Amantadine reduces levodopa-induced dyskinesias in parkinsonian monkeys.
Identifieur interne : 004357 ( PubMed/Corpus ); précédent : 004356; suivant : 004358Amantadine reduces levodopa-induced dyskinesias in parkinsonian monkeys.
Auteurs : P J Blanchet ; S. Konitsiotis ; T N ChaseSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1998.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Amantadine (administration & dosage), Amantadine (adverse effects), Animals, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (adverse effects), Dopamine Agents (administration & dosage), Dopamine Agents (adverse effects), Dose-Response Relationship, Drug, Dyskinesia, Drug-Induced (drug therapy), Dyskinesia, Drug-Induced (physiopathology), Injections, Subcutaneous, Levodopa (administration & dosage), Levodopa (adverse effects), Macaca fascicularis, Neurologic Examination (drug effects), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (physiopathology), Receptors, N-Methyl-D-Aspartate (drug effects), Receptors, N-Methyl-D-Aspartate (physiology).
- MESH :
- chemical , administration & dosage : Amantadine, Antiparkinson Agents, Dopamine Agents, Levodopa.
- chemical , adverse effects : Amantadine, Antiparkinson Agents, Dopamine Agents, Levodopa.
- chemical , drug effects : Receptors, N-Methyl-D-Aspartate.
- chemical , physiology : Receptors, N-Methyl-D-Aspartate.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Neurologic Examination.
- drug therapy : Dyskinesia, Drug-Induced, Parkinson Disease, Secondary.
- physiopathology : Dyskinesia, Drug-Induced, Parkinson Disease, Secondary.
- Animals, Dose-Response Relationship, Drug, Injections, Subcutaneous, Macaca fascicularis.
Abstract
The antidyskinetic potential of the glutamate NMDA receptor channel blocker amantadine was evaluated in four levodopa-primed parkinsonian monkeys using two different regimens (1.25 or 2.5 mg/kg administered subcutaneously twice daily for 3-6 days). When administered with a relatively low dose of levodopa, amantadine produced a near-total suppression of choreiform dyskinesias and a substantial reduction in dystonic dyskinesias at the expense of a significant reduction in antiparkinsonian response. With a high dose of levodopa, amantadine had a smaller but still significant effect on dyskinesias without altering the antiparkinsonian response. These results lend support to the view that glutamate receptor-mediated mechanisms contribute to levodopa-induced dyskinesias. They also suggest that amantadine could alleviate such complications in parkinsonian patients, especially with careful dose optimization.
DOI: 10.1002/mds.870130507
PubMed: 9756148
Links to Exploration step
pubmed:9756148Le document en format XML
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Konitsiotis</name></author><author><name sortKey="Chase, T N" sort="Chase, T N" uniqKey="Chase T" first="T N" last="Chase">T N Chase</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9756148</idno><idno type="pmid">9756148</idno><idno type="doi">10.1002/mds.870130507</idno><idno type="wicri:Area/PubMed/Corpus">004357</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Amantadine reduces levodopa-induced dyskinesias in parkinsonian monkeys.</title><author><name sortKey="Blanchet, P J" sort="Blanchet, P J" uniqKey="Blanchet P" first="P J" last="Blanchet">P J Blanchet</name><affiliation><nlm:affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892-1406, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Konitsiotis, S" sort="Konitsiotis, S" uniqKey="Konitsiotis S" first="S" last="Konitsiotis">S. 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When administered with a relatively low dose of levodopa, amantadine produced a near-total suppression of choreiform dyskinesias and a substantial reduction in dystonic dyskinesias at the expense of a significant reduction in antiparkinsonian response. With a high dose of levodopa, amantadine had a smaller but still significant effect on dyskinesias without altering the antiparkinsonian response. These results lend support to the view that glutamate receptor-mediated mechanisms contribute to levodopa-induced dyskinesias. They also suggest that amantadine could alleviate such complications in parkinsonian patients, especially with careful dose optimization.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9756148</PMID><DateCreated><Year>1999</Year><Month>01</Month><Day>05</Day></DateCreated><DateCompleted><Year>1999</Year><Month>01</Month><Day>05</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>5</Issue><PubDate><Year>1998</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Amantadine reduces levodopa-induced dyskinesias in parkinsonian monkeys.</ArticleTitle><Pagination><MedlinePgn>798-802</MedlinePgn></Pagination><Abstract><AbstractText>The antidyskinetic potential of the glutamate NMDA receptor channel blocker amantadine was evaluated in four levodopa-primed parkinsonian monkeys using two different regimens (1.25 or 2.5 mg/kg administered subcutaneously twice daily for 3-6 days). When administered with a relatively low dose of levodopa, amantadine produced a near-total suppression of choreiform dyskinesias and a substantial reduction in dystonic dyskinesias at the expense of a significant reduction in antiparkinsonian response. With a high dose of levodopa, amantadine had a smaller but still significant effect on dyskinesias without altering the antiparkinsonian response. These results lend support to the view that glutamate receptor-mediated mechanisms contribute to levodopa-induced dyskinesias. They also suggest that amantadine could alleviate such complications in parkinsonian patients, especially with careful dose optimization.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Blanchet</LastName><ForeName>P J</ForeName><Initials>PJ</Initials><AffiliationInfo><Affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892-1406, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Konitsiotis</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Chase</LastName><ForeName>T N</ForeName><Initials>TN</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></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov 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RefType="CommentIn"><RefSource>Mov Disord. 1998 Sep;13(5):851</RefSource><PMID Version="1">9756161</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000547">Amantadine</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015259">Dopamine 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UI="D008252">Macaca fascicularis</DescriptorName></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="N" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016194">Receptors, N-Methyl-D-Aspartate</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate 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