Novel antiepileptic drug levetiracetam decreases dyskinesia elicited by L-dopa and ropinirole in the MPTP-lesioned marmoset.
Identifieur interne : 003716 ( PubMed/Checkpoint ); précédent : 003715; suivant : 003717Novel antiepileptic drug levetiracetam decreases dyskinesia elicited by L-dopa and ropinirole in the MPTP-lesioned marmoset.
Auteurs : Michael P. Hill [Royaume-Uni] ; Erwan Bezard ; Steven G. Mcguire ; Alan R. Crossman ; Jonathan M. Brotchie ; Ann Michel ; Renee Grimée ; Henrik KlitgaardSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2003.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Animals, Anticonvulsants (pharmacology), Anticonvulsants (therapeutic use), Antiparkinson Agents (adverse effects), Callithrix, Dopamine Agents (adverse effects), Dopamine Agents (metabolism), Drug Synergism, Drug Therapy, Combination, Female, Indoles (adverse effects), Levodopa (adverse effects), Male, Parkinsonian Disorders (chemically induced), Parkinsonian Disorders (drug therapy), Parkinsonian Disorders (metabolism), Piracetam (analogs & derivatives), Piracetam (pharmacology), Piracetam (therapeutic use).
- MESH :
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Antiparkinson Agents, Dopamine Agents, Indoles, Levodopa.
- chemical , analogs & derivatives : Piracetam.
- chemical , metabolism : Dopamine Agents.
- chemical , pharmacology : Anticonvulsants, Piracetam.
- chemical , therapeutic use : Anticonvulsants, Piracetam.
- chemically induced : Parkinsonian Disorders.
- drug therapy : Parkinsonian Disorders.
- metabolism : Parkinsonian Disorders.
- Animals, Callithrix, Drug Synergism, Drug Therapy, Combination, Female, Male.
Abstract
Long-term dopamine replacement therapy of Parkinson's disease leads to the occurrence of dyskinesias. Altered firing patterns of neurons of the internal globus pallidus, involving a pathological synchronization/desynchronization process, may contribute significantly to the genesis of dyskinesia. Levetiracetam, an antiepileptic drug that counteracts neuronal (hyper)synchronization in animal models of epilepsy, was assessed in the MPTP-lesioned marmoset model of Parkinson's disease, after coadministration with (1) levodopa (L-dopa) or (2) ropinirole/L-dopa combination. Oral administration of levetiracetam (13-60 mg/kg) in combination with either L-dopa (12 mg/kg) alone or L-dopa (8 mg/kg)/ropinirole (1.25 mg/kg) treatments was associated with significantly less dyskinesia, in comparison to L-dopa monotherapy during the first hour after administration. Thus, new nondopaminergic treatment strategies targeting normalization of abnormal firing patterns in basal ganglia structures may prove useful as an adjunct to reduce dyskinesia induced by dopamine replacement therapy without affecting its antiparkinsonian action.
DOI: 10.1002/mds.10542
PubMed: 14639671
Affiliations:
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pubmed:14639671Le document en format XML
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<front><div type="abstract" xml:lang="en">Long-term dopamine replacement therapy of Parkinson's disease leads to the occurrence of dyskinesias. Altered firing patterns of neurons of the internal globus pallidus, involving a pathological synchronization/desynchronization process, may contribute significantly to the genesis of dyskinesia. Levetiracetam, an antiepileptic drug that counteracts neuronal (hyper)synchronization in animal models of epilepsy, was assessed in the MPTP-lesioned marmoset model of Parkinson's disease, after coadministration with (1) levodopa (L-dopa) or (2) ropinirole/L-dopa combination. Oral administration of levetiracetam (13-60 mg/kg) in combination with either L-dopa (12 mg/kg) alone or L-dopa (8 mg/kg)/ropinirole (1.25 mg/kg) treatments was associated with significantly less dyskinesia, in comparison to L-dopa monotherapy during the first hour after administration. Thus, new nondopaminergic treatment strategies targeting normalization of abnormal firing patterns in basal ganglia structures may prove useful as an adjunct to reduce dyskinesia induced by dopamine replacement therapy without affecting its antiparkinsonian action.</div>
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