</term><term>Neurologic Examination</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Skills</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callithrix</term><term>Dose-Response Relationship, Drug</term><term>Drug Administration Schedule</term><term>Female</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In contrast to levodopa (L-dopa), de novo administration of the D2-like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2-like selective dopamine agonist ropinirole with that of bromocriptine and L-dopa to induce dyskinesia in MPTP-treated common marmosets. MPTP-treated common marmosets were treated with placebo, L-dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L-dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L-dopa-treated group (p < 0.05). However, in a separate group of marmosets previously primed with L-dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L-dopa in a dose-dependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L-dopa to produce dyskinesia while similarly improving motor performance in drug-naive MPTP-treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L-dopa priming has occurred. These results predict a similar response to ropinirole and other long-acting dopamine agonists in L-dopa-naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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