Cell reports
April 23, 2024
Adeeti Aggarwal, Jennifer Luo, Helen Chung et al.
17 citations
Traveling cortical waves in the 3-6 Hz range coordinate neuronal activity across visual and parietal cortex only in brain states where perception is possible. In awake mice, visual stimuli reset spontaneous waves, producing stimulus-evoked feedback waves that entrain neurons. Under anesthesia, visual stimuli fail to disrupt spontaneous waves. During ketamine-induced dissociation, spontaneous waves themselves traverse the cortex caudally and entrain neurons, mimicking the stimulus-evoked pattern seen in wakefulness. Thus, coordinated neuronal assemblies orchestrated by traveling waves emerge in states that allow perception, but only the awake state reliably links this coordination to external visual input.
The Journal of neuroscience : the official journal of the Society for Neuroscience
May 14, 2025
Diego G Dávila, Andrew McKinstry-Wu, Max B Kelz et al.
5 citations
During wakefulness, people respond to external stimuli, while in dreams or drug-induced dissociated states, vivid internal experiences occur with reduced perception of the outside world. The brain's activity near a critical point between damped and exploding oscillations is linked to conscious experience, and this signature appears in both normal wakefulness and dissociative states but not in dreamless sleep or anesthesia. Using high-density EEG in human male volunteers given escalating ketamine doses, activity became progressively more stable, especially at higher frequencies, as dissociative symptoms increased. This stabilization correlated with reduced ability to perceive external stimuli, not with conscious experience itself. Combining statistical and dynamical measures of criticality may help distinguish wakefulness, dissociation, and unconsciousness.
Nature communications
April 3, 2025
Joseph Cichon, Thomas T Joseph, Xinguo Lu et al.
A single dose of inhaled nitrous oxide (N2O) rapidly and durably activates a specific population of neurons in the cingulate cortex of rodents exposed to chronic stress. This activation rescues a stress-induced hypoactivity state in layer V (L5) pyramidal neurons and is necessary for N2O's antidepressant-like effects. Although N2O is believed to work primarily by blocking NMDA receptors, L5 neurons still activate when NMDA receptor function is inhibited. Instead, N2O inhibits calcium-sensitive potassium (SK2) channels, driving L5 neuron activity and antidepressant-like effects. These findings identify a novel molecular and circuit mechanism for N2O's fast antidepressant action.