Orientation Processing Deficits in Amblyopia: Neural Bases to Functional Implications

项目总结 弱视是一种空间视觉障碍，尽管视网膜图像质量和眼睛健康良好。它会影响2%-3%的 人群和几乎总是发展为早期不对准(斜视)或屈光度不相等 屈光参差(屈光参差)或形觉剥夺(白内障)。大多数关于人类弱视的研究都集中在阈值上 对于对比度、大小或偏移，但显著的知觉扭曲已经通过要求弱视者 描述或绘制清晰可见的高对比度字母、环形和正弦栅格。可能会出现形式扭曲 至少和日常生活中视觉分辨率的丧失一样是个大问题。形状由局部方向定义， 而初级视觉皮质(V1)的几乎所有神经元都调整了方向，突显了它在大脑中的重要性 解析可视图像。弱视患者绘制的栅格的可复制系统知觉失真是 无法用神经扰乱模型或神经映射中的系统变化来解释，但与 V1中方位的神经编码错误，同时也涉及后来皮质中的解码机制 区域。我们的研究团队和临床医生建议检查神经发育和功能 利用我们最新的心理物理学、电生理学和模型研究光栅失真的意义 弱视的开/关系统失衡、大脑皮层地图形成、定向 跨V1的处理，以及用于感知3-D形状、对象的并行方位信号的处理 姿势和镜像对称。我们的目标是将定向编码中错误的神经发展建模为 屈光参差和斜视引起的开关不平衡的后果，限制了方向性 V1神经元的调谐和空间分辨率，并缩小弱视眼的眼优势柱。 我们还将检查弱视眼睛中的定向处理错误是否会使其难以达到更高水平 任务依赖于方位提示，或者是否有某种补偿机制，如果同伴的眼睛完成了任务 正常情况下，会过度补偿，或者因为缺少立体声音响而难以校准 发育过程中的单目线索。心理生理和电生理数据显示弱视 也涉及V1后皮质区域的异常，表明生理变化可能是 在可能具有较长可塑性窗口的较高皮质区域中传播和放大。此外, 黄斑变性患者在被动观看视觉刺激时无反应的V1区域可能是 通过让受试者参与与刺激相关的任务而被激活，暗示自上而下对 可塑性。我们用来识别重要视觉任务中的缺陷的刺激可以用来触发 来自高级大脑区域的自上而下的信号，作为未来知觉恢复治疗设计的一部分 成年后的表现，这将补充改善视力和双眼视力的治疗。 最大的回报可能来自直接测试来自这些任务的自上而下的信号是否重新激活 成人弱视患者定向选择性V1神经元的可塑性。

PROJECT SUMMARY Amblyopia is a disorder of spatial vision despite good retinal image quality and eye health. It affects 2-3% of the population and almost always develops with early misalignment (strabismus) or unequal refractive power (anisometropia), or form deprivation (cataract). Most studies on human amblyopia concentrate on thresholds for contrast, size or offset, but striking perceptual distortions have been documented by asking amblyopes to describe or draw clearly visible high-contrast letters, rings, and sinusoidal gratings. Form distortions are likely to be at least as big a problem as loss of visual resolution for daily life. Forms are defined by local orientations, and almost all neurons in primary visual cortex (V1) are tuned for orientation, highlighting its importance in parsing visual images. The replicable systematic perceptual distortions of gratings drawn by amblyopes are unexplainable with a neural scrambling model or a systematic shift in the neural map, but are compatible with errors in the neural encoding of orientation in V1, while also involving decoding mechanisms in later cortical areas. Our team of researchers and clinicians proposes to examine the neural development and functional implications of the grating distortions by using our recent psychophysics, electrophysiology and modeling results in the domains of ON/OFF system imbalance in amblyopia, cortical map formation, orientation processing across V1, and the processing of parallel orientation signals for perceptions of 3-D shape, object pose and mirror symmetry. We aim to model the neural development of errors in orientation encoding as a consequence of ON-OFF imbalance caused by anisometropia and strabismus, which limits the orientation tuning and spatial resolution of V1 neurons and shrinks the ocular dominance columns for the amblyopic eye. We will also examine if orientation processing errors in the amblyopic eye make it difficult to do higher level tasks that rely on orientation cues, or if there is some compensatory mechanism, and if the fellow eye performs normally, overcompensates, or is handicapped because the lack of stereo makes it difficult to calibrate monocular cues during development. Psychophysical and electrophysiological data suggest that amblyopia also involves abnormalities in cortical areas after V1, suggesting that physiological changes may be propagated and amplified in higher cortical areas that may have prolonged windows of plasticity. In addition, regions of V1 that are unresponsive during passive viewing of visual stimuli in macular degeneration, can be activated by engaging the subjects in a stimulus-related task, suggesting a role for top-down influences on plasticity. The stimuli we use to identify deficits in functionally important visual tasks could be used to trigger top-down signals from higher brain areas as part of the design of future treatments for recovery of perceptual performance in adulthood, which would supplement treatments for improving visual acuity and binocularity. Possibly the biggest payoff could come from directly testing if top-down signals from these tasks reactivate plasticity in orientation selective V1 neurons in adult amblyopes.