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Max B Kelz

7 papers in the library · 66 citations · publishing 2018-2025

Papers

Brain network motifs are markers of loss and recovery of consciousness

Scientific Reports February 16, 2021 Catherine Duclos, Danielle Nadin, Yacine Mahdid et al. 28 citations

Three-node network motifs—recurring patterns of connections—reorganize in the brain during anesthetic-induced unconsciousness and recovery. In nine healthy volunteers undergoing a 3-hour anesthesia protocol, electroencephalography (EEG) recordings in the alpha band (8–13 Hz) showed that two specific motifs (motifs 1 and 5) changed their topology significantly between responsive and unresponsive states. Motif 1 consisted of long-range chain-like connections, while motif 5 comprised short-range loop-like connections. The topological reorganization of motif 5 preceded the return of responsiveness, and motif 1 accompanied it, suggesting these motifs may help reveal neural correlates of consciousness.

Neural assemblies coordinated by cortical waves are associated with waking and hallucinatory brain states.

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.

Cognitive and Neurophysiological Recovery Following Electroconvulsive Therapy: A Study Protocol

Frontiers in Psychiatry May 14, 2018 Ben J Palanca, Hannah R. Maybrier, Angela M. Mickle et al. 16 citations

Electroconvulsive therapy (ECT) deliberately induces generalized seizures to treat severe psychiatric illness, offering a chance to study how consciousness, cognition, and brain activity recover after seizures. Fifteen patients with treatment-resistant major depressive disorder will receive right unilateral ECT under etomidate anesthesia. They will then undergo three treatments in randomized order: etomidate plus ECT, ketamine plus ECT, and ketamine plus sham ECT, repeated for six total sessions. Cognitive tests assess sensorimotor speed, working memory, and executive function before and after each treatment. The study will measure time to return of responsiveness, cognitive recovery trajectories, postictal delirium, and EEG changes. It aims to develop biomarkers for tailoring cognitive and emotional recovery in ECT patients.

The Administration of Ketamine Is Associated with Dose-Dependent Stabilization of Cortical Dynamics in Humans.

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.

Nitrous oxide activates layer 5 prefrontal neurons via SK2 channel inhibition for antidepressant effect.

Nature Communications April 3, 2025 Joseph Cichon, Thomas 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.

Nitrous Oxide activates layer 5 prefrontal neurons via SK2 channel inhibition for antidepressant effect

Joseph Cichon, Thomas Joseph, Xinguo Lu et al.

A single dose of inhaled nitrous oxide (N2O) rapidly activates layer V (L5) pyramidal neurons in the cingulate cortex of rodents exposed to chronic stress, rescuing a stress-associated hypoactivity state. This activation persists after exposure and is necessary for N2O's antidepressant-like effects. Although N2O is believed to act primarily through NMDA-receptor antagonism, L5 neurons activate even when NMDA-receptor function is blocked. Instead, N2O-induced inhibition of calcium-sensitive potassium (SK2) channels drives specific L5 activity and the ensuing antidepressant-like effects. These results indicate that N2O's fast antidepressant action relies on novel molecular actions in distinct cortical cell types.

Nitrous Oxide activates layer 5 prefrontal cortical neurons via SK2 channel inhibition for antidepressant effect

Joseph Cichon, Thomas Joseph, Andrzej Z Wasilczuk et al.

A single dose of inhaled nitrous oxide (N2O) rapidly and specifically activates layer V (L5) pyramidal neurons in the prefrontal cortex of rodents exposed to chronic stress. This activation reverses a stress-linked hypoactivity state, persists after N2O exposure, and is necessary for the antidepressant effect. The activation occurs independently of NMDA-receptor function and synaptic activity, contrary to N2O's purported mechanism. Instead, N2O inhibits calcium-sensitive potassium (SK2) channels, driving both rapid and sustained L5 activity and antidepressant-like effects. The findings suggest a novel molecular target for fast-acting antidepressants.