In a double‑blind, dose‑dependent study, psilocybin impaired temporal reproduction and sensorimotor synchronisation for intervals longer than roughly 2–3 seconds and slowed preferred tapping rate, alongside working‑memory deficits and increased reports of depersonalisation/derealisation. These findings implicate 5‑HT2A/1A‑mediated disruption of duration processing for longer intervals and voluntary control of movement speed, and represent the first systematic demonstration of psilocybin’s selective effects on temporal processing.
Hallucinogenic psilocybin is known to alter the subjective experience of time. However, there is no study that systematically investigated objective measures of time perception under psilocybin. Therefore, we studied dose-dependent effects of the serotonin (5-HT)2A/1A receptor agonist psilocybin (4-phosphoryloxy-N, N-dimethyltryptamine) on temporal processing, employing tasks of temporal reproduction, sensorimotor synchronization and tapping tempo. To control for cognitive and subjective changes, we assessed spatial working memory and conscious experience. Twelve healthy human volunteers were tested under placebo, medium (115μg/kg), and high (250μg/kg) dose conditions, in a double-blind experimental design. Psilocybin was found to significantly impair subjects’ ability to (1) reproduce interval durations longer than 2.5 sec, (2) to synchronize to inter-beat intervals longer than 2 sec and (3) caused subjects to be slower in their preferred tapping rate. These objective effects on timing performance were accompanied by working-memory deficits and subjective changes in conscious state, namely increased reports of ‘depersonalization’ and ‘derealization’ phenomena including disturbances in subjective ‘time sense.’ Our study is the first to systematically assess the impact of psilocybin on timing performance on standardized measures of temporal processing. Results indicate that the serotonin system is selectively involved in duration processing of intervals longer than 2 to 3 seconds and in the voluntary control of the speed of movement. We speculate that psilocybin’s selective disruption of longer intervals is likely to be a product of interactions with cognitive dimensions of temporal processing -presumably via 5-HT2A receptor stimulation.
Papers cited by this study that are also in Blossom
Hasler, F., Grimberg, U., Benz, M. A. et al. · Psychopharmacology (2004)
Umbricht, A., Vollenweider, F. X., Schmid, L. et al. · Neuropsychopharmacology (2003)
Vollenweider, F. X., Vollenweider-Scherpenhuyzen, M. F. I., Bäbler, A. et al. · NeuroReport (1998)
Papers in Blossom that reference this study
Temporal processing is essential for perception and motor control, and evidence indicates that different neural mechanisms subserve distinct time ranges and tasks. Previous work has implicated dopaminergic fronto-striatal circuits in timing, and patients with lesions or disorders affecting these systems show impaired accuracy and increased variability in time estimation and motor timing. Hallucinogens such as psilocybin reliably alter the subjective experience of time, yet prior studies had not systematically examined objective, standardised measures of temporal processing under psilocybin in humans. Wittmann and colleagues designed a double-blind, placebo-controlled within-subject experiment to test dose-dependent effects of psilocybin (a mixed 5-HT2A/1A agonist) on multiple aspects of temporal processing. The study employed temporal reproduction, sensorimotor synchronization and tapping tasks—chosen to probe timing below and above an approximate 2–3 second boundary—as well as assessments of spatial working memory and subjective conscious state, with the hypothesis that psilocybin would selectively impair longer-interval timing because of its known effects on attention and working memory.
