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戏剧性的进展。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 全世界。此外，两个小组正在积极植入和开发皮质电子设备 植入物。第一个光遗传学临床试验已经开始，未来两年可能还会有更多的临床试验 好几年了。在十年内，许多盲人可能会得到广泛的选择 用于视力恢复，这依赖于截然不同的技术。 植入电子器件与视网膜或视网膜潜在神经生理学的相互作用 皮质意味着这些技术中的大多数提供的视觉将与 视力正常。这项提议的问题是--大脑皮层的可塑性在帮助 患者使用这种人工视觉输入吗？ 在过去的15年里，我们的研究小组一直在生成计算模型，开发出 使用生理和心理物理数据的组合，可以预测感知 患者可能会体验到各种视力恢复技术。我们建议使用 这些模型在视觉正常的参与者中模拟了四个关键的神经生理学 视力恢复技术固有的失真： 目的1.视网膜刺激时异常神经元群体反应：同时刺激 开和关牢房。 目的2.空间扭曲：刺激视网膜神经节细胞轴突。 目的3.异常皮质神经元群体反应：由V1神经引起的扭曲 建筑。 目的4.慢速光发生动力学导致的时间模糊。 我们的目标是使用正常视力的参与者，观看扭曲的视觉输入，作为虚拟的 患者了解哪些时空扭曲可以通过可塑性来补偿，以及 在器件设计中必须加以补偿。这将为设备制造商提供 对视觉知觉适应性的能力和限度有更细微的理解。 最后，这项工作将为大脑皮层的基本机制提供新的见解 通过询问在成年后是否有可能重新配置基本的构建块来实现可塑性 视觉感知的能力？

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?