De novo administration of ropinirole and bromocriptine induces less dyskinesia than L-dopa in the MPTP-treated marmoset.
Identifieur interne : 004477 ( PubMed/Corpus ); précédent : 004476; suivant : 004478De novo administration of ropinirole and bromocriptine induces less dyskinesia than L-dopa in the MPTP-treated marmoset.
Auteurs : R K Pearce ; T. Banerji ; P. Jenner ; C D MarsdenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1998.
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, 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), Receptors, Dopamine D2 (agonists), Receptors, Dopamine D2 (physiology).
- 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 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.
DOI: 10.1002/mds.870130207
PubMed: 9539335
Links to Exploration step
pubmed:9539335Le document en format XML
<record><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><nlm:affiliation>Neurodegenerative Diseases Research Centre, Biomedical Sciences Division, King's College , London, England.</nlm:affiliation></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></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><nlm:affiliation>Neurodegenerative Diseases Research Centre, Biomedical Sciences Division, King's College , London, England.</nlm:affiliation></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><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9539335</PMID><DateCreated><Year>1998</Year><Month>06</Month><Day>15</Day></DateCreated><DateCompleted><Year>1998</Year><Month>06</Month><Day>15</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>13</Volume><Issue>2</Issue><PubDate><Year>1998</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>De novo administration of ropinirole and bromocriptine induces less dyskinesia than L-dopa in the MPTP-treated marmoset.</ArticleTitle><Pagination><MedlinePgn>234-41</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pearce</LastName><ForeName>R K</ForeName><Initials>RK</Initials><AffiliationInfo><Affiliation>Neurodegenerative Diseases Research Centre, Biomedical Sciences Division, King's College , London, England.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Banerji</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Jenner</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Marsden</LastName><ForeName>C D</ForeName><Initials>CD</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007211">Indoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017448">Receptors, Dopamine D2</NameOfSubstance></Chemical><Chemical><RegistryNumber>030PYR8953</RegistryNumber><NameOfSubstance UI="C046649">ropinirole</NameOfSubstance></Chemical><Chemical><RegistryNumber>3A64E3G5ZO</RegistryNumber><NameOfSubstance UI="D001971">Bromocriptine</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001971">Bromocriptine</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002144">Callithrix</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004305">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004334">Drug Administration Schedule</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004409">Dyskinesia, Drug-Induced</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007211">Indoles</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009048">Motor Skills</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009460">Neurologic Examination</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010302">Parkinson Disease, Secondary</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017448">Receptors, Dopamine D2</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000819">agonists</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>4</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>4</Month><Day>16</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>4</Month><Day>16</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9539335</ArticleId><ArticleId IdType="doi">10.1002/mds.870130207</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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