Frontiers in pharmacology
January 1, 2018
Joaquín González, José P Prieto, Paola Rodríguez et al.
31 citations
Ibogaine, a psychedelic alkaloid with anti-addictive properties, acutely increases wakefulness and suppresses REM sleep in rats. In a study with polysomnographic recordings over six hours, rats given ibogaine (20 or 40 mg/kg) spent more time awake and less time in slow wave sleep and REM sleep compared to controls. REM sleep latency increased with the higher dose. The wake-promoting and slow wave sleep effects occurred in the first two hours, while REM suppression lasted throughout the recording. Lower doses increased locomotion; higher doses caused tremor and flat body posture. Head shake response, linked to 5HT2A receptor activation, was unchanged. The findings suggest ibogaine produces a waking state with prolonged REM suppression and a dose-dependent motor profile.
bioRxiv (Cold Spring Harbor Laboratory)
June 29, 2020
Joaqúın González, Matías Cavelli, Santiago Castro‐zaballa et al.
5 citations
preprint
Ibogaine, a psychedelic alkaloid with anti-addictive properties, produces a waking state that shares brain-wave traits with REM sleep. In rats, ibogaine increased gamma oscillation power in the brain but made those oscillations less coherent and less complex than normal waking levels. This pattern mirrors REM sleep features within the gamma frequency band, providing biological evidence for the long-standing hypothesis that ibogaine induces a dream-like state while awake—a phenomenon called oneirogenesis. The findings offer an empirical basis for understanding how ibogaine's unique subjective effects may contribute to its anti-addictive potential.
Behavioural brain research
January 5, 2025
Santiago Castro-Zaballa, Joaquín González, Matías Cavelli et al.
4 citations
In cats, high-frequency oscillations (HFO, >100 Hz) in the brain's electrical activity are linked to breathing during wakefulness but not during sleep. A sub-anesthetic dose of ketamine increases the power of these HFO, and they remain tied to the inhalation phase of respiration. The enhanced HFO appear to originate in the olfactory bulb and travel to the prefrontal cortex. Blocking the nostrils reduces the ketamine-enhanced HFO in both regions. Auditory stimulation does not affect these oscillations. The findings suggest that ketamine's enhancement of respiration-coupled HFO may disrupt cortical information processing, potentially contributing to its neuropsychiatric effects.