VISUAL DEFICITS RELATED TO DOPAMINE DEFICIENCY IN EXPERIMENTAL-ANIMALS AND PARKINSONS-DISEASE PATIENTS
VISUAL DEFICITS RELATED TO DOPAMINE DEFICIENCY IN EXPERIMENTAL-ANIMALS AND PARKINSONS-DISEASE PATIENTS
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DOI：
10.1016/0166-2236(90)90113-o
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发表时间：
1990-07-01
影响因子：
15.9
通讯作者：
BODISWOLLNER, I
中科院分区：
文献类型：
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作者：
BODISWOLLNER, I
在帕金森氏病患者和这种疾病的猴模型中，使用空间和时间对比敏感度的心理物理学和电生理学测量已经显示出视觉缺陷。这些研究暗示了多巴胺在灵长类视觉中的重要作用。有电生理学和神经化学证据表明，至少部分问题是由系统性多巴胺能缺乏引起的视网膜处理受损。一些赤字已被证明，与生理学研究一致，表明多巴胺能神经元的中心-周围相互作用可能会受到影响。视网膜多巴胺（DI和De）受体在灵长类视觉中的调节作用以及这些受体在突触前多巴胺能缺陷中的平衡尚未确定。在认知负荷任务中使用正弦光栅刺激可以增加对多巴胺缺乏综合征中视觉缺陷的行为后果的理解，自从James Parkinson于1817年首次描述以来，人们已经接受帕金森病（PD）是一种运动系统疾病，具有影响基底神经节的特定神经病理学改变，主要是多巴胺能神经元。因此，当大量患有PD的患者被报道2具有异常的视觉诱发电位（VEP）时，这是令人惊讶的，这表明视觉通路（可能是视网膜）中的多巴胺能缺乏。最初，这一想法几乎没有得到进一步的支持。现在，有相当多的心理物理学和电生理学证据证明，人类和动物的多巴胺能缺乏导致视觉功能障碍。本文综述了PD患者的视觉研究。此外，在猴子实验诱导帕金森综合征的数据被认为是在试图从细胞研究中获得的数据与行为证据。视网膜和纹状体黑质多巴胺受体机制的一些共同的方面突出。最后，对PD患者感觉视觉和认知视觉功能障碍之间的可能关系进行了讨论。Malmfors于1963年首次观察到儿茶酚胺耗竭对视力的影响。他记录到利血平处理的老鼠对光有明显的敏感性：它们会避开光照并闭上眼睛。然而，与此同时，这些动物的瞳孔很小，正如人们所期望的那样，使用利血平，
In patients affected by Parkinson's disease, and in the monkey model of this disease, visual defects have been shown using psychophysical and electrophysiological measures of spatial and temporal contrast sensitivity. These studies imply an essential role for dopamine m primate vision. There is electrophysiological and neurochemical evidence to suggest that at least part of the problem is impaired retinal processing caused by systemic dopaminergic deficiency. Some of the deficits that have been demonstrated, consistent with physiological studies, suggest that center-surround interaction of neurons may suffer as a consequence of dopaminergic deficiency. The role of the regulation of retinal dopamine (DI and De) r~ ceptors in primate vision and of the balance of these receptors in presynaptic dopaminergic defMency is not yet determined. Using sinusoidal grating stimuli in cognitively loaded tasks may increase understanding of the behavioral consequences of visual deficits seen in dopamine deficiency syndromes.Since the original description by James Parkinson in 1817~ it has become accepted that Parkinson's disease (PD) is exclusively a motor system disorder with specific neuropathological changes affecting the basal ganglia, predominantly dopaminergic neurons. So it was surprising when a large number of patients suffering from PD were reported 2 to have abnormal visual evoked potentials (VEPs), suggesting dopaminergic deficiency in the visual pathway, probably the retina. Initially, there was little further support for this idea. Now, there is considerable psychophysical and electrophysiological evidence attesting to visual dysfunction as a result of dopaminergic deficiency in both humans and animals. This review summarizes vision studies of humans with PD. In addition, data on experimentally induced parkinsonism in monkeys is considered in an attempt to link behavioral evidence with data obtained from cellular studies. Some common aspects of retinal and striatonigral dopamine receptor mechanisms are highlighted. Finally, the possible relationship between sensory-visual and cognitive-visual dysfunction in PD is discussed. The first observations concerning the effect of catecholamine depletion on vision were made by Malmfors in 19633. He recorded that reserpinized rats had pronounced sensitivity to light: they turn away from illumination and close their eyes. Yet at the same time, the pupils of these animals were small, as indeed one would expect from using reserpine, which