Open AccessRestoration of the Dopamine Transporter through Cell Therapy Improves Dyskinesia in a Rat Model of Parkinson’s Disease
Author(s) -
Doris Tomas,
Davor Stanić,
H. Chua,
Kylie White,
Wah Chin Boon,
Malcolm Horne
Publication year - 2016
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0153424
Subject(s) - dopamine transporter , dyskinesia , dopamine , dopamine plasma membrane transport proteins , parkinson's disease , striatum , transporter , medicine , pharmacology , dopamine receptor d3 , levodopa , neuroscience , disease , dopaminergic , biology , endocrinology , genetics , gene
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.