Capacity Limitations in the Cortex

描述(由申请人提供)：这个项目解决了功能电路的作用，这是关于认知的最基本和最引人注目的事实，它的能力有限(例如，在打电话时很难写电子邮件)。尽管人类认知具有非凡的力量和灵活性，但大多数认知机制所依赖的“在线”工作空间令人惊讶地有限，只能同时表示几个项目。理解能力受限的神经生物学是至关重要的，因为能力的下降与精神分裂症和ADHD等一系列神经精神疾病有关。事实上，有人建议，为提高被诊断为ADHD的儿童的工作记忆容量而设计的培训可以缓解症状，并可能提高液体智力。这增加了一种可能性，即对认知的一个基本方面的治疗改进可能会导致一系列可能被证明是症状性而不是原发病的疾病的改善，如注意力缺陷障碍、执行功能低下等。然而，尽管能力限制在人类中得到了很好的研究(这可能是研究最充分的认知现象)，但它从未在动物大脑中进行过研究。因此，有关其神经基础的根本问题尚未得到解决。我们的实验室将通过在人类身上进行容量限制测试，并使用我们独特的方法，同时从猴子大脑不同区域的多个电极进行记录，来做到这一点。这将使我们能够确定容量限制的方式、地点和原因，例如它在皮质处理中出现在哪里，达到容量后项目如何从记忆中丢失，以及为什么神经编码会导致容量限制。我们将检验容量限制的两个主要理论(狭缝模型与信息负荷模型)以及与人类工作记忆容量限制最相关的目标皮质区域：前额叶皮质、顶叶后皮质和中层视觉皮质(即V4区)。通过比较它们之间的信息丢失的相对神经潜伏期，我们可以确定大脑皮质处理中的能力限制出现在哪里，以及它是自下而上还是自上而下的现象。

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.