Twelve healthy, right-handed volunteers (six men, six women; mean age 26.8 years, SD 3.6) recruited in Zürich participated after medical and psychiatric screening and informed consent. Exclusion criteria included hearing or vision problems, major psychiatric disorder in self or first-degree relatives, and regular substance abuse. Six participants reported prior limited psilocybin use; seven had sporadic cannabis use. The Swiss authorities authorised psilocybin administration and the protocol received local ethics approval. A within-subject, counterbalanced design compared placebo, medium dose (MD; 115 µg/kg, mean absolute dose ≈8.2 mg) and high dose (HD; 250 µg/kg, mean absolute dose ≈17.6 mg) psilocybin on three separate days at least 14 days apart. Assessments occurred at baseline (t0), at peak drug effects (t1; about 90 min after administration) and at a post-peak time (t2; 240 min). Psychometric measures (AMRS at 0, 80 and 280 min; 5D-ASC at 110 min) and the spatial span (SSP) from CANTAB (at 0, 100 and 360 min) were included to index subjective state and spatial working memory. Temporal tasks comprised: (1) temporal reproduction of six standard intervals—three short (1500, 2000, 2500 ms) and three long (4000, 4500, 5000 ms)—each presented eight times in random order; participants reproduced intervals by key press after a fixed 2000 ms pause; (2) sensorimotor synchronization to regular tone sequences with inter-onset intervals of 700, 1000, 2000 and 4000 ms, recording mean asynchrony, standard deviation of asynchrony and percent of missed synchronizations (defined as taps occurring >120 ms after tone onset); and (3) tapping tasks measuring self-paced (personal) and maximum tapping speeds (median inter-tap interval and stability measured via coefficient of variance). Spatial working memory was assessed with the SSP (span length recorded). Subjective effects were measured using the 5D-ASC (five main factors including 'oceanic boundlessness' and an item cluster 'altered time sense') and the 60-item Adjective Mood Rating Scale (AMRS) with multiple subscales. Psilocybin and matched placebo capsules were administered orally; subjective effects typically emerged within 20–40 min and peaked around 60–90 min. Statistical analyses used repeated measures ANOVAs with factors of treatment (placebo, MD, HD), measurement time (t0, t1, t2) and, where applicable, interval or subscale. The primary interaction of interest was treatment × measurement time. Planned contrasts compared changes from t0 to t1 and t0 to t2 between drug and placebo (alpha adjusted for the number of contrasts per measure). Data were natural-log transformed to reduce non-normality (a constant added when necessary), and Greenhouse–Geisser corrections were applied when sphericity was violated. Pearson correlations pooled MD and HD data where significant at both doses; only correlations significant at both doses were considered robust.
Temporal reproduction: For short intervals (1.5–2.5 s) only the effect of interval duration was significant, with no treatment or time effects. For long intervals (4–5 s) there were significant main effects of interval and measurement time, and a significant treatment × measurement time interaction (F = 3.2, p = 0.025). Follow-up analyses showed that HD psilocybin produced a significant under-reproduction of long intervals at peak (t1) compared with baseline (contrast F = 13.0, p = 0.004), whereas MD and placebo did not show this time-dependent change. The underestimation had largely returned by t2 (no significant t2 vs t0 contrast). Analysis of reproduction variability found a main effect of measurement time for long intervals but no significant treatment × time interaction for stability measures. Sensorimotor synchronization: Mean asynchrony analyses indicated significant effects of measurement time (p = 0.001) and interval (p < 0.001), and a measurement time × treatment interaction (F = 3.9, p = 0.009). The interaction reflected that MD psilocybin produced a significant change from baseline to peak when compared with placebo (contrast t1 vs t0: p = 0.003); HD showed a marginal difference against placebo (p = 0.057). When examined within dose conditions, MD showed significant effects of both interval and measurement time (measurement-time contrast t1 vs t0: p = 0.002). For HD, interval, measurement time and their interaction reached significance (interval × measurement-time interaction p = 0.012), with a marginal t1 vs t0 contrast (p = 0.039). The authors note that smaller mean asynchronies under drug do not indicate improved synchronization but reflect increased reaction-time asynchronies (missed anticipations). The standard deviation of asynchrony (stability) was influenced strongly by interval length (larger variability for longer intervals) but showed no treatment or time effects. Percent missed synchronizations occurred mainly for the 2000 ms and 4000 ms intervals; there were significant main effects of treatment (p = 0.018) and interval (p = 0.002), but the treatment × measurement time interaction was not significant, although descriptively more missed synchronizations occurred at peak psilocybin. Tapping speed: Personal (self-paced) tapping