Restoration of the Dopamine Transporter through Cell Therapy Improves Dyskinesia in a Rat Model of Parkinson's Disease

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 Transport...

Full description

Saved in:
Bibliographic Details
Published in:PloS one 2016-04, Vol.11 (4), p.e0153424-e0153424
Main Authors: Tomas, D, Stanic, D, Chua, H K, White, K, Boon, W C, Horne, M
Format: Article
Language:English
Subjects:
Aberration
Alcohol
Analysis
Animals
Behavior, Animal - drug effects
Biology and Life Sciences
Brain - metabolism
Brain - pathology
Care and treatment
Cell Line
Cell- and Tissue-Based Therapy
Cellular therapy
Cloning
Complications and side effects
Disease Models, Animal
Dopamine
Dopamine - metabolism
Dopamine Plasma Membrane Transport Proteins - genetics
Dopamine Plasma Membrane Transport Proteins - metabolism
Dopamine transporter
Dyskinesia
Dyskinesia, Drug-Induced - etiology
Dyskinesia, Drug-Induced - metabolism
Dyskinesia, Drug-Induced - therapy
Grafts
Health aspects
Laboratory animals
Levodopa - administration & dosage
Levodopa - pharmacology
Male
Medicine and Health Sciences
Mental health
Mice
Movement disorders
Neostriatum
Neural Stem Cells - cytology
Neural Stem Cells - metabolism
Neural Stem Cells - transplantation
Neural transmission
Neurodegeneration
Neurodegenerative diseases
Neurosciences
Oxidopamine - toxicity
Parkinson Disease - metabolism
Parkinson Disease - pathology
Parkinson Disease - therapy
Parkinson's disease
Physical Sciences
Rats
Rats, Wistar
Research and Analysis Methods
Restoration
Rodents
Stem cells
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0153424