Proceedings of the National Academy of Sciences of the United States of America
October 15, 2024
Yihan Sophy Xiong, Jacob 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.
PLoS Computational Biology
August 18, 2021
Indie C. Garwood, S. Chakravarty, Jacob Donoghue et al.
32 citations
Ketamine, an anesthetic that blocks NMDA receptors, produces alternating bursts of gamma (25-50 Hz) and slow-delta (0.1-4 Hz) brain oscillations. A hidden Markov model fitted to local field potentials from two non-human primates and electroencephalograms from nine humans quantified these dynamics. Gamma activity lasted on average 2.2 seconds in one primate, 1.2 in the other, and 2.5 in humans; slow-delta lasted 1.6, 1.0, and 1.8 seconds respectively. Five sub-states with regular sequential transitions were identified. These findings provide quantitative constraints for models of rhythm generation underlying ketamine-induced altered arousal.
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.
bioRxiv Preprint Server
April 3, 2024
Elie Adam, Marek Kowalski, Oluwaseun Akeju et al.
5 citations
preprint
Ketamine, an NMDA-receptor antagonist, produces sedation, analgesia, and dissociation at low doses and unconsciousness at high doses, generating gamma oscillations (>25 Hz) in the EEG at both doses, with slow-delta oscillations (0.1-4 Hz) interrupting gamma at high doses. Using a biophysical model of cortical circuits, the authors show how NMDA-receptor antagonism by ketamine leads to disinhibition in neuronal circuits, and how the disinhibited interaction between NMDA-receptor-mediated excitation and GABA-receptor-mediated inhibition generates gamma oscillations at both doses and slow-delta oscillations at high doses. This work reveals general mechanisms for oscillatory brain dynamics distinct from previous reports and offers insights into ketamine's action as an anesthetic and therapy for treatment-resistant depression.
medRxiv Preprint Server
November 12, 2020
Indie C. Garwood, Sourish Chakravarty, Jacob Donoghue et al.
preprint
Ketamine, an anesthetic and psychoactive drug, produces alternating patterns of brain activity: bursts of gamma oscillations (30-50 Hz) and slow oscillations (0.1-10 Hz). A hidden Markov model (HMM) was applied to brainwave data from two non-human primates and nine human subjects receiving anesthetic doses of ketamine. The model revealed distinct states corresponding to gamma bursts and slow oscillations, with intermediate states. Mean gamma burst durations were 2.5 seconds (non-human primate 1), 1.2 seconds (non-human primate 2), and 2.7 seconds (humans). Mean slow oscillation durations were 1.6 seconds, 0.7 seconds, and 2.8 seconds, respectively. This framework provides quantitative constraints for understanding how ketamine alters states of consciousness.