Synaptic remodeling of neuronal circuits in early retinal degeneration.
Synaptic remodeling of neuronal circuits in early retinal degeneration.
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DOI：
10.3389/fncel.2015.00395
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发表时间：
2015
影响因子：
5.3
通讯作者：
Kerschensteiner D
中科院分区：
文献类型：
--
作者：
Soto F;Kerschensteiner D
光感受器退化是导致失明的主要原因，也是人类最常见的神经退化形式之一。对小鼠模型的研究表明，突触功能障碍往往先于光感受器退化，而从光感受器到双极细胞的异常突触输入会导致视网膜内部电路变得过度活跃。在这里，我们提供一个简短的概述常用的小鼠模型的光感受器退化。然后，我们讨论对早期突触功能障碍引发的外部视网膜和内部视网膜过度活动引发的电路重构的见解。我们在突触功能和活性的其他实验操作的背景下讨论这些见解。对视网膜回路的可塑性和早期重塑的了解将是设计成功的视力挽救策略的关键。
Photoreceptor degenerations are a major cause of blindness and among the most common forms of neurodegeneration in humans. Studies of mouse models revealed that synaptic dysfunction often precedes photoreceptor degeneration, and that abnormal synaptic input from photoreceptors to bipolar cells causes circuits in the inner retina to become hyperactive. Here, we provide a brief overview of frequently used mouse models of photoreceptor degenerations. We then discuss insights into circuit remodeling triggered by early synaptic dysfunction in the outer and hyperactivity in the inner retina. We discuss these insights in the context of other experimental manipulations of synaptic function and activity. Knowledge of the plasticity and early remodeling of retinal circuits will be critical for the design of successful vision rescue strategies.