Diabetic retinopathy is now well understood as a neurovascular disease. Significant deficits early in diabetes are found in the inner retina that consists of bipolar cells that receive inputs from rod and cone photoreceptors, ganglion cells that receive inputs from bipolar cells, and amacrine cells that modulate these connections. These functional deficits can be measured in vivo in diabetic humans and animal models using the electroretinogram (ERG) and behavioral visual testing. Early effects of diabetes on both the human and animal model ERGs are changes to the oscillatory potentials that suggest dysfunctional communication between amacrine cells and bipolar cells as well as ERG measures that suggest ganglion cell dysfunction. These are coupled with changes in contrast sensitivity that suggest inner retinal changes. Mechanistic in vitro neuronal studies have suggested that these inner retinal changes are due to decreased inhibition in the retina, potentially due to decreased gamma aminobutyric acid (GABA) release, increased glutamate release, and increased excitation of retinal ganglion cells. Inner retinal deficits in dopamine levels have also been observed that can be reversed to limit inner retinal damage. Inner retinal targets present a promising new avenue for therapies for early-stage diabetic eye disease.

中文翻译：

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早期糖尿病对视网膜内神经元的影响

糖尿病性视网膜病变现在被很好地理解为一种神经血管疾病。糖尿病早期的显着缺陷存在于视网膜内部，包括接收来自视杆和视锥细胞光感受器的输入的双极细胞、接收来自双极细胞的输入的神经节细胞以及调节这些连接的无长突细胞。这些功能缺陷可以测量体内在糖尿病人和动物模型中使用视网膜电图 (ERG) 和行为视觉测试。糖尿病对人类和动物模型 ERG 的早期影响是振荡电位的变化，表明无长突细胞和双极细胞之间的通讯功能障碍，以及 ERG 测量表明神经节细胞功能障碍。这些与表明内部视网膜变化的对比敏感度变化相结合。机械的体外神经元研究表明，这些视网膜内部变化是由于视网膜抑制减少，可能是由于 γ 氨基丁酸 (GABA) 释放减少、谷氨酸释放增加和视网膜神经节细胞兴奋增加。还观察到多巴胺水平的内部视网膜缺陷可以逆转以限制内部视网膜损伤。视网膜内靶点为早期糖尿病眼病的治疗提供了一条有希望的新途径。