Tomas D, Stanic D, Chua H K, White K, Boon W C, Horne M
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Australia, 3010.
Department of Medicine, University of Melbourne, St Vincent's Hospital, Fitzroy, Victoria, Australia, 3065.
PLoS One. 2016 Apr 14;11(4):e0153424. doi: 10.1371/journal.pone.0153424. eCollection 2016.
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.
帕金森病的运动障碍很可能是由于纹状体内多巴胺水平过高所致。其机制可能是异常合成，也可能是多巴胺转运体缺乏或缺失。在本研究中，我们检验了在纹状体内恢复多巴胺转运体表达可减轻运动障碍这一假设。我们将稳定表达多巴胺转运体的c17.2细胞移植到患有运动障碍的大鼠体内。接受表达多巴胺转运体移植的大鼠的运动障碍有所减轻。旨在增加纹状体内多巴胺转运体的策略可能有助于治疗与人类帕金森病相关的运动障碍。
