Mechanisms of visual learning in cortical blindness

皮质失明的视觉学习机制

• 批准号: 8698756
• 负责人: Krystel R Huxlin
• 金额: $ 37.85万
• 依托单位: UNIVERSITY OF ROCHESTER
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-08-01 至 2016-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8698756
• 关键词: Adult; Anatomy; Area; Awareness; Biological Preservation; Blindness; Brain; Bypass; Characteristics; Complex; Conscious; Cortical Blindness; Data; Discrimination; Elderly; Eye; Functional Magnetic Resonance Imaging; Goals; Human; Individual; Knowledge; Learning; Link; Location; Macaca; Measures; Mediating; Modality; Modeling; Motion; Neurons; Noise; Pathway interactions; Patients; Perceptual learning; Process; Property; Protocols documentation; Psychological Transfer; Psychophysics; Pulvinar structure; Recovery; Recruitment Activity; Rehabilitation therapy; Role; Shapes; Specificity; Stimulus; Testing; Training; Unconscious State; Vision; Visual; Visual Cortex; Visual Fields; Visual Pathways; Visual Psychophysics; Visual system structure; Work; aging population; area V1; area V4; area striata; base; blind; brain pathway; design; disability; extrastriate visual cortex; improved; information processing; meetings; orientation selectivity; relating to nervous system; research study; response; retinotopic; signal processing; superior colliculus Corpora quadrigemina; treatment strategy; visual information; visual learning; visual process; visual processing

DESCRIPTION (provided by applicant): Damage to the adult primary visual cortex (V1) causes a loss of conscious vision over the same part of the visual field in both eyes (cortical blindness - CB). This increasingly common cause of permanent disability in older, adult humans is still considered untreatable. Our long-term objective is to define a new paradigm for understanding visual recovery after permanent visual cortex damage. Our goal is to characterize the properties of and signal processing mechanisms that enable visual relearning and recovery in CB. Knowing what mechanisms and brain pathways mediate recovery will allow us to predict the extent to which vision can be recovered, as well as the quality and modality of recovered vision that can be attained in a given individual. We will meet our objective and goal by testing the primary hypothesis that after V1 damage, training-induced relearning in CB fields depends on motion processing for its initiation. This is based on our preliminary findings that motion training in CB fields transfers to static orientation discriminations not normally perceivable in blindsight. However, without the initial motion training, these static discriminations cannot be relearned. While training could work via a variety of mechanisms, our preliminary findings suggest the following alternatives, to be tested here: 1) training stimulates the motion processing complex hMT+ to more effectively process visual information from CB fields, including that needed for static orientation discriminations, 2) training stimulates the motion pathway to reactivate other visual areas (incl. parts of V1, V2, V3, V4, V01) and their pre-existing processing abilities, or 3) training alters readout of information from hMT+/other areas. Aim 1 will use visual psychophysics to test the hypothesis that static orientation relearning depends on learning in the motion pathway, and to measure specificity of learning for trained directions/orientations. Aim 2 will use the perceptual template model (PTM) and psychophysical tests of spatial suppression to test the hypothesis that relearning in CB fields occurs via 1) changes in tuning of basic orientation or direction channels, possibly via changes in spatial suppression within these channels, or 2) that training improves the readout of these channels. Aim 3 will use functional MRI (fMRI) to measure changes in functional anatomy associated with relearning in CB fields. We will test the hypothesis that visual training: 1) alters the blind field's retinotopic representation either in just hMT+ or both in hMT+ and other visual areas (V1, V2, V3, V4, V01); 2) increases direction and/or orientation specificity in just hMT+ or both in hMT+ and V1, V2, V3, V4, V01 or 3) none of the above. Our results will provide critical information about brain pathways and signal processing mechanisms stimulated by training to evoke visual relearning in CB fields. This knowledge is essential theoretically to better understand the type and degree of plasticity possible in damaged, adult visual systems, and to improve our treatment strategies for humans suffering from the disability induced by permanent visual cortical damage.

描述（由申请人提供）：对成人原发性视觉皮层（V1）的损害会导致两只眼睛的视野的同一部分（皮质失明-CB）导致有意识的视力丧失。在年龄较大的成年人中，这种永久残疾的日益普遍原因仍然被认为是不可治疗的。我们的长期目标是定义一个新的范式，以理解永久视觉皮层损害后视觉​​恢复。我们的目标是表征能够在CB中进行视觉重新学习和恢复的信号处理机制的属性和信号处理机制。知道哪些机制和大脑途径介导恢复将使我们能够预测可以恢复视力的程度，以及在给定个人中可以实现的恢复视力的质量和方式。我们将通过测试主要假设来实现我们的目标和目标，即在V1损坏后，CB领域训练引起的重新学习取决于其启动的运动处理。这是基于我们的初步发现，即CB场中的运动训练转移到静态方向区分，通常在盲目的角度不可感知。但是，如果没有初步的运动训练，这些静态歧视就无法重新学习。 While training could work via a variety of mechanisms, our preliminary findings suggest the following alternatives, to be tested here: 1) training stimulates the motion processing complex hMT+ to more effectively process visual information from CB fields, including that needed for static orientation discriminations, 2) training stimulates the motion pathway to reactivate other visual areas (incl. parts of V1, V2, V3, V4, V01) and their pre-existing处理能力，或3）培训会改变HMT+/其他领域的信息的读数。 AIM 1将使用视觉心理物理学来检验以下假设：静态取向重新学习取决于运动途径中的学习，并测量训练有素的方向/方向的学习特异性。 AIM 2将使用感知模板模型（PTM）和空间抑制的心理物理测试来检验以下假设：CB领域中的重新学习是通过1）通过1）进行基本定向或方向通道的调整而发生的变化，这可能是通过这些通道内空间抑制的变化来进行的，或者可以通过这些通道内的空间抑制，或者2）训练这些渠道的读数可以改善这些渠道的读数。 AIM 3将使用功能性MRI（fMRI）来测量与CB场中重新学习相关的功能解剖结构的变化。我们将测试视觉训练的假设：1）在仅在HMT+中或HMT+和其他视觉区域（V1，V2，V3，V3，V4，V01）中改变盲田的视网膜表示形式； 2）仅在HMT+中增加方向和/或方向的特异性，或在HMT+和V1，V2，V3，V4，V4，V01或3中增加方向和/或方向的特异性。我们的结果将提供有关通过训​​练唤起CB领域视觉重新学习的脑通路和信号处理机制的关键信息。从理论上讲，这些知识对于更好地了解受损的成人视觉系统可能的可塑性类型和程度至关重要，并改善了我们对由永久视觉皮质损害造成的残疾的人类的治疗策略。