Neuronal plasticity of the inner retina has been observed in response to photoreceptor degeneration. Typically, this phenomenon has been considered maladaptive and may preclude vision restoration in the blind. However, several recent studies utilizing triggered photoreceptor ablation have shown adaptive responses in bipolar cells expected to support normal vision. Whether such homeostatic plasticity occurs during progressive photoreceptor degenerative disease to help maintain normal visual behavior is unknown. We addressed this issue in an established mouse model of Retinitis Pigmentosa caused by the P23H mutation in rhodopsin. We show robust modulation of the retinal transcriptomic network, reminiscent of the neurodevelopmental state, and potentiation of rod – rod bipolar cell signaling following rod photoreceptor degeneration. Additionally, we found highly sensitive night vision in P23H mice even when more than half of the rod photoreceptors were lost. These results suggest retinal adaptation leading to persistent visual function during photoreceptor degenerative disease.

中文翻译：

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视网膜的稳态可塑性与视网膜退行性疾病期间夜视的维持有关

已经观察到内部视网膜的神经元可塑性响应光感受器变性。通常，这种现象被认为是适应不良的，可能会妨碍盲人的视力恢复。然而，最近几项利用触发光感受器消融的研究表明，双极细胞的适应性反应有望支持正常视力。这种稳态可塑性是否在进行性光感受器退行性疾病期间发生以帮助维持正常的视觉行为尚不清楚。我们在由视紫质中的 P23H 突变引起的色素性视网膜炎小鼠模型中解决了这个问题。我们展示了视网膜转录组网络的强大调制，让人联想到神经发育状态，以及杆状光感受器变性后杆 - 杆双极细胞信号传导的增强。此外，我们发现 P23H 小鼠具有高度敏感的夜视能力，即使超过一半的视杆光感受器丢失。这些结果表明视网膜适应导致光感受器退行性疾病期间的持续视觉功能。