Mechanisms and Perceptual Consequences of Somatosensory Cortical Plasticity

描述(由申请人提供)：这项建议的资金将用于培训申请人对能够执行复杂触觉辨别任务的人类和非人类灵长类动物进行综合心理物理研究和神经生理学研究。这些实验解决了与躯体感觉皮质可塑性有关的两个基本问题。首先，我们将通过描述在一项任务中诱导的可塑性是否会改变执行其他任务的能力，来确定触觉训练后的皮质可塑性是否改变了相关的感知能力。虽然许多研究表明，大脑皮质是可塑性的，但这种可塑性如何与知觉总体上相关还不得而知。其次，我们将研究注意力诱导可塑性的机制。众所周知，注意刺激对于学习发生是很重要的。以往的研究表明，非人灵长类动物在同时刺激多个手指时，在初级躯体感觉皮层3b区(SI，3b)发展出新的多指表征。此外，众所周知，选择性注意改变了体感神经元的放电频率和神经元之间的同步放电程度。我们在这里测试注意力是否通过同步性和假定的Hebbian机制的变化导致可塑性。为了解决这种可塑性的知觉相关性的第一个问题，在目标1中，我们将确定用多位数刺激训练人类的单个和多位数触觉空间知觉会发生什么。我们假设，多位触觉空间敏锐度将以牺牲一位数触觉空间敏锐度为代价而增加。研究结果将有助于更好地理解学习机制。它还将有助于描述局灶性肌张力障碍的症状与触觉输入的关系，以及如何在康复过程中指导可塑性。我们还讨论了注意力如何作用于可塑性机制，以及可能控制注意力信号的区域在学习过程中如何改变。在目标2中，我们将研究注意力对皮质可塑性的作用，并测试驱动可塑性的潜在机制：可塑性是否与注意诱导的皮质同步性有关？在目标2a中，我们将从SI，3b中的细胞对记录动物在接受相同触觉刺激的同时参与多位数触觉任务或视觉任务的过程。我们预测，在触觉任务中，细胞对将表现出更多的同步性，这将对应于更大的感受野扩展。我们还预测，参与触觉刺激的动物将比参与视觉任务的动物表现出更大的SI，3b MAP可塑性。在目标2b中，我们将分析动物学习触觉任务时同时从腹外侧额叶皮质(VLPFC)记录的数据。这一区域与躯体感觉皮质相连，并与多感觉注意机制和触觉工作记忆有关。我们预测，VLPFC活动将预测躯体感觉可塑性和注意同步性。因此，这一目标将检验为什么注意力是诱导/增强可塑性所必需的准确解释。这样的结果将帮助我们更好地理解认知状态如何与学习过程中发生的大脑过程相互作用。 公共卫生相关性：我们希望了解在触觉辨别任务训练后皮质的可塑性如何影响触觉知觉，以及注意力如何改变初级躯体感觉反应以增强可塑性。我们将研究的特定类型的可塑性与局灶性肌张力障碍有关；因此，了解这些机制将指导未来对这种疾病的治疗。此外，通过准确地了解注意力如何改变大脑结构，我们可以描述感觉运动技能发展和学习的机制，以指导教育和康复。

DESCRIPTION (provided by applicant): Funds for this proposal will be used to train the applicant to perform combined psychophysical studies of humans and neurophysiological studies of non-human primates able to perform complex tactile discrimination tasks. The experiments address two fundamental questions related to somatosensory cortical plasticity. First, we will determine if cortical plasticity following tactile training alters related perceptual abilities, by describing if plasticity induced during one task alters ability in performing other tasks. While many studies have shown that the cortex is plastic, it is unknown how this plasticity is related to perception in general. Second, we will investigate the mechanisms by which attention induces plasticity. It is well known that attending to stimuli is important for learning to occur. Previous studies have shown that non-human primates attending to simultaneous stimulation of multiple digits develop novel multi-digit representations in primary somatosensory cortex, area 3b (SI, 3b). Furthermore, it is known that selective attention changes somatosensory neurons' firing rate and the degree of synchronous firing between neurons. We test here whether attention causes plasticity via changes in synchrony and putative Hebbian mechanisms. To address the first question of the perceptual relevance of this plasticity, in Aim 1, we will determine what happens to single and multi-digit tactile spatial-perception as a result of training humans with multi-digit stimuli. We hypothesize that multi-digit tactile spatial acuity will increase at the expense of single digit tactile spatial acuity. The results will provide a better understanding of the mechanisms of learning. It will also help describe how symptoms of focal dystonia are related to tactile input, and how to direct plasticity during rehabilitation. We also address how attention acts upon mechanisms of plasticity and how regions that presumably control attentional signals are altered during learning. In aim 2 we will investigate the role of attention on cortical plasticity, and test a potential mechanism that drives plasticity: is plasticity is related to attentionally- induced cortical synchrony? In aim 2a we will record from cell pairs in SI, 3b while an animal attends to a multi-digit tactile task or a visual task while receiving the same tactile stimulation. We predict that cell pairs will exhibit more synchrony during the tactile task and this will correspond to greater receptive field expansion. We also predict that animals attending to a tactile stimulus will show greater SI, 3b map plasticity than animals attending to a visual task. In aim 2b, we will analyze data recorded simultaneously from the ventrolateral prefrontal cortex (vLPFC) while the animal learns the tactile task. This area is connected with somatosensory cortices, and is implicated in multisensory attentional mechanisms and tactile working memory. We predict that vLPFC activity will predict somatosensory plasticity and attentional synchrony. This aim will therefore test a precise explanation as to why attention is necessary to induce/enhance plasticity. Such results would help us to better understand how cognitive states interact with brain processes that occur during learning. PUBLIC HEALTH RELEVANCE: We wish to understand how cortical plasticity following training on a tactile discrimination task influences tactile perception and how attention alters primary somatosensory responses to enhance plasticity. The specific type of plasticity we will study is implicated in focal dystonia; therefore understanding these mechanisms will guide future treatments of this disorder. In addition, by knowing exactly how attention alters brain structure we can describe mechanisms of sensorimotor skill development and learning to guide education and rehabilitation.