Capacity Limitations in the Cortex

皮层的容量限制

• 批准号: 8103576
• 负责人: EARL K MILLER
• 金额: $ 37.94万
• 依托单位: MASSACHUSETTS INSTITUTE OF TECHNOLOGY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-03-07 至 2015-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8103576
• 关键词: Address; Adult; Animals; Area; Attention; Attention Deficit Disorder; Attention deficit hyperactivity disorder; Brain; Child; Code; Cognition; Cognition Disorders; Cognitive; Color; Diagnosis; Disease; Electrodes; Electronic Mail; Employee Strikes; Foundations; Human; Impaired cognition; Individual; Intelligence; Laboratories; Lead; Learning; Liquid substance; Location; Macaca; Memory; Mental disorders; Modality; Modeling; Monkeys; Motor; Neurobiology; Neurons; Parietal Lobe; Pattern; Performance; Population; Positioning Attribute; Prefrontal Cortex; Process; Property; Relative (related person); Research; Research Infrastructure; Role; Schizophrenia; Sensory; Short-Term Memory; Signal Transduction; Stimulus; Symptoms; Technology; Telephone; Testing; Therapeutic; Training; Visual; Visual Cortex; Writing; area V4; base; cognitive function; design; executive function; flexibility; improved; information processing; insight; neuromechanism; neurophysiology; neuropsychiatry; relating to nervous system; research study; theories

DESCRIPTION (provided by applicant): This project addresses the role of functional circuitry of the most fundamental and striking fact about cognition, its limited capacity (e.g., it is difficult to write an email while talking on the phone). Despite the remarkable power and flexibility of human cognition, the "online" workspace that most cognitive mechanisms depend upon is surprisingly limited, capable of representing only a few items simultaneously. Understanding the neurobiology of capacity limitations is critical because a reduction in capacity has been tied to a host of neuropsychiatric diseases such as schizophrenia and ADHD. In fact, training designed to increase capacity of working memory in children diagnosed with ADHD has been suggested to alleviate symptoms and may be able to improve fluid intelligence. This raises the possibility that therapeutic improvement to one bedrock aspect of cognition could lead to improvements in a wide range of what may prove to be symptomatic, rather than primary, ills, such as attention deficit disorder, poor executive function, etc. However, while capacity limitations are well-studied in humans (it may be the most well-studied cognitive phenomenon), it has never been investigated in the animal brain. Thus, fundamental questions about its neural basis have not yet been addressed. Our laboratory will do so by using a test of capacity limitations in humans and by using our unique approach of recording from many electrodes simultaneously in different areas of the monkey brain. This will allow us to determine the how, where, and why of capacity limitations, such as where it arises in cortical processing, how items are lost from memory after capacity is reached, and why neural coding leads to a capacity limitation. We will test the two major theories of capacity limitations (slot model vs information-load model) and target cortical areas most associated with working memory capacity limitations in humans: the prefrontal cortex, posterior parietal cortex, and mid-level visual cortex (i.e., area V4). By comparing the relative neural latencies for information loss between them, we can determine where capacity limitations arise in cortical processing and whether it is a bottom-up or top-down phenomenon. PUBLIC HEALTH RELEVANCE: We will use multiple-electrode technology to record from multiple areas of the macaque cortex during a visual, working memory capacity task. We will determine the neural substrates of where, when, and how capacity limitations arise in cortical processing by evaluating where, when, and how neural information is degraded when capacity is exceeded. Understanding the neural substrates of working memory capacity limitations will provide important insights towards both normal (e.g., IQ performance & fluid intelligence) and abnormal (e.g., ADHD & schizophrenia) cognitive functions that have not yet been explored at the neurophysiological level.

描述（由申请人提供）：该项目介绍了有关认知最基本和最引人注目的事实的功能电路的作用，其能力有限（例如，在电话上交谈时很难写电子邮件）。尽管人类认知具有显着的力量和灵活性，但大多数认知机制依赖的“在线”工作空间令人惊讶地有限，能够同时同时代表少数项目。了解能力限制的神经生物学至关重要，因为能力的降低与精神分裂症和ADHD等神经精神疾病有关。实际上，已经建议培训旨在增加诊断为多动症儿童的工作记忆能力以减轻症状，并可能能够改善流体智能。这增加了一种认知的基岩方面的治疗性改善可能会导致在广泛的范围内的改善，这可能被证明是有症状的，而不是主要的疾病，例如注意力不足障碍，执行功能差等。但是，尽管人类的能力限制是在人类中得到充分研究的（这可能是最良好的认知能力现象），但它从未受过研究。因此，尚未解决有关其神经基础的基本问题。我们的实验室将通过对人类的容量限制进行测试，并通过同时在猴子大脑不同区域同时使用我们的许多电极记录方法来实现这一目标。这将使我们能够确定能力限制的方式，何处和原因，例如在皮质处理中产生的位置，在达到容量后如何从内存中损失的项目以及为什么神经编码导致容量限制。我们将测试两个主要限制的主要理论（插槽模型与信息负载模型）和与人类工作记忆能力限制最相关的皮质区域：前额叶皮层，壁壁皮层和中级视觉皮层（即区域V4）。通过比较它们之间信息丢失的相对神经延迟，我们可以确定皮质加工中的容量限制以及它是自下而上的还是自下而上的现象。 公共卫生相关性：在视觉，工作记忆容量任务中，我们将使用多电极技术从猕猴皮层的多个区域记录。我们将通过评估超过容量时在何处，何时何地，何时以及如何降解神经信息来确定皮层处理中的何处，何时以及如何产生容量限制的神经基质。了解工作记忆能力局限性的神经基板将为正常（例如IQ性能和流体智能）和异常（例如ADHD和精神分裂症）认知功能提供重要的见解，这些认知功能尚未在神经生理学水平上探索。