Plasticity during visual/vestibular conflict

视觉/前庭冲突期间的可塑性

• 批准号: 9825191
• 负责人: Dora Angelaki
• 金额: $ 53.67万
• 依托单位: NEW YORK UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-09-03 至 2021-09-02
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9825191
• 关键词: Plasticity; during; visual; vestibular; conflict

 DESCRIPTION (provided by applicant): The neural mechanisms of sensory conflict and plasticity are not well understood, yet common in everyday life. If sensory conflict is not ameliorated or reduced, problems to human health, such as motion sickness, can be harmful. Perceptual plasticity can ameliorate motion sickness by reducing sensory conflict. Here we hypothesize that multisensory plasticity enables our senses to dynamically adapt to each other and the external environment. Recent work using human/monkey psychophysics has distinguished two multisensory plasticity mechanisms, "unsupervised" and "supervised". How and where multisensory plasticity takes place in the brain is unknown and this proposal explores specific hypotheses about its neural basis. In aim 1, we will search for neural correlates of adult multisensory plasticity in single cortical neuron activity and population responses from the dorsal medial superior temporal area (MSTd) and ventral intraparietal area (VIP). In aim 2, we will search for direct links between neuronal activity and multisensory plasticity using reversible chemical inactivation. The aims outlined here test the hypothesis that unsupervised plasticity occurs in the relatively low- level multisensory cortical area MSTd, whereas supervised plasticity occurs in higher-level multisensory VIP, an area thought closer to where the perceptual decisions that guide behavior are formed. Results from aim 1 about neuronal tuning curve shifts, choice probabilities and noise correlations will be used to compute population thresholds as well as simulate specific cortical lesions. These model simulations will be directly compared with the inactivation experiments in aim 2, thus providing novel information about neural decoding. Results from these experiments are critical for understanding the neural basis of multisensory plasticity, a fundamental operation our brain performs throughout our lives. Our combined use of psychophysics, single cell and population responses, causal manipulations while monitoring perception, as well as computational modeling, represents a state-of-the-art approach and ensures substantial successes.

 描述(申请人提供)：感觉冲突和可塑性的神经机制还不是很清楚，但在日常生活中很常见。如果感觉冲突没有得到改善或减少，对人类健康的问题，如晕车，可能是有害的。知觉可塑性可以通过减少感觉冲突来缓解晕动病。在这里，我们假设多感官的可塑性使我们的感官能够动态地适应彼此和外部环境。最近利用人类/猴子心理物理学的研究区分了两种多感官可塑性机制，即“无监督”和“有监督”。多感官可塑性在大脑中如何以及在哪里发生尚不清楚，这项提议探索了关于其神经基础的具体假设。在目标1中，我们将寻找成人的神经关联 背侧单个皮层神经元活动和群体反应的多感觉可塑性 内侧上颞区(MSTd)和腹侧顶内区(VIP)。在目标2中，我们将使用可逆的化学失活来寻找神经元活动和多感觉可塑性之间的直接联系。这里概述的目的是测试这一假说，即无监督可塑性发生在相对较低水平的多感觉皮质区域MSTd，而有监督可塑性发生在较高水平的多感觉VIP区域，这一区域被认为更接近于指导行为的知觉决定形成的地方。来自目标1的关于神经元调谐曲线移动、选择概率和噪声相关性的结果将被用于计算种群阈值以及模拟特定的皮质损伤。这些模型模拟将直接与AIM 2中的失活实验进行比较，从而提供关于神经解码的新信息。这些实验的结果对于理解多感觉可塑性的神经基础至关重要，多感觉可塑性是我们的大脑在一生中执行的一项基本操作。我们结合使用心理物理学、单细胞和群体反应、监测感知的因果处理以及计算建模，代表了一种最先进的方法，并确保了实质性的成功。