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中文摘要
翻译
描述(由申请人提供):认知和系统神经科学中一个关键的未解决的问题是,重复暴露于感知刺激如何导致神经元反应(重复抑制,或RS)减少,但对相同刺激的行为反应(行为启动)更有效和快速。我们将使用硬脑膜下皮质电图(ECoG)来阐明视觉对象命名过程中皮层激活和重复抑制的精细时间动态(Specific Aim 1),以及事件相关功能相互作用的动态(Specific Aim 2)。我们将使用这些动态来测试RS神经机制竞争模型的关键预测,以及这些机制如何与行为启动相关。更具体地说,我们将检验RS和行为启动可以通过“有效相互作用”模型更好地解释的假设,在该模型中,行为启动源于观察RS的位点之间功能相互作用的增加。为此,ECoG的激活将通过高频(伽马)振荡、低频谱扰动和erp来索引。我们还将使用定量方法来测量ECoG记录点之间伽马频率的动态事件相关因果相互作用,以及分析综合网络活动的其他方法。为了进一步测试我们的模型(特异性Aims),我们还将使用皮层电刺激映射(ESM)暂时干扰ECoG部位的功能,在Aims 1和Aims 2中观察到RS和增强的功能相互作用。我们将测试这些短暂的功能“损伤”是否不仅在初始刺激暴露时干扰RS和重复刺激时增加的功能相互作用,而且还会干扰重复刺激的命名潜伏期的启动。这样做是为了验证我们的模型预测的RS和功能相互作用与行为启动有因果关系的假设。与海马依赖的外显记忆相比,行为启动是一种基于新皮质功能的内隐学习和记忆的基本机制,该项目有望为RS的神经机制及其与行为启动的关联提供新的见解。这些见解将为认知心理学和功能性神经影像学的研究提供信息,这些研究使用RS和启动来探测正常认知的神经基质,以及与皮层功能障碍相关的认知障碍,例如阿尔茨海默氏痴呆症。此外,该研究有望通过改进ECoG功能定位技术,在癫痫的外科治疗中产生临床影响。
英文摘要
DESCRIPTION (provided by applicant): A key unresolved question in cognitive and systems neuroscience is how repeated exposure to perceptual stimuli results in reduced neuronal responses (repetition suppression, or RS) but more efficient and rapid behavioral responses (behavioral priming) to the same stimuli. We will use subdural electrocorticography (ECoG) to elucidate the fine temporal dynamics of cortical activation and repetition suppression (Specific Aim 1), as well as the dynamics of event-related functional interactions (Specific Aim 2), during visual object naming. We will use these dynamics to test key predictions of competing models of the neural mechanisms of RS and how these mechanisms relate to behavioral priming. More specifically, we will test the hypothesis that RS and behavioral priming can be better explained by an "effective interaction" model in which behavioral priming arises from an increase in functional interactions between sites where RS is observed. For this purpose ECoG activation will be indexed by high frequency (gamma) oscillations, low frequency spectral perturbations, and ERPs. We will also use quantitative methods for measuring dynamic event-related causal interactions in gamma frequencies between ECoG recording sites, as well as other methods for analyzing integrative network activity. To further test our model (Specific Aim3), we will also use electrocortical stimulation mapping (ESM) to temporarily interfere with function at ECoG sites where RS and increased functional interactions were observed in Aims 1 and 2. We will test whether these transient functional "lesions" during initial stimulus exposure not only interfere with RS and increased functional interactions during repeated stimulus exposure, but also interfere with priming of naming latencies for repeated stimuli. This will be done to test the hypothesis that the RS and functional interactions predicted by our model are causally linked to behavioral priming. This project is expected to provide new insights into the neural mechanisms underlying RS and its association with behavioral priming, which is a fundamental mechanism of implicit learning and memory based on neocortical function, in contrast to hippocampal-dependent explicit memory. These insights will inform studies in cognitive psychology and functional neuroimaging that use RS and priming to probe the neural substrates of normal cognition, as well as cognitive impairments associated with cortical dysfunction, e.g. in Alzheimer's dementia. In addition, the research is expected to have a clinical impact in the surgical management of epilepsy by improving ECoG techniques for functional mapping. PUBLIC HEALTH RELEVANCE: The research plan will use EEG measures of human brain activity discovered in the previous funding period to investigate the mechanisms by which more exposure to perceptual stimuli result in reduced brain responses but more efficient and rapid behavioral responses to the same stimuli. To answer this question, we will study the temporal sequence by which brain areas are activated and interact with each other when humans name novel versus repeated visual objects. This research could lead to better methods for mapping brain function in patients undergoing surgical treatment for epilepsy.
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Investigation of the Cortical Communication (CORTICOM) System
  • 批准号:
    10256610
  • 项目类别:
  • 资助金额:
    $230.97万
  • 财政年份:
    2020
  • 负责人:
    NATHAN E CRONE
  • 依托单位:
Brain-Computer Interface Implant for Severe Communication Disability
Brain-Computer Interface Implant for Severe Communication Disability
Brain-Computer Interface Implant for Severe Communication Disability
国内基金
海外基金
新型F-18标记香豆素衍生物PET探针的研制及靶向Alzheimer's Disease 斑块显像研究
  • 批准号:
    81000622
  • 项目类别:
    青年科学基金项目
  • 资助金额:
    20.0万元
  • 批准年份:
    2010
  • 负责人:
    梁胜
  • 依托单位:
阿尔茨海默病(Alzheimer's disease,AD)动物模型构建的分子机理研究
  • 批准号:
    31060293
  • 项目类别:
    地区科学基金项目
  • 资助金额:
    26.0万元
  • 批准年份:
    2010
  • 负责人:
    郭亚芬
  • 依托单位:
跨膜转运蛋白21(TMP21)对引起阿尔茨海默病(Alzheimer'S Disease)的γ分泌酶的作用研究