Proceedings of the National Academy of Sciences of the United States of America
October 15, 2024
Yihan Sophy Xiong, Jacob A Donoghue, Mikael Lundqvist et al.
32 citations
Predictive coding in the cortex relies on predictions fed back from deep layers via alpha/beta oscillations (8–30 Hz) that inhibit gamma (40–100 Hz) and spiking carrying sensory input forward. Intracranial recordings in macaques during passive auditory oddball tasks showed that in the awake state alpha/beta oscillations inhibited processing of predictable sounds. Propofol-induced loss of consciousness eliminated this alpha/beta modulation in sensory cortex and reduced alpha/beta coherence between sensory and frontal areas. Consequently, oddball stimuli evoked enhanced gamma power, late spiking, and superficial layer sinks in auditory cortex, indicating a disinhibited state. However, differential spiking to oddballs in higher-order cortex was lost, likely due to disrupted spike-field coupling. These findings constrain theories of consciousness.
Proceedings of the National Academy of Sciences of the United States of America
May 28, 2024
Elie Adam, Marek Kowalski, Oluwaseun Akeju et al.
30 citations
Ketamine, an NMDA-receptor antagonist, produces sedation and dissociation at low doses and unconsciousness at high doses, while generating gamma oscillations (>25 Hz) in the EEG that are interrupted by slow-delta oscillations (0.1–4 Hz) at high doses. Using a biophysical model of cortical circuits, the authors show how NMDA-receptor antagonism leads to disinhibition in neuronal circuits, and how disinhibited interaction between NMDA-receptor-mediated excitation and GABA-receptor-mediated inhibition produces gamma oscillations at both doses and slow-delta oscillations at high doses. This work reveals general mechanisms for generating oscillatory brain dynamics and provides insights into ketamine's actions as an anesthetic and therapy for treatment-resistant depression.
Cell reports
May 27, 2025
Alexandra G Bardon, Jesus J Ballesteros, Scott L Brincat et al.
8 citations
Two anesthetics with different molecular actions, ketamine and dexmedetomidine, both increase phase locking of neural oscillations in the prefrontal cortex of nonhuman primates during loss of responsiveness. Within a hemisphere, neighboring prefrontal subregions become less phase-aligned, possibly due to large traveling waves. However, homologous areas across hemispheres become more aligned in phase. These distinct patterns of cortical phase alignment, markedly different from waking states, may represent a common mechanism by which diverse anesthetics produce loss of responsiveness.