Abstract
L-dopa remains the mainstay treatment for Parkinson's disease (PD), although in later stages, treatment is complicated by L-dopa-induced dyskinesias (LID). Current evidence links LID to excessive striatal L-dopa-derived dopamine (DA) release, while the possibility of a direct involvement of L-dopa itself in LID has been largely ignored. Here we show that L-dopa can alter basal ganglia activity and produce LID without enhancing striatal DA release in parkinsonian non-human primates. These data may have therapeutic implications for the management of advanced PD since they suggest that LID could result from diverse mechanisms of action of L-dopa.
MeSH terms
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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / adverse effects
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Animals
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Benserazide / adverse effects
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Benserazide / pharmacokinetics
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Corpus Striatum / drug effects
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Corpus Striatum / metabolism
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Disease Models, Animal
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Dopamine / metabolism
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Dopamine Agents / adverse effects*
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Dopamine Agents / pharmacokinetics
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Drug Combinations
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Dyskinesias / etiology*
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Dyskinesias / metabolism
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Female
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Levodopa / adverse effects*
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Levodopa / pharmacokinetics
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Macaca mulatta
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Male
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Parkinson Disease / metabolism
Substances
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Dopamine Agents
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Drug Combinations
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benserazide, levodopa drug combination
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Levodopa
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Benserazide
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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
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Dopamine