tempo slowed under HD psilocybin at peak. Median inter-tap intervals increased to 949.0 ms (SD 390.0) at t1 versus 692.2 ms (SD 274.6) at baseline, with a significant contrast t1 vs t0 in the HD condition (p = 0.004); no significant change was observed for MD. A main effect of measurement time on tapping stability (coefficient of variance) was observed, but there was no treatment effect. Maximum tapping speed (~150 ms inter-tap intervals) showed main effects of measurement time (p = 0.001) and treatment (p = 0.026) but no significant measurement time × treatment interaction; tapping stability at maximum speed was unaffected by psilocybin, and the authors suggest the main treatment effect may reflect chance differences across sessions rather than a drug effect. Spatial span (working memory): A significant treatment × measurement time interaction was found for SSP span length (p = 0.003). Planned contrasts indicated that HD psilocybin impaired spatial span at peak compared with placebo (contrast p < 0.011); MD did not produce a significant decrement. Subjective measures: Psilocybin produced dose-dependent increases across 5D-ASC dimensions (treatment main effect F = 14.2, p < 0.001) with a treatment × subscale interaction (p = 0.016). All five subscales showed significant treatment effects at peak after correction; notable increases included 'oceanic boundlessness' (OB), anxious ego dissolution, visionary restructuralization and reduction of vigilance. The ASC item 'altered time sense' increased significantly (ANOVA p = 0.009; HD vs placebo contrast p = 0.017). AMRS subscales revealed multiple treatment × time interactions: significant effects were reported for inactivation, tiredness, dazed state, introversion, emotional excitability and dreaminess, among others, with contrasts often significant at t1 vs t0 for MD and/or HD. Correlations: No significant correlations were found between spatial span length and temporal reproduction underestimation for the long intervals (r between −0.17 and 0.16). A strong negative correlation emerged between spatial span length and the OB subscore (r = −0.73, p < 0.001), and regression analysis implicated the OB items 'depersonalization' (r = −0.83, p < 0.0001) and 'altered time sense' (r = −0.69, p < 0.001) as major contributors. Temporal-processing measures did not correlate significantly with 5D-ASC subscales, although there was a non-significant trend (r ≈ 0.4–0.6) linking greater underestimation of 4.5–5 s intervals with higher 'altered time sense' scores.
Wittmann and colleagues interpret their results as evidence that psilocybin alters objective timing performance in humans, but selectively so: impairments occurred for interval durations longer than approximately 2–3 seconds across temporal reproduction and sensorimotor synchronization tasks, and personal tapping tempo slowed at peak HD psilocybin. No consistent drug effects were found for shorter intervals or for maximum tapping speed. From these patterns the researchers infer that psilocybin's timing effects likely reflect disruption of cognitively mediated stages of temporal processing—attention, short-term/working memory or decision processes—rather than a basic alteration of an internal pacemaker or accumulator mechanism. The authors link their findings to prior literature showing a temporal-integration window near 2–3 seconds and to studies in which working-memory loading selectively impaired timing for intervals above 2 seconds. The concurrent impairment of spatial working memory under HD psilocybin supports the notion that cognitive processes contribute to the observed timing deficits, although the absence of significant correlations between the objective timing measures and working-memory performance is taken to reflect limited power and relatively small effect sizes in this small sample rather than disconfirming the hypothesis. Slowing of self-paced tapping but preserved maximum tapping is discussed in terms of separable neural control modes for voluntary (feedback) versus maximal (feed-forward) movement frequencies and is consistent with cortical rather than cerebellar or basal ganglia–only effects; the authors note prior imaging evidence of left-sided dorsolateral overactivation under psilocybin that related to depersonalization phenomena. Pharmacologically, the study indicates involvement of the serotonin 5-HT2A/1A system in duration processing in the seconds range, either directly or indirectly via interactions with dopaminergic and glutamatergic systems. The authors acknowledge limitations including small sample size, modest effect sizes and the inability to disentangle receptor-specific contributions; they recommend future work using receptor-selective antagonists, larger samples, concurrent probing of different working-memory domains (e.g. verbal vs spatial), and comparisons with clinical populations (for example, unmedicated acute schizophrenic patients) to clarify similarities and differences between psilocybin-induced effects and timing deficits observed in schizophrenia. The researchers also emphasise that the pattern of selective impairment argues against a non-specific loss of task engagement as an explanation.
