De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset
Identifieur interne : 005034 ( Main/Exploration ); précédent : 005033; suivant : 005035De 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.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Adult animal, Agonist, Animals, Antiparkinson Agents (pharmacology), Antiparkinson agent, Bromocriptine, Bromocriptine (pharmacology), Callithrix, Chemotherapy, Comparative study, D2 Dopamine receptor, De novo, Dose activity relation, Dose-Response Relationship, Drug, Drug Administration Schedule, Dyskinesia, Dyskinesia, Drug-Induced (physiopathology), Female, Indoles (pharmacology), Levodopa, Levodopa (pharmacology), Male, Monkey, Motor Skills (drug effects), Motor Skills (physiology), Neurologic Examination (drug effects), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Parkinson disease, Parkinson's disease, Receptors, Dopamine D2 (agonists), Receptors, Dopamine D2 (physiology), Ropinirole, Toxicity, Treatment.
- 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
Affiliations:
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Le document en format XML
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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>Adult animal</term><term>Agonist</term><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson agent</term><term>Bromocriptine</term><term>Bromocriptine (pharmacology)</term><term>Callithrix</term><term>Chemotherapy</term><term>Comparative study</term><term>D2 Dopamine receptor</term><term>De novo</term><term>Dose activity relation</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</term><term>Levodopa (pharmacology)</term><term>Male</term><term>Monkey</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 disease</term><term>Parkinson's disease</term><term>Receptors, Dopamine D2 (agonists)</term><term>Receptors, Dopamine D2 (physiology)</term><term>Ropinirole</term><term>Toxicity</term><term>Treatment</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><keywords scheme="Pascal" xml:lang="fr"><term>Agoniste</term><term>Animal adulte</term><term>Antiparkinsonien</term><term>Bromocriptine</term><term>Chimiothérapie</term><term>De novo</term><term>Dyskinésie</term><term>Etude comparative</term><term>Lévodopa</term><term>Parkinson maladie</term><term>Relation dose réponse</term><term>Ropinirole</term><term>Récepteur dopaminergique D2</term><term>Singe</term><term>Toxicité</term><term>Traitement</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</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><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><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></region><name sortKey="Banerji, Tara" sort="Banerji, Tara" uniqKey="Banerji T" first="Tara" last="Banerji">Tara Banerji</name><name sortKey="David Marsden, C" sort="David Marsden, C" uniqKey="David Marsden C" first="C." last="David Marsden">C. David Marsden</name><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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