Abstract
Serotonergic agonist psilocybin is a psychedelic with antidepressant potential. Sleep may interact with psilocybin’s antidepressant properties like other antidepressant drugs via induction of neuroplasticity. The main aim of the study was to evaluate the effect of psilocybin on sleep architecture on the night after psilocybin administration. Regarding the potential antidepressant properties, we hypothesized that psilocybin, similar to other classical antidepressants, would reduce rapid eye movement (REM) sleep and prolong REM sleep latency. Moreover, we also hypothesized that psilocybin would promote slow-wave activity (SWA) expression in the first sleep cycle, a marker of sleep-related neuroplasticity. Twenty healthy volunteers (10 women, age 28–53) underwent two drug administration sessions, psilocybin or placebo, in a randomized, double-blinded design. Changes in sleep macrostructure, SWA during the first sleep cycle, whole night EEG spectral power across frequencies in non-rapid eye movement (NREM) and REM sleep, and changes in subjective sleep measures were analyzed. The results revealed prolonged REM sleep latency after psilocybin administration and a trend toward a decrease in overall REM sleep duration. No changes in NREM sleep were observed. Psilocybin did not affect EEG power spectra in NREM or REM sleep when examined across the whole night. However, psilocybin suppressed SWA in the first sleep cycle. No evidence was found for sleep-related neuroplasticity, however, a different dosage, timing, effect on homeostatic regulation of sleep, or other mechanisms related to antidepressant effects may play a role. Overall, this study suggests that potential antidepressant properties of psilocybin might be related to changes in sleep.
Highlights
Psilocybin (O-phosphoryl-4hydroxy-N, N-dimethyltryptamine) and its active metabolite psilocin (4-hydroxy-N, N-dimethyltryptamine) are the main psychoactive components of psychedelic mushrooms
It was locally observed only in averaged occipital derivations (t (13) −2.29, p 0.039, r 0.54, large effect) in the psilocybin relative to the placebo condition (Figure 1), a trend decrease in EEG relative delta power was observed at the averaged central derivations in the psilocybin relative to the placebo condition (t (16) −1.861, p 0.081, r 0.42, medium effect)
The main finding of this study is that psilocybin significantly increased rapid eye movement (REM) sleep onset latency and showed a trend toward reduced REM sleep duration on the first night after
Summary
Psilocybin (O-phosphoryl-4hydroxy-N, N-dimethyltryptamine) and its active metabolite psilocin (4-hydroxy-N, N-dimethyltryptamine) are the main psychoactive components of psychedelic mushrooms. Psilocybin doses of 0.04–0.43 mg/kg cause alterations in perception, cognition, and emotions, while eliciting long-term changes in well-being and mood in both healthy and psychiatric subjects (Dos Santos et al, 2016; Korcák et al, 2019; Barrett et al, 2020). These longlasting positive changes lead to an exploration of the therapeutic potential of psychedelics as well as the mechanisms underlying this potential. It has been shown that serotonergic psychedelics including psilocybin via 5-HT2A receptors promote neuroplasticity (Ly et al, 2018), a fundamental mechanism of neuronal adaptation that is disrupted in depression (CarhartHarris and Goodwin, 2017) and restored by antidepressant treatments including selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs) or electroconvulsive therapy (ECT) (Hayley and Littlejohn, 2013)
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