Regulation of Anatomical Plasticity and Perceptual Learning by NgR1

描述（由申请人提供）：新的感觉体验和改善的运动表现改变了大脑皮层中的结构性突触连接，但这种解剖可塑性对感知学习的功能贡献尚不清楚。最近，新兴的技术，在体内反复成像神经元结构的树突棘作为一个潜在的学习基板的重塑集中注意力。然而，解决脊柱重塑和学习之间的关系的一个主要障碍是确定脊柱动力学是否是特定的皮质区域，神经元的身份和学习任务。 由于胡须的地形表示和胡须使用的可控性、可量化性，体感皮层（桶皮层）中的桶场一直是检查感觉体验期间脊柱重塑的有利系统。差距跨越任务是一种自动化的、定量的感知学习任务，其依赖于通过触须检测两个平台之间的间隙。这些实验结合联合收割机慢性在体成像的树突棘在桶皮质与这种知觉学习任务，以调查是否和如何重建的速度可以指定的速度知觉学习。 为了检验脊柱重塑的速率报告感知学习的速率的假设，随后的组合成像和学习实验利用了nogo-66受体（NgR 1）突变小鼠的表型，这些小鼠学习这项任务更快。NgR 1是一种神经元蛋白，调节受损和完整中枢神经系统的可塑性。NgR 1突变体从脊髓损伤和中风中恢复得更好;成年NgR 1突变体也显示出一种通常局限于发育关键期的视觉可塑性。NgR 1如何调节脊柱重塑和感知学习不仅可以提高对解剖可塑性如何有助于学习的理解，而且可以揭示这种受体在损伤后和发育过程中控制可塑性的保守机制。

DESCRIPTION (provided by applicant): Novel sensory experience and improved motor performance modify structural synaptic connectivity in the cerebral cortex, yet the functional contribution of this anatomical plasticity to perceptual learning is unclear. Recently, emerging techniques for repeatedly imaging neuronal structures in vivo has focused attention upon the remodeling of dendritic spines as a potential substrate for learning. However, a major obstacle to resolving the relationship between spine remodeling and learning is determining if spine dynamics are specific to cortical region, neuronal identity and learning task. The barrel field in somatosensory cortex (barrel cortex) has been a favored system for examining spine remodeling during sensory experience due to the topographical representation of whiskers and controlled, quantifiable nature of whisker use. The gap crossing task is an automated, quantitative perceptual learning task that relies on detection of a gap between two platforms by the whiskers. These experiments combine chronic in vivo imaging of dendritic spines in barrel cortex with this perceptual learning task to investigate if and how the rate of spine remodeling may specify the rate of perceptual learning. To test the hypothesis that the rate of spine remodeling reports the rate of perceptual learning, subsequent combined imaging and learning experiments exploit the phenotype of nogo-66 receptor (NgR1) mutant mice that learn this task faster. NgR1 is a neuronal protein that regulates plasticity in both the injured and intact central nervous system. NgR1 mutants recover better from spinal cord injury and stroke; adult NgR1 mutants also display a form of visual plasticity normally confined to a developmental critical period. How NgR1 regulates both spine remodeling and perceptual learning may improve not only understanding of how anatomical plasticity contributes to learning, but may reveal conserved mechanisms by which this receptor governs plasticity after injury and during development as well.