Psychometric data were analysed using a one-, two-or three-way repeated measures ANOVA. Analysed factors were (1) treatment (placebo, MD psilocybin, HD psilocybin), (2) time of measurement (t 0 , t 1 , t 2 ) and -where applicable -(3) measures or subscales (different temporal intervals in a timing task or subscales on a questionnaire). The interaction of treatment ϫ time of measurement was considered as the main source of information since the effect of psilocybin should occur at t 1 and to a lesser degree at t 2 , in contrast to the placebo condition. In cases where a significant interaction effect was observed, simple a priori contrasts compared differences between placebo and both MD and HD psilocybin. These drug dose effects were considered in respect to changes over time from both t 0 to t 1 and t 0 to t 2 (four contrasts). In some cases we looked at the three treatment conditions separately. Then, time of measurement (t 0 , t 1 , t 2 ) was the main factor in three drug conditions followed by two contrasts each (t 0 to t 1 and t 0 to t 2 ). Pearson's correlation analysis was used to compare relative change in performance on the temporal-processing tasks, the spatial span working memory test and the 5D-ASC rating scale. Only those correlations found to be significant at both medium and high doses were considered. For these cases, the low and high dose data were pooled to calculate a single Pearson's r value for that measure. To minimize the possible effects of non-normal distribution in the data sets, we transformed all data prior to analysis by applying a natural log transform. In the case that negative values had to be transformed, a constant was added to the variable to make sure that all values were positive. Additionally, Greenhouse-Geisser adjustment of degrees of freedom was applied to the data set when, according to the Mauchly test, sphericity of the sample distributions could not be assumed. Significance levels were set to values of p < 0.05. However, since multiple comparisons were planned for each measure, the risk of Type I error increases (incorrect rejection of null hypothesis). To ensure overall protection level, only those planned contrasts associated with the decisive interaction for hypothesis testing (e.g. time of measurement ϫ treatment) on each measure are reported. Nevertheless, we adjusted the alpha level for each measure to the amount of contrasts that were applied (e.g. two contrasts: p < 0.025, four contrasts: p < 0.0125) as well as for the number of ANOVAs that were calculated for different subscales of a task.
Our investigation clearly revealed that the 5-HT 2A /5-HT 1A mixed agonist psilocybin alters time perception and temporal control of behaviour in humans. These results confirm self-reports that hallucinogens cause strong alterations in spatial and temporal perceptionand extend these psychometric findings by showing the specific ways in which objective measures of temporal processing can be affected. Psilocybin was found to affect an individual's capacity to accurately reproduce interval lengths longer than 3 seconds, synchronize a motor response (finger tap) to regular auditory beats with intervals longer than 2 seconds, and to slow down the personal tapping tempo (preferred tapping rate). No impairment of performance was observed for shorter lengths on the sensorimotor synchronization and the reproduction task. This indicates that the effects found at the longer intervals were likely a product of interactions with cognitive dimensions of temporal processing instead of interactions with the proposed basic pacemaker/accumulator mechanisms of the brain. Several studies on timing point to a temporal-integration interval of approximately 2 to 3 sec that can be found in perception and motor performance (for reviews, see. Durations of temporal intervals in the temporalreproduction task are estimated precisely with intervals up to approximately 2 to 3 sec, whereas longer intervals are substantially underestimated. A temporal limitation of anticipatory planning is also observed in the sensorimotor syn-chronization task. The ability to synchronize accurately becomes substantially weaker when the inter-stimulus interval is longer than 2 sec. Our pharmacological approach contributes to these findings, as psilocybin mildly affects only those intervals of longer duration in each task. One of the few time perception studies under LSD in humans adds to our results: subjects did not show distortions in the ability to identify durations of visual stimuli in the range between 300 ms and 1 sec although they reported changes in the subjective passage of time. In respect to the current model of timing with multiple processing stages, the disturbed timing abilities for sensorimotor synchronization and duration reproduction we show here could