Humans possess the useful ability to monitor and control our own cognition, a phenomenon known as metacognition. This ability is essential to our sense of volition, confidence, and self-awareness, giving metacognition a broad clinical relevance. Functional magnetic resonance imaging (fMRI) and lesion studies suggest which particular brain regions may contribute to metacognitive processes, but the neural basis of metacognition remains to be explored. The primary goal of this proposal is to elucidate neuronal mechanisms underlying metacognition. To do this, existing metacognition behavioral paradigms will be adapted into a visual oculomotor task suitable for neurophysiology. The first specific aim is to test the hypothesis that the new metacognition task elicits metacognitive behavior. An operational definition of metacognitive behavior will be established, and psychophysical results will be analyzed to determine whether they meet the established criteria. The second specific aim is to test the hypothesis that metacognitive processes can be characterized at the single cell level. Single neuron activity will be recorded from specific cortical sites during performance of the metacognition task. Based on cortical regions previously established as important for visual, oculomotor, and higher cognitive functioning, and guided by metacognition fMRI studies, single neurons will be recorded from frontal eye field (FEF), dorsolateral prefrontal cortex (DLPFC), and supplementary eye field (SEF). Predictions will be tested regarding the types of responses likely to arise in each of these cortical regions. The third specific aim is to establish the functional roles of each of the cortical areas using reversible inactivation during performance of the metacognition task. This researched proposed herein will begin to elucidate the neural basis of metacognition, and will provide a foundation for future metacognition research.

Public Health Relevance

The research proposed herein will begin to elucidate the neural basis of metacognition, and will provide a foundation for future metacognition research. Metacognitive deficits have been implicated in a range of pathologies, such as schizophrenia, Parkinson's disease, and Alzheimer's disease. Understanding the neural basis of metacogntion will help understand how to treat patients with such disorders. Currently, metacognition-based therapies are also being used as a tool to treat obsessive-compulsive disorder, post-traumatic stress disorder, and to improve learning in mentally disabled individuals.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31MH087094-02
Application #
7924564
Study Section
Special Emphasis Panel (ZRG1-F02B-Y (20))
Program Officer
Vogel, Michael W
Project Start
2009-09-01
Project End
2011-06-14
Budget Start
2010-09-01
Budget End
2011-06-14
Support Year
2
Fiscal Year
2010
Total Cost
$24,582
Indirect Cost
Name
University of Pittsburgh
Department
Neurosciences
Type
Schools of Arts and Sciences
DUNS #
004514360
City
Pittsburgh
State
PA
Country
United States
Zip Code
15213
Middlebrooks, Paul G; Sommer, Marc A (2012) Neuronal correlates of metacognition in primate frontal cortex. Neuron 75:517-30
Middlebrooks, Paul G; Sommer, Marc A (2011) Metacognition in monkeys during an oculomotor task. J Exp Psychol Learn Mem Cogn 37:325-37