Increased dopamine turnover after partial loss of dopaminergic neurons: compensation or toxicity?
Increased dopamine turnover after partial loss of dopaminergic neurons: compensation or toxicity?
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DOI：
10.1016/s1353-8020(02)00019-6
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发表时间：
2002-09
影响因子：
4.1
通讯作者：
M. Zigmond;T. Hastings;R. Perez
中科院分区：
文献类型：
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作者：
M. Zigmond;T. Hastings;R. Perez
6-羟基多巴胺 (6-OHDA) 已被证明是研究帕金森病 (PD) 的重要工具；它还强调了这种疾病可能部分由 6-OHDA 对多巴胺神经元施加的氧化应激引起的可能性。在这篇综述中，我们对与氧化应激在帕金森病中的作用相关的几项研究进行了评论，这些研究极大地受益于杰拉尔德·科恩的工作，我们在本次研讨会上纪念他。首先，我们讨论使用 6-OHDA 来制作 PD 动物模型；其次，我们对多巴胺的神经毒性作用的研究进行评论；最后，我们讨论了酪氨酸羟化酶部分通过与 α-突触核蛋白相互作用进行调节的发现。我们认为帕金森病与多巴胺周转增加有关，这不仅可以减轻疾病的直接症状，还有助于其进展。
6-Hydroxydopamine (6-OHDA) has proven a valuable tool in the study of Parkinson's disease (PD); it has also served to emphasize the possibility that this disorder may result in part from the sort of oxidative stress that 6-OHDA exerts on dopamine neurons. In this review we comment on several lines of our research related to the role of oxidative stress in PD, research that has benefited greatly from the work of Gerald Cohen whose memory we honor at this symposium. First, we discuss our use of 6-OHDA to produce an animal model of PD; second, we comment on our studies on dopamine's neurotoxic effects; and finally, we discuss our finding that tyrosine hydroxylase is regulated in part by an interaction with α-synuclein. We suggest that PD is associated with an increase in dopamine turnover, which may not only reduce the immediate symptoms of the disease but also contribute to its progression.