reflect impairments of short-term memory, attention or decision-making mechanisms, rather than the alteration of the pacemaker-accumulator clock (the basic internal timing mechanism). This is especially supported by the concurrent deficits observed in working memory in the present study. Converging evidence exists for the involvement of working memory in temporal reproduction. Processing of a secondary task that influences working-memory capacity interferes with the encoding and reproducing of durations in the domain of seconds.showed that a secondary working-memory task affected the accuracy of synchronization only with inter-stimulus intervals above 2 seconds. With inter-stimulus intervals below 2 seconds the memory task had no influence on performance. In a group of elderly subjects, working memory capacity correlated with performance in a temporal reproduction task with durations of 5 and 14 seconds. Frontal regions known to be closely linked with working-memory function, particularly dorsolateral and frontomedial corticesare active during temporal reproductions of time intervals of Effects of psilocybin on time sense 61 a few seconds. Given the selective effect of psilocybin on the longer duration intervals in both the temporal reproduction and sensory synchronization tasks it seems that the temporal disturbance observed is induced through interference with cognitive processes like attention and working memory. The fact that no correlations were found between performance on the workingmemory and temporal-processing tasks, should not be considered as evidence against this hypothesized role of working memory in the observed timing impairments. Rather it is likely to reflect the small sample size combined with the relatively small effect sizes seen in both the timing measurements and the working memory. In fact, the small impairments observed for the timing measures may reflect a relative insensitivity of working memory performance to psilocybin, a claim supported by the finding that psilocybin had no significant effect on working memory at either the median dose used in this study (115 µ g/kg) or a higher dose (215 µ g/kg) used in a separate study. However, further studies are warranted to corroborate this interpretation. Moreover, it is also possible that other working-memory functions such as verbal working memory might be more significantly associated with the timing tasks. Whereas the maximum-tapping speed was unaffected by psilocybin, the tapping tempo in a voluntarily chosen tempo was significantly slower during peak effects of HD psilocybin as compared to baseline and post-peak time of that condition. This finding is consistent with several lines of evidence showing that the control of motor speed can basically be characterized by two distinct sensorimotor processes functioning with different frequencies. For example, movements with a frequency of 1 to 2 Hz are under voluntary control and allow the collection of somatosensory information (feedback control), while movements at maximum speed with frequencies of 5 Hz and above require only coarse pre-attentive control (feed-forward control). These two sensorimotor modes appear to be controlled by distinct neural networks. Injury of the cerebellum can lead to dysdiadochokinesia, the inability to alternate agonist and antagonist muscles with maximum speed. In contrast, metabolic dysfunction of the basal ganglia such as in Parkinson's disease can lead to the inability to tap at a slower pace, patients showing the so-called hastening phenomenon. In another study, tapping in a self-paced tempo was slowed down in patients with left-hemispheric lesions to the brain, whereas maximum-tapping speed was not influenced by lesions in either side of the cortex. The effect of HD psilocybin on personal tapping tempo, leading to a slower pace of the regular finger taps at peak time, could be the result of the drug influencing cortical sites of the brain, including those of the left hemisphere. In partial support of such a hypothesis we have previously found that psilocybin caused left-over-right sided dorsolateral overactivation that significantly correlated with depersonalization phenomena using FDG-PET imaging. Psilocybin-induced dose-dependent changes to subjective measures of conscious state, i.e. the loosening of ego boundaries, changes in affect and perceptual distortions as previously reported in detail, included the expected changes in time perception as indexed by the 5D-ASC item 'altered time sense'. Although we found no correlation between working-memory deficits and the objective timing measures used, we did find significant correlations between workingmemory impairment and subjective measures of altered time sense and depersonalization experiences measured by the OB subscale of the 5D-ASC. The trend towards