Amantadine reduces levodopa-induced dyskinesias in parkinsonian monkeys.
Identifieur interne : 005029 ( Ncbi/Curation ); précédent : 005028; suivant : 005030Amantadine reduces levodopa-induced dyskinesias in parkinsonian monkeys.
Auteurs : P J Blanchet [États-Unis] ; 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
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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><idno type="wicri:Area/PubMed/Curation">004357</idno><idno type="wicri:Area/PubMed/Checkpoint">004506</idno><idno type="wicri:Area/Ncbi/Merge">005029</idno><idno type="wicri:Area/Ncbi/Curation">005029</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 wicri:level="1"><nlm:affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892-1406, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892-1406</wicri:regionArea><wicri:noRegion>Maryland 20892-1406</wicri:noRegion></affiliation></author><author><name sortKey="Konitsiotis, S" sort="Konitsiotis, S" uniqKey="Konitsiotis S" first="S" last="Konitsiotis">S. 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></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>Amantadine (administration & dosage)</term><term>Amantadine (adverse effects)</term><term>Animals</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (adverse effects)</term><term>Dopamine Agents (administration & dosage)</term><term>Dopamine Agents (adverse effects)</term><term>Dose-Response Relationship, Drug</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Injections, Subcutaneous</term><term>Levodopa (administration & dosage)</term><term>Levodopa (adverse effects)</term><term>Macaca fascicularis</term><term>Neurologic Examination (drug effects)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Receptors, N-Methyl-D-Aspartate (drug effects)</term><term>Receptors, N-Methyl-D-Aspartate (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Amantadine</term><term>Antiparkinson Agents</term><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Amantadine</term><term>Antiparkinson Agents</term><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, N-Methyl-D-Aspartate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, N-Methyl-D-Aspartate</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>Neurologic Examination</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease, Secondary</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>Dose-Response Relationship, Drug</term><term>Injections, Subcutaneous</term><term>Macaca fascicularis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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