Plasticity of feedback inputs from Higher Order Visual Areas into Primary Visual Cortex

从高阶视觉区域到初级视觉皮层的反馈输入的可塑性

• 批准号: 10240287
• 负责人: Samuel Parkins
• 金额: $ 4.6万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-08-01 至 2024-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10240287
• 关键词: Address; Adult; Affect; Anterolateral; Area; Attention; Axon; Blindness; Brain; Cells; Code; Equilibrium; Feedback; Injections; Jaw; Knowledge; Label; Lateral; Life; Light; Maps; Measures; Methods; Modeling; Motion; Mus; Nature; Neurodegenerative Disorders; Neurons; Opsin; Parvalbumins; Pathway interactions; Population; Process; Reporter; Reporting; Research; Retina; Sensory; Source; Stroke; Synapses; Synaptic plasticity; Techniques; Testing; Thalamic structure; Transgenic Mice; V1 neuron; Vision; Visual; Visual Cortex; Visual system structure; Whole-Cell Recordings; Work; area striata; deprivation; excitatory neuron; expectation; experience; experimental study; extrastriate visual cortex; falls; genetic manipulation; in vivo imaging; in vivo two-photon imaging; inhibitory neuron; optogenetics; recruit; response; visual deprivation; visual information; visual stimulus

Project Summary Processing of sensory experience, which is essential for navigating and interacting with the world, relies heavily on feedback inputs from higher-order cortical areas. This is further emphasized in the visual system where the connectivity between higher-order visual areas and the primary visual cortex (V1) provides context to the information we see, and allows us to pay attention to important aspects of the visual stimuli. It is well documented that V1 undergoes plastic changes in response to altered visual experience. For instance, in response to visual deprivation, V1 adapts by changing the strength of its connections in a layer specific manner. More specifically, our lab has shown that after visual deprivation, lateral connections in layer 2/3 increase in strength without changes in feedforward connections from layer 4. These changes were readily observed in adult mice, which suggests that visual deprivation is an effective means to produce plasticity in the adult brain. Feedback projections from higher-order visual areas constitute one of the major lateral inputs to V1 layer 2/3 neurons. Visual deprivation-induced plasticity has been studied extensively in V1, but whether and how higher-order visual areas adapt to changes in visual experience is currently unknown. I propose to fill this knowledge gap by first investigating if the strength of the dense feedback projections from higher-order visual areas into V1 layer 2/3 is increased after visual deprivation (Aim1). Additionally, inhibitory circuitry is important in modulating responses of neurons and provides another way of controlling plasticity. I will investigate the connections between higher-visual areas and inhibitory cells in V1 layer 2/3 and determine how vison loss changes the strength of these connections (Aim2). Lastly, I will investigate how loss of these feedback projections affects the spontaneous activity of neurons in V1 layer 2/3 (Aim 3). The results obtained from this work will shed light on how inputs from higher-order visual areas to V1 adapt to the loss of vision, and how these inputs contribute to spontaneous activity in V1. Furthermore, because my proposed study will be done in adults, the results will provide mechanistic understanding on the innate plasticity in the adult visual system, and provide us with potential targets to promote V1 plasticity that could compensate for loss of visual function.

项目摘要 感官体验的处理对于导航和与世界互动至关重要， 主要依赖于来自高级皮层区域的反馈输入。这一点在视觉系统中得到了进一步强调 高级视觉区域和初级视觉皮层（V1）之间的连接提供了背景 我们看到的信息，并允许我们关注视觉刺激的重要方面。公 记录了V1经历塑性变化以响应改变的视觉体验。例如在 作为对视觉剥夺的反应，V1通过改变其在特定层中的连接强度来适应 方式更具体地说，我们的实验室已经表明，在视觉剥夺后，第2/3层的横向连接 在不改变来自层4的前馈连接的情况下增加强度。这些变化是显而易见的。 在成年小鼠中观察到，这表明视觉剥夺是产生可塑性的有效手段， 成人大脑来自高阶视觉区的反馈投射构成了V1的主要横向输入之一 2/3层神经元。视觉剥夺诱导的可塑性已经在V1中得到了广泛的研究，但是 高阶视觉区域如何适应视觉体验的变化目前是未知的。我建议把这个 通过首先调查来自高阶视觉的密集反馈投影的强度， 视觉剥夺后，V1层2/3的面积增加（Aim 1）。此外，抑制回路也很重要， 调节神经元的反应，并提供了另一种控制可塑性的方法。我会调查 V1层2/3中的高视觉区和抑制细胞之间的联系，并确定vison损失如何 改变这些连接的强度（Aim 2）。最后，我将研究如何失去这些反馈， 投射影响V1层2/3中神经元的自发活动（Aim 3）。由此获得的结果 这项工作将阐明从高阶视觉区到V1的输入如何适应视力的丧失，以及如何 这些输入有助于V1的自发活动。此外，由于我的研究将在 成年人，结果将提供对成人视觉系统先天可塑性的机械理解， 为我们提供了促进V1可塑性的潜在目标，可以补偿视觉功能的丧失。