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Cortical high-frequency oscillations (≈ 110 Hz) in cats are state-dependent and enhanced by a subanesthetic dose of ketamine.

Santiago Castro-Zaballa, Joaquín González, Matías Cavelli, Diego M. Mateos, Claudia Pascovich, Adriano B. L. Tort, Mark Jeremy Hunt, Pablo Torterolo

Behavioural Brain Research January 5, 2025 DOI: 10.1016/j.bbr.2024.115231 (opens in new tab)

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Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Sample size 4
Population Cats
Intervention subanesthetic dose of ketamine
Dose sub-anesthetic dose
Topics Esketamine Ketamine
Keywords Anesthesia Cognition Gamma Hfo Rem Psychedelics hallucinogens Entheogens Psychoactive drugs Brain activity Brain rhythms Consciousness awareness Perception Ketamine an
Citations 4
Key findings Ketamine enhances high-frequency oscillations in the cat cortex that are coupled with respiration during wakefulness, and these oscillations originate in the olfactory bulb and stream toward the prefrontal cortex.

Abstract

Ketamine is an NMDA receptor antagonist that has antidepressant and anesthetic properties. At subanesthetic doses, ketamine induces transient psychosis in humans, and is used to model psychosis in experimental animals. In rodents, subanesthetic doses of ketamine increase the power of high-frequency oscillations (HFO, > 100 Hz) in the electroencephalogram (EEG), a frequency band linked to cognitive functions. However, to date, the effects of ketamine in carnivores and primates have been poorly investigated. Here, we examined in the cat, cortical HFO during wakefulness, sleep, and after administering a sub-anesthetic dose of ketamine. Four cats were prepared with cortical electrodes for chronic polysomnographic recordings in head-restrained conditions. The cortical HFO power, connectivity, direction of the information flow using Granger Causality (GC) analysis, their relationships with respiratory activity, and the effect of auditory stimulation were analyzed. During wakefulness, but not during sleep, we found that HFO were coupled with the inspiratory phase of the respiration. After ketamine administration, HFO power was enhanced and remained associated with the inspiratory phase. GC analysis suggests that ketamine-enhanced HFO originate from the olfactory bulb (OB) and stream towards the prefrontal cortex (Pf). Accordingly, occluding the nostrils significantly reduced the power of the ketamine-enhanced HFO in both the OB and Pf. Finally, auditory stimulation did not affect HFO. In conclusion, the HFO are associated with respiration during wakefulness, but not during sleep. The enhancement of this rhythm by ketamine may disrupt cortical information processing, which could contribute to some of the neuropsychiatric effects associated with ketamine.

Comparable studies

Other experimental studies on ketamine, most cited first.

Study Year Design Participants
Ketamine activates psychosis and alters limbic blood flow in schizophrenia Schizophrenic individuals 1995 Experimental study
The spectral exponent of the resting EEG indexes the presence of consciousness during unresponsiveness induced by propofol, xenon, and ketamine Healthy participants 2019 Controlled experimental study n = 15
Ketamine Increases Human Motor Cortex Excitability to Transcranial Magnetic Stimulation Normal human subjects 2003 Experimental study n = 7
Evidence that Subanesthetic Doses of Ketamine Cause Sustained Disruptions of NMDA and AMPA-Mediated Frontoparietal Connectivity in Humans Human participants 2015 Experimental study
Simultaneous population pharmacokinetic modelling of ketamine and three major metabolites in patients with treatment‐resistant bipolar depression Patients with treatment-resistant bipolar depression 2012 Population pharmacokinetic analysis n = 9

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