Ketamine, a drug that blocks NMDA receptors, impairs episodic memory. Using fMRI, brain activity was measured in healthy volunteers during memory encoding and retrieval under two intravenous doses of ketamine in a double-blind, placebo-controlled, randomized, within-subjects design. Encoding and retrieval were separated across two study-test cycles to isolate drug effects on each process. Results suggest that ketamine increases left frontal activation when elaborative semantic processing is needed during encoding, and successful encoding on the drug relies on additional incidental non-verbal processing. At retrieval, ketamine appears to impair access to contextual features of studied items. Even when behavior appears normal, ketamine alters recruitment of key brain regions for episodic memory.
Patterns of functional interactions across distributed brain regions are thought to provide a scaffold for conscious processing, with topological changes seen in loss of consciousness. Using resting-state fMRI in healthy participants at baseline and two levels of propofol-induced sedation, the study found a persistent modular brain architecture but significant reorganization of brain hubs that formed parts of a wider rich-club collective. Reduced strength of rich-club connectivity was significantly associated with poorer performance on a semantic judgment task, highlighting the importance of this higher-order topological feature for conscious cognition.
A multi-level oddball task reveals that local and global prediction-error responses interact, challenging the view that the global effect reflects a distinct processing mode beyond predictive coding. Sedation modulates this interaction, suggesting conscious awareness may not be confined solely to the global processing level.