Capacity Limitations in the Cortex

描述（由申请人提供）：本项目探讨了功能电路在认知中最基本、最显著的作用，即其有限的容量（例如，打电话时很难写电子邮件）。尽管人类认知具有非凡的能力和灵活性，但大多数认知机制所依赖的“在线”工作空间却令人惊讶地有限，只能同时表示少数几个项目。理解能力限制的神经生物学是至关重要的，因为能力的降低与许多神经精神疾病有关，如精神分裂症和多动症。事实上，对被诊断为多动症的儿童进行训练，以提高他们的工作记忆能力，这已经被认为可以缓解症状，并可能提高他们的流体智力。这增加了一种可能性，即对认知的一个基本方面的治疗改善可能会导致广泛的症状性疾病的改善，而不是原发性疾病，如注意力缺陷障碍，执行功能差等。然而，虽然能力限制在人类身上得到了很好的研究（它可能是研究得最充分的认知现象），但在动物大脑中却从未得到过研究。因此，关于其神经基础的基本问题尚未得到解决。我们的实验室将通过对人类容量限制的测试，以及使用我们独特的方法，同时记录猴子大脑不同区域的多个电极。这将使我们能够确定容量限制的方式，位置和原因，例如它在皮层处理中出现的位置，达到容量后项目如何从记忆中丢失，以及为什么神经编码导致容量限制。我们将测试容量限制的两种主要理论（槽模型与信息负荷模型）和目标皮质区域最相关的工作记忆容量限制在人类：前额叶皮层，后顶叶皮层和中层视觉皮层（即区域V4）。通过比较它们之间相对的信息丢失的神经潜伏期，我们可以确定在皮层处理中出现的能力限制，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.