Abstract
Ibogaine is a potent psychedelic alkaloid that has been the focus of intense research because of its intriguing anti-addictive properties. According to anecdotic reports, ibogaine has been originally classified as an oneirogenic psychedelic; i.e., induces a dream-like cognitive activity while awake. However, the effects of ibogaine administration on wakefulness (W) and sleep have not been thoroughly assessed. The main aim of our study was to characterize the acute effects of ibogaine administration on W and sleep. For this purpose, polysomnographic recordings on chronically prepared rats were performed in the light phase during 6 h. Animals were treated with ibogaine (20 and 40 mg/kg) or vehicle, immediately before the beginning of the recordings. Furthermore, in order to evaluate associated motor behaviors during the W period, a different group of animals was tested for 2 h after ibogaine treatment on an open field with video-tracking software. Compared to control, animals treated with ibogaine showed an increase in time spent in W. This effect was accompanied by a decrease in slow wave sleep (SWS) and rapid-eye movements (REM) sleep time. REM sleep latency was significantly increased in animals treated with the higher ibogaine dose. While the effects on W and SWS were observed during the first 2 h of recordings, the decrement in REM sleep time was observed throughout the recording time. Accordingly, ibogaine treatment with the lower dose promoted an increase on locomotion, while tremor and flat body posture were observed only with the higher dose in a time-dependent manner. In contrast, head shake response, a behavior which has been associated in rats with the 5HT2A receptor activation by hallucinogens, was not modified. We conclude that ibogaine promotes a waking state that is accompanied by a robust and long-lasting REM sleep suppression. In addition, it produces a dose-dependent unusual motor profile along with other serotonin-related behaviors. Since ibogaine is metabolized to produce noribogaine, further experiments are needed to elucidate if the metabolite and/or the parent drug produced these effects.
Highlights
Ibogaine is a natural occurring indole alkaloid found in the root bark of the shrub Tabernanthe iboga, originally from Congo and Gabon, as well as in other plants of the Apocynaceae family (Lavaud and Massiot, 2017)
This dream-like activity does not produce the typical interferences in thinking, identity distortions, and space–time alteration produced by the traditional psychedelics drugs such as lysergic acid diethylamide (LSD), mescaline, and dimethyltryptamine (DMT), which are pharmacologically classified as 5-HT2A receptor agonists (Naranjo, 1973; Glennon, 1990; Lotsof, 1995; Nichols, 2016)
The total amount of rapid-eye movements (REM) sleep was diminished in animals treated with ibogaine 20 mg/kg (I20) [F(2,14) = 19.3, p < 0.01] and I40 [F(2,14) = 19.3, p < 0.005]
Summary
Ibogaine is a natural occurring indole alkaloid found in the root bark of the shrub Tabernanthe iboga, originally from Congo and Gabon, as well as in other plants of the Apocynaceae family (Lavaud and Massiot, 2017) It has become widely known in the western world because of its claimed properties to reduce addiction to drugs of abuse and craving (Alper et al, 1999). An early report in cats described that the administration of ibogaine (2–10 mg/kg doses) produced an activation of the electroencephalogram (EEG) that resembles the effect of the electrical stimulation of the activating reticular system (Schneider and Sigg, 1957) This effect was reduced in the classical “decerebrate” animal model, suggesting that the reticular formation plays a key role in the ibogaine effects. The opposite effect was found when other tabernanthine derivatives (claimed as methoxy-16 ibogaine tartrate and methoxy-16 tabernanthine tartrate) were administered (Da Costa et al, 1980; Da Costa-Rochette et al, 1981)
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