A rat model of Parkinsonism shows depletion of dopamine in the retina
A rat model of Parkinsonism shows depletion of dopamine in the retina
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DOI：
10.1016/j.neuint.2006.08.001
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发表时间：
2007-01-01
影响因子：
4.2
通讯作者：
Schmidt, Werner J.
中科院分区：
文献类型：
--
作者：
Biehlmaier, Oliver;Alam, Mesbah;Schmidt, Werner J.
视网膜多巴胺（DA）缺乏是帕金森病（PD）视功能障碍发病机制的重要特征。已经提出了在大鼠中复合物]（鱼藤酮）的全身抑制作为PD的模型。在这项研究中，我们调查了是否系统性抑制复合物I可以诱导视网膜DA能细胞的损害，类似于PD患者视网膜细胞的破坏。鱼藤酮（2.5mg/kg i. p.，每日一次）给药60天。神经化学上，鱼藤酮处理的大鼠显示纹状体和黑质中DA的消耗。此外，视网膜DA能无长突细胞的数量显着减少鱼藤酮治疗animals.This研究是第一个给突出走向更深层次的理解系统性复合物I抑制（鱼藤酮作为一种环境毒素）和两者之间的连接，DA能变性的黑质纹状体通路，并在DA能无长突细胞的视网膜。(c)2006爱思唯尔有限公司保留所有权利。
The retinal dopamine (DA) deficiency is an important feature of the pathogenesis in Parkinson's disease (PD) visual dysfunction. Systemic inhibition of complex] (rotenone) in rats has been proposed as a model of PD. In this study, we investigated whether systemic inhibition of complex I can induce impairment of DA-ergic cells in the retina, similar to the destruction of retinal cells found in PD patients. Rotenone (2.5 mg/kg i.p., daily) was administered over 60 days. Neurochemically, rotenone treated rats showed a depletion of DA in the striatum and substantia nigra SN). In addition, the number of retinal DA-ergic amacrine cells was significantly reduced in the rotenone treated animals.This study is the first one giving highlight towards a deeper understanding of systemic complex I inhibition (rotenone as an environmental toxin) and the connection between both, DA-ergic degeneration in the nigrostriatal pathway, and in the DA-ergic amacrine cells of the retina. (c) 2006 Elsevier Ltd. All rights reserved.