Learning to see again: biological constraints on cortical plasticity and the implications for sight restoration technologies

摘要 在过去的十年里，视力恢复领域取得了巨大的进步。两种类型的 视网膜植入物已经获得商业批准，其他几种设计正在开发中 国际吧此外，两个小组正在积极植入和开发皮层电子 植入物.第一个光遗传学临床试验已经开始，未来两个月可能会有许多其他试验。 年在十年内，许多盲人可能会得到广泛的选择， 用于视力恢复，这取决于广泛不同的技术。 植入电子设备与视网膜的潜在神经生理学之间的相互作用， 皮质意味着这些技术中的大多数提供的视觉将与 正常的视力。这个提议的问题是--大脑皮层可塑性在帮助 病人利用这种人工视觉输入？ 在过去的15年里，我们的研究小组一直在生成计算模型， 使用生理和心理物理数据的组合，可以预测感知 患者可能会经历各种视力恢复技术。我们建议使用 这些模型模拟，在视觉正常的参与者，四个关键的神经生理 视觉恢复技术中固有的失真： 目标1。视网膜刺激过程中的异常神经元群体反应：同时刺激 开和关的细胞。 目标2.空间扭曲：视网膜神经节细胞轴突的刺激。 目标3。异常皮层神经元群体反应：V1神经元诱导的畸变 架构 目标4。由于光遗传学动力学缓慢导致的时间模糊。 我们的目标是使用正常视力的参与者，将扭曲的视觉输入视为“虚拟” 患者学习哪些时空扭曲可以通过可塑性来补偿， 这在器件设计中必须得到补偿。这将为设备制造商提供 更细致入微地理解视知觉适应性的能力和局限性。 最后，这项工作将提供新的见解有关的基本机制，皮层 可塑性的问题，在成年后，是否有可能重新配置基本的积木， 视觉感知？

ABSTRACT The field of sight restoration has made dramatic progress over the last decade. Two types of retinal implants have been commercially approved, and several other designs are in development worldwide. In addition, two groups are actively implanting and developing cortical electronic implants. The first optogenetic clinical trial has begun, with many others likely in the next two years. Within a decade, many blind individuals are likely to be offered a wide range of options for sight restoration that depend on widely different technologies. Interactions between implant electronics and the underlying neurophysiology of the retina or cortex mean that the vision provided by most of these technologies will differ substantially from normal sight. The question of this proposal is – What role can cortical plasticity play in helping patients make use of this artificial visual input? Over the past 15 years our research group has been generating computational models, developed using a combination of physiological and psychophysical data, which can predict the percepts that patients might experience for a variety of sight recovery technologies. We propose to use these models to simulate, within visually normal participants, four critical neurophysiological distortions inherent in sight restoration technologies: Aim 1. Abnormal neuronal population responses during retinal stimulation: Simultaneous stimulation of on and off cells. Aim 2. Spatial distortions: Stimulation of retinal ganglion cell axons. Aim 3. Abnormal cortical neuronal population responses: Distortions induced by the V1 neural architecture. Aim 4. Temporal blurring due to slow optogenetic kinetics. Our goal is to use normally sighted participants, viewing distorted visual input, as ‘virtual patients’ to learn which spatiotemporal distortions can be compensated for by plasticity, and which must be compensated for in device design. This will provide device manufacturers with a more nuanced understanding of the abilities and limits of visual perceptual adaptability. Finally, this work will provide novel insights regarding the fundamental mechanisms of cortical plasticity by asking whether, in adulthood, it is possible to reconfigure the fundamental building blocks of visual perception?