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（由申请人提供）：感觉冲突和可塑性的神经机制尚未被充分理解，但在日常生活中很常见。如果感觉冲突得不到改善或减少，对人类健康的问题（例如晕动病）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。最近使用人类/猴子心理物理学的工作区分了两种多感觉可塑性机制：“无监督”和“监督”。多感觉可塑性在大脑中如何以及在何处发生尚不清楚，该提议探讨了有关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 单个皮质神经元活动的多感觉可塑性和背侧群体反应 内侧上颞区 (MSTd) 和腹侧顶内区 (VIP)。在目标 2 中，我们将利用可逆化学失活来寻找神经元活动与多感觉可塑性之间的直接联系。这里概述的目标测试了以下假设：无监督可塑性发生在相对较低水平的多感觉皮质区域 MSTd，而监督可塑性发生在较高水平的多感觉 VIP，该区域被认为更接近形成指导行为的感知决策的区域。目标 1 关于神经元调谐曲线位移、选择概率和噪声相关性的结果将用于计算群体阈值以及模拟特定的皮质病变。这些模型模拟将直接与目标 2 中的失活实验进行比较，从而提供有关神经解码的新颖信息。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，这是我们的大脑在我们一生中执行的基本操作。我们结合使用心理物理学、单细胞和群体反应、监测感知的因果操作以及计算模型，代表了最先进的方法，并确保取得实质性成功。