Bodis-Wollner I
Department of Neurology, Mount Sinai School of Medicine, CUNY 10029.
Trends Neurosci. 1990 Jul;13(7):296-302. doi: 10.1016/0166-2236(90)90113-o.
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 in 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 (D1 and D2) receptors in primate vision and of the balance of these receptors in presynaptic dopaminergic deficiency 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.
在帕金森病患者以及该疾病的猴子模型中，通过空间和时间对比敏感度的心理物理学和电生理学测量方法，已显示出视觉缺陷。这些研究表明多巴胺在灵长类动物视觉中起着至关重要的作用。有电生理学和神经化学证据表明，至少部分问题是由全身性多巴胺能缺乏导致的视网膜处理受损。一些已被证实的缺陷与生理学研究一致，表明神经元的中心 - 外周相互作用可能因多巴胺能缺乏而受到影响。视网膜多巴胺（D1和D2）受体调节在灵长类动物视觉中的作用以及这些受体在突触前多巴胺能缺乏中的平衡尚未确定。在认知负荷任务中使用正弦光栅刺激可能会增进对多巴胺缺乏综合征中视觉缺陷行为后果的理解。
