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.
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.
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