Abstract
The dyskinesia of Parkinson's Disease is most likely due to excess levels of dopamine in the striatum. The mechanism may be due to aberrant synthesis but also, a deficiency or absence of the Dopamine Transporter. In this study we have examined the proposition that reinstating Dopamine Transporter expression in the striatum would reduce dyskinesia. We transplanted c17.2 cells that stably expressed the Dopamine Transporter into dyskinetic rats. There was a reduction in dyskinesia in rats that received grafts expressing the Dopamine Transporter. Strategies designed to increase Dopamine Transporter in the striatum may be useful in treating the dyskinesia associated with human Parkinson's Disease.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Behavior, Animal / drug effects
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Brain / metabolism
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Brain / pathology
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Cell Line
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Cell- and Tissue-Based Therapy
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Disease Models, Animal
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Dopamine / metabolism*
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Dopamine Plasma Membrane Transport Proteins / genetics
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Dopamine Plasma Membrane Transport Proteins / metabolism*
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Dyskinesia, Drug-Induced / etiology
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Dyskinesia, Drug-Induced / metabolism
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Dyskinesia, Drug-Induced / therapy
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Levodopa / administration & dosage
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Levodopa / pharmacology
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Male
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Mice
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Neural Stem Cells / cytology
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Neural Stem Cells / metabolism
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Neural Stem Cells / transplantation*
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Oxidopamine / toxicity
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Parkinson Disease / metabolism
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Parkinson Disease / pathology
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Parkinson Disease / therapy
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Rats
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Rats, Wistar
Substances
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Dopamine Plasma Membrane Transport Proteins
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Levodopa
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Oxidopamine
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Dopamine
Grants and funding
MH is an NHMRC Practitioner Fellow. WCB is a Fred P. Archer Fellow. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.