Development of Visual Function

视觉功能的发展

• 批准号: 9360625
• 负责人: Lynne Kiorpes
• 金额: $ 39.63万
• 依托单位: NEW YORK UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1985
• 资助国家: 美国
• 起止时间: 1985-09-30 至 2019-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9360625
• 关键词: Affect; Amblyopia; Animal Model; Animals; Area; Area Analyses; Behavior; Behavioral; Binocular Vision; Blindness; Child; Code; Contrast Sensitivity; Data; Development; Discrimination; Disease; Electrodes; Evaluation; Eye; Form Perception; Foundations; Functional disorder; Goals; Human; Impairment; Individual; Inherited; Knowledge; Learning; Macaca; Masks; Measurement; Measures; Methods; Modeling; Monkeys; Nature; Neurons; Ocular Dominance; Pathway interactions; Pattern; Performance; Plant Roots; Play; Population; Property; Psychophysics; Research; Resolution; Role; Series; Signal Transduction; Site; Social Welfare; Stimulus; Stream; Testing; Texture; Utah; Vision; Vision Disorders; Visual; Visual Cortex; Visual Fields; Visual Pathways; Visual system structure; Work; area V1; area V4; awake; base; behavior measurement; developmental disease; disability; effective intervention; experience; experimental study; extrastriate visual cortex; monocular; multi-electrode arrays; neural correlate; neuromechanism; neurophysiology; nonhuman primate; perceptual organization; prevent; public health relevance; relating to nervous system; response; spatial vision; vision development; visual processing

 DESCRIPTION (provided by applicant): Amblyopia is a developmental disorder of vision that affects 3-5% of children in the US. The goals of our work are to identify the neural mechanisms underlying the visual deficits and to evaluate specific hypotheses for the neural disorder. We study a nonhuman primate model for the human visual system so that we can directly assess the neural correlates of developmental visual disability without compromising the visual welfare of any child. The proposed work aims to evaluate the neural disorder of amblyopia with a series of matched behavioral and neurophysiological studies. Since amblyopia is predominantly a disorder of spatial vision, we plan to target the ventral visual cortical pathway. The framework for the research is to contrast two mechanistic hypotheses: 1) amblyopia is a disorder arising primarily at the first stages of cortical processing that is then passed along through subsequent levels of processing, essentially unmodified, or 2) amblyopia results from a cascade of deficits that emerge from a series of changes in cortical processing as signals traverse the ventral pathway. The planned experiments will directly evaluate neural activity as it relates to amblyopic performance deficits in ventral stream cortical areas V1, V2, and V4. We will use tasks ranging from low-level to higher-order to capture the range of individual losses in these three areas: Monocular and dichoptic contrast masking, second order contrast discrimination, naturalistic texture discrimination, and Gabor contour integration, as well as basic characterization of the first-order spatial deficit. The same stimuli will be employed for behavioral and neurophysiological testing in individual subjects. The recordings will be conducted in awake, behaving amblyopes with multi-electrode "Utah" arrays placed in the three ventral stream areas simultaneously. The goal is to record single and multi-unit activity simultaneously in foveal representations of the three target visual areas; we will also separately assess responses in the parafoveal visual field representation of V4. We will use population decoding and correlational analyses to compare behavioral performance and neural activity between the eyes of amblyopes, between amblyopes and controls, between different visual areas, and across specific visual tasks. The results will be used to evaluate and refine the current views on the neural disorder in amblyopia. In addition, we will learn about the neural mechanisms underlying form perception in normal individuals. Our research will ultimately inform efforts to treat and prevent amblyopia development in children.

 描述（由适用提供）：弱视是一种影响美国3-5％儿童的视力障碍。我们工作的目标是确定视觉缺陷的基础神经元机制，并评估神经元疾病的特定假设。我们研究了人类视觉系统的非人类私人模型，以便我们可以直接评估发育视觉障碍的神经元相关性，而不会损害任何儿童的视觉福利。提出的工作旨在通过一系列匹配的行为和神经生理研究来评估弱视的神经元疾病。由于弱视主要是空间视力的障碍，因此我们计划针对腹侧视觉皮质途径。该研究的框架是对比两个机械假设进行对比：1）弱点是一种疾病，主要是在皮层处理的第一阶段引起的疾病，然后通过随后的处理水平（本质上没有修改）通过，弱视是由定义的级联产生的，这些定义是由一系列的变化而导致的。计划的实验将直接评估与通风流的皮质区域V1，V2和V4中的弱视性能防御措施有关的中性活性。我们将使用从低级到高阶的任务来捕获这三个领域的个体损失范围：单眼和二分法对比度掩盖，二阶对比度歧视，自然主义纹理歧视以及Gabor轮廓整合，以及一阶空间赤字的基本表征。在个别受试者中，将采用相同的刺激进行行为和神经生理测试。录音将在清醒中进行，以多电极“犹他州”阵列的行为弱小，简单地放置在三个腹流区域。目的是仅在三个目标视觉区域的动脉表示中记录单个和多单元活动。我们还将分别评估V4的副视觉场表示中的响应。我们将使用人群解码和相关分析来比较弱视的眼睛之间的行为表现和神经活动，在不同的视觉区域之间以及特定的视觉任务之间，弱视和控制之间，弱视和控制之间。结果将用于评估和完善有关弱视神经元疾病的当前观点。此外，我们将了解正常个体中基础形式感知的神经元机制。我们的研究最终将为治疗和预防儿童弱视发展的努力提供帮助。