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首页> 外文期刊>The Journal of Comparative Neurology >Morphological impairments in retinal neurons of the scotopic visual pathway in a monkey model of Parkinson's disease.
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Morphological impairments in retinal neurons of the scotopic visual pathway in a monkey model of Parkinson's disease.

机译:帕金森氏病猴子模型中暗视视觉通路的视网膜神经元形态受损。

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摘要

Physiological abnormalities resulting from death of dopaminergic neurons of the central nervous system in Parkinson's disease also extend to the retina, resulting in impaired visual functions. In both parkinsonian patients and animal models, low levels of dopamine and loss of dopaminergic cells in the retina have been reported. However, the morphology and connectivity of their postsynaptic neurons, the amacrine cells, have not been analyzed. Here we report, with macaques chronically treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) as a model of Parkinson's disease, that morphological impairments in dopaminergic retinal neurons and their plexus in the inner retina are accompanied by an immunoreactivity decrease in gamma-aminobutyric acidergic and glycinergic amacrine cells. Especially deteriorated were AII amacrine cells, the main neuronal subtype postsynaptic to dopaminergic cells, which exhibited a marked loss of lobular appendages and dendritic processes. Concomitantly, electrical synapses among AII cells, as well as chemical synapses between these and rod bipolar cells, were highly deteriorated in parkinsonian monkeys. These results highlight that the scotopic visual pathway is severely impaired in the parkinsonian condition and provide a morphological basis for a number of abnormalities found in electrophysiological and psychophysical trials in Parkinson's disease patients and animal models. J. Comp. Neurol. 493:261-273, 2005. (c) 2005 Wiley-Liss, Inc.
机译:由帕金森氏病中枢神经系统的多巴胺能神经元死亡引起的生理异常也延伸到视网膜,导致视觉功能受损。在帕金森氏病患者和动物模型中,都已经报道了视网膜中低水平的多巴胺和多巴胺能细胞的丢失。但是,尚未分析其突触后神经元,无长突细胞的形态和连通性。在这里,我们报道了用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)长期治疗的猕猴作为帕金森氏病的模型,多巴胺能视网膜神经元及其内视网膜神经丛的形态受损伴随着γ-氨基丁酸能和甘氨酸能的无长突细胞的免疫反应性降低。尤其恶化的是AII amacrine细胞,其是突触后的多巴胺能细胞的主要神经元亚型,表现出明显的小叶附肢和树突突消失。随之而来的是,帕金森氏猴中的AII细胞之间的电突触以及这些与杆状双极细胞之间的化学突触高度恶化。这些结果表明,在帕金森病中暗视视觉通路受到严重损害,并为在帕金森氏病患者和动物模型中进行的电生理和心理物理试验发现的许多异常现象提供了形态学基础。 J.比较神经元。 493:261-273,2005.(c)2005 Wiley-Liss,Inc.

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