correlations for the duration underestimation above 3 seconds and the OB item 'altered time sense' merits further studies seeking to investigate the relationship between alterations in temporal processing and experiences of self. The pharmacological basis of the experience of time and temporal processing is only vaguely understood. Pharmacological manipulations in animal and human studies indicate that dopaminergic agonists and antagonists influence timing processes -supposedly by increasing and decreasing (respectively) clock speed. The detrimental effect of the DA antagonist haloperidol on duration discrimination with base intervals of 50 ms has been interpreted as resulting from a slowing down of the clock rate. Studies in patients with Parkinson's disease show that dopaminergic agonists can improve motor timing. It appears that dopaminergic neurotransmission within striatal and cortical sites is strongly connected to temporal processing, leading to the postulation of a cortico-striato-thalamo-cortical system involved in sensorimotor timing. The present results indicate that the serotonin system is also involved in temporal processing, either directly as a component of one of the basic processing stages in the model of timing or indirectly by influencing dopaminergic or glutaminergic transmission as we have previously shown in PET studies of psilocybin model psychosis. When taking into account the different levels of the timing model that are an integrative part of the cognitive system, several neurotransmitter systems play a decisive role in temporal processing in the range of seconds., for example, discovered that the dopamine receptor antagonist haloperidol as well as benzodiazepine midazolam had detrimental effects on duration discrimination of intervals ranging around 1 second whereas processing of 50-ms intervals was only affected by haloperidol. These results were discussed as influences via disruption of transmitter-guided cognitive processes such as attention and working memory. The author concluded that any pharmacological treatment that affected working-memory capacity would interfere with temporal processing of intervals in the longer time range. It has to be noted that we did not find effects of psilocybin on durations below 2 seconds. This discrepancy can only be resolved in future studies that consider task-specific and pharmacological factors. In addition to comparing possible task-related differences between the duration discrimination task and the sensorimotor tasks used in our study, selective effects of individual pharmacological substances will probably be accounted for by the inconsistencies found over different studies. In the study presented here, the 5-HT 2A/1A receptor agonist psilocybin affected time intervals in sensorimotor synchronization and temporal reproduction only above 2 to 3 seconds and only self-paced tapping (and not maximum tapping). These effects can also be interpreted as following the disruption of cognitively mediated temporal-processing stages. Moreover, as we are reporting the specific effects of the drug concerning the time domain, we can rule out the possibility that a generally decreased capacity of subjects to interact with the environment or a decreased interest for the experimental task produced the effects shown. Our main goal was to elucidate whether psilocybin induced specific effects on temporal control of behaviour and, if so, whether these would be a function of the duration of the processed time interval -an effect we did find. In future studies the possible relationship between duration processing and underlying cognitive functions including different aspects of working memory -for example, taking into account differences between spatial and verbal working memory -needs to be further investigated by concurrently probing other dimensions of attention and working memory. Further studies with specific 5-HT 1A , 5-HT 2A and dopamine receptor antagonists are needed to tease out the relative contribution of each of these receptor systems to the observed effects. In respect to the use of psilocybin in modelling endogenous psychosis, temporal processing deficits have been observed in chronic medicated schizophrenics at both short and long intervalswhereas our current findings indicate that only longer interval processing is affected by psilocybin. It would be of interest to see whether the use of the same paradigm in healthy subjects with psilocybin and unmedicated acute schizophrenic subjects would show the same disparity of effects. Moreover, as some effects could be seen on a descriptive level but differences failed to reach the significance level it would be interesting to investigate whether increasing the number of participating subjects may yield further effects of the psilocybin intervention.
