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Ketamine increases fronto-posterior functional connectivity during meta-perceptual confidence ratings
Mirko Lehmann1, Claudia Neumann2, Sven Wasserthal3
1Department of Psychology, University of Bonn, Kaiser-Karl-Ring 9, 53111 Bonn, Germany.
Behavioural Brain Research
|May 17, 2022
Summary
Ketamine impaired metacognition, impacting confidence in decisions but not perception itself. This study explored glutamate
Area of Science:
- Neuropsychopharmacology
- Cognitive Neuroscience
- Neuroimaging
Background:
- Glutamate is crucial for metacognition, but its role across different cognitive functions is not fully understood.
- Investigating the N-methyl-D-aspartate (NMDA) receptor system's impact on metacognition is essential for understanding its broader implications.
Purpose of the Study:
- To examine the effects of ketamine, an NMDA receptor antagonist, on metacognition within a perceptual decision-making task.
- To assess how ketamine influences both metacognitive performance and underlying neural activity using functional magnetic resonance imaging (fMRI).
Main Methods:
- A randomized, double-blind, placebo-controlled, and preregistered fMRI study.
- Participants performed a two-alternative forced-choice task with trial-by-trial metacognitive confidence ratings.
- A psychotomimetic dose of ketamine was administered to assess its impact on brain function and behavior.
Main Results:
- Ketamine significantly worsened metacognitive performance, specifically affecting confidence judgments.
- No significant effects of ketamine were found on perceptual accuracy, response times, or metacognitive bias.
- Exploratory analysis revealed altered functional connectivity patterns in brain regions associated with metacognition under ketamine.
Conclusions:
- Ketamine disrupts metacognitive processes, highlighting the role of the NMDA receptor system in metacognitive integrity.
- Findings suggest that ketamine may alter neural representations involved in metacognitive evaluation.
- This research contributes to understanding the neurochemical basis of metacognition and its disruption.

