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.

项目概要 感官体验的处理对于导航和与世界互动至关重要，它依赖于 很大程度上依赖于来自高阶皮质区域的反馈输入。这在视觉系统中得到进一步强调 高阶视觉区域和初级视觉皮层 (V1) 之间的连接提供了上下文 我们看到的信息，使我们能够关注视觉刺激的重要方面。很好 据记载，V1 会因视觉体验的改变而发生塑性变化。例如，在 为了响应视觉剥夺，V1 通过改变特定层中的连接强度来适应 方式。更具体地说，我们的实验室表明，在视觉剥夺之后，第 2/3 层的横向连接 在不改变第 4 层前馈连接的情况下增加强度。这些变化很容易实现 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 成人的大脑。来自高阶视觉区域的反馈投影构成了 V1 的主要横向输入之一 第 2/3 层神经元。视觉剥夺引起的可塑性已在 V1 中得到广泛研究，但是否和 高阶视觉区域如何适应视觉体验的变化目前尚不清楚。我建议填写这个 通过首先调查来自高阶视觉的密集反馈投影的强度是否可以弥补知识差距 视觉剥夺后进入 V1 层 2/3 的区域增加（目标 1）。此外，抑制电路也很重要 调节神经元的反应并提供另一种控制可塑性的方法。我将调查 较高视觉区域和 V1 层 2/3 中的抑制细胞之间的连接，并确定视力丧失的方式 改变这些连接的强度（目标2）。最后，我将研究如何丢失这些反馈 投射影响 V1 层 2/3 神经元的自发活动（目标 3）。由此得到的结果 这项工作将揭示从高阶视觉区域到 V1 的输入如何适应视力丧失，以及如何 这些输入有助于 V1 的自发活动。此外，因为我提议的研究将在 对于成年人，研究结果将为成人视觉系统的先天可塑性提供机械理解，并且 为我们提供了促进 V1 可塑性的潜在目标，从而可以补偿视觉功能的损失。