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

基本信息

批准号：
10673202
负责人：
Samuel Parkins
金额：
$ 4.77万
依托单位：
JOHNS HOPKINS UNIVERSITY
依托单位国家：
美国
项目类别：
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/10673202
关键词：
Address Adult Affect Anterolateral Area Attention Axon Blindness Brain Cells Code Compensation Darkness Equilibrium Feedback Injections Jaw Knowledge Label Lateral Life Maps Measures Methods Modeling Motion Mus Nature Neurodegenerative Disorders Neurons Opsin Parvalbumins Pathway interactions Population Process Reporter Reporting Research Retina Sensory Source Stream Stroke Synapses Synaptic plasticity Techniques Testing Thalamic structure Transgenic Mice V1 neuron Vision Visual Visual Cortex Visual System Whole-Cell Recordings Work area striata deprivation excitatory neuron expectation experience experimental study extrastriate visual cortex falls genetic manipulation hippocampal pyramidal neuron in vivo imaging in vivo two-photon imaging inhibitory neuron optogenetics recruit response visual deprivation visual information visual processing visual stimulus

项目摘要

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，这对于与世界进行导航和互动至关重要大量的反馈输入来自高阶皮质区域。在视觉系统中进一步强调了这一点高阶视觉区域和主要视觉皮层（V1）之间的连通性提供了上下文对于我们看到的信息，并允许我们关注视觉刺激的重要方面。很好记录，V1会因改变视觉体验而进行塑料变化。例如，在对视觉剥夺的响应，V1通过在特定层的特定层中改变其连接的强度来适应方式。更具体地说，我们的实验室表明，在视觉剥夺后，第2/3层的横向连接强度的提高而没有第4层的进发电连接变化。这些变化很容易在成年小鼠中观察到，这表明视觉剥夺是在成人大脑。高阶视觉区域的反馈预测构成了V1的主要侧向输入之一第2/3层神经元。视觉剥夺引起的可塑性已在V1中进行了广泛的研究，但是是否和当前未知的高阶视觉区域如何适应视觉体验的变化。我建议填补这个通过首先调查高阶视觉的密集反馈预测的强度，通过知识差距视觉剥夺后，V1 2/3层的区域增加（AIM1）。另外，抑制电路很重要在调节神经元的反应中，并提供了另一种控制可塑性的方式。我将调查 V1第2/3层中较高视野和抑制细胞之间的连接，并确定Vison损失如何改变这些连接的强度（AIM2）。最后，我将调查这些反馈的损失投影影响V1层2/3中神经元的自发活动（AIM 3）。从此获得的结果工作将阐明从高阶视觉区域到V1的投入如何适应视力的丧失，以及如何这些输入有助于V1中的自发活动。此外，因为我建议的研究将在成人，结果将对成人视觉系统中的先天可塑性提供机械理解，以及为我们提供潜在的目标，以促进可以弥补视觉功能丧失的V1可塑性。