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Evens, R., Uyar, A., Gosslau, E. et al. · Psychological Medicine (2026)
Scholle, P., Wenke, Š., Nekovářová, T. et al. · Journal of Psychopharmacology (2026)
Stoliker, D., Novelli, L., Vollenweider, F. X. et al. · Biological Psychiatry (2024)
Ekins, T. G., Brooks, I., Kailasa, S. et al. · Biorxiv (2023)
Mallaroni, P., Mason, N. L., Reckweg, J. T. et al. · Clinical Pharmacology and Therapeutics (2023)
Nayak, S., Bradley, M. K., Kleykamp, B. A. et al. · Journal of Clinical Psychiatry (2023)
Sadibolova, R., Murray-Lawson, C., Family, N. et al. · Biorxiv (2023)
Michael, P., Luke, D., Robinson, O. · Frontiers in Psychology (2023)
Prugger, J., Derdiyok, E., Dinkelacker, J. et al. · Scientific Data (2022)
Gattuso, J. J., Perkins, D., Ruffell, S. G. D. et al. · International Journal of Neuropsychopharmacology (2022)
van Elk, M., Yaden, D. B. · Neuroscience and Biobehavioral Reviews (2022)
Kopra, E., Ferris, J. A., Winstock, A. R. et al. · Journal of Psychopharmacology (2022)
Balaet, M. · Frontiers in Neuroscience (2022)
Sekula, A. D., Downey, L., Puspanathan, P. · Frontiers in Psychology (2022)
Dursun, S. M., Kelly, J. R., Gillan, C. M. et al. · Frontiers in Psychiatry (2021)
Garcia-Romeu, A., Darcy, S., Jackson, H. et al. · Current Topics in Behavioral Neurosciences (2021)
Ballentine, G., Friedman, S. F., Bzdok, D. · Science Advances (2021)
Hirschfeld, T., Schmidt, T. T. · Journal of Psychopharmacology (2021)
Aday, J. S., Bloesch, E. K., Wood, J. R. et al. · Reviews In The Neuroscience (2021)
Galvão-Coelho, N. L., Marx, W., Sinclair, J. et al. · Psychopharmacology (2021)
Barrett, F. S., Krimmel, S. R., Griffiths, R. R. et al. · NeuroImage (2020)
Kangaslampi, S., Hausen, A., Rauteenmaa, T. · Journal of Psychoactive Drugs (2020)
Yanakieva, S., Polychroni, N., Family, N. et al. · Psychopharmacology (2018)
Bayne, T., Carter, O. · Neuroscience of Consciousness (2018)
Swanson, L. R. · Frontiers in Pharmacology (2018)
Kraehenmann, R. · Current Neuropharmacology (2017)
Kaelen, M. · Imperial College London (2017)
Preller, K. H., Vollenweider, F. X. · Behavioral Neurobiology of Psychedelic Drugs (2016)
Nour, M. R., Evans, J., Nutt, D. J. et al. · Frontiers in Human Neuroscience (2016)
Dos Santos, R. G., Balthazar, F. M., Bouso, J. C. et al. · Journal of Psychopharmacology (2016)
Nichols, D. E. · Pharmacological Reviews (2016)
McKenna, D., Riba, J. · Current Topics in Behavioral Neurosciences (2016)
Kometer, M., Vollenweider, F. X. · Behavioral Neurobiology of Psychedelic Drugs (2016)
Lebedev, A. V., L€ Ovd En, M., Rosenthal, G. et al. · Human Brain Mapping (2015)
Nutt, D. J., Carhart-Harris, R. L. · Current Drug Abuse Reviews (2015)
Halberstadt, A. L. · Behavioural Brain Research (2014)
Tylš, F., Páleníček, T., Horacek, J. · European Neuropsychopharmacology (2013)
Bogenschutz, M. P. · Current Drug Abuse Reviews (2013)
Hanks, J. B., González-Maeso, J. · ACS Chemical Neuroscience (2012)
Sinke, C., Halpern, J. H., Zedler, M. et al. · Consciousness and Cognition (2012)
Quednow, B. B., Kometer, M., Geyer, M. A. et al. · Neuropsychopharmacology (2011)
Van Amsterdam, J., Opperhuizen, A., Van Den Brink, W. · Regulatory Toxicology and Pharmacology (2011)
Studerus, E., Kometer, M., Hasler, F. et al. · Journal of Psychopharmacology (2010)
Johnson, M. W., Richards, W. A., Griffiths, R. R. · Journal of Psychopharmacology (2008)
Wittmann, M., Hasler, F., Vollenweider, F. X. · Neuroscience Letters (2008)
Carter, O. L., Hasler, F. ;., Pettigrew, J. D. et al. · Psychopharmacology (2007)