In a double-blind, placebo-controlled study using ultra-high-field multimodal imaging, psilocybin produced region-specific alterations in glutamate in humans that predicted the subjective experience of ego dissolution. Specifically, higher medial prefrontal glutamate was associated with negatively experienced ego dissolution, while lower hippocampal glutamate predicted positively experienced ego dissolution, suggesting a neurochemical mechanism that may underlie therapeutic effects.
There is growing interest in the therapeutic utility of psychedelic substances, like psilocybin, for disorders characterized by distortions of the self-experience, like depression. Accumulating preclinical evidence emphasizes the role of the glutamate system in the acute action of the drug on brain and behavior; however this has never been tested in humans. Following a double-blind, placebo-controlled, parallel group design, we utilized an ultra-high field multimodal brain imaging approach and demonstrated that psilocybin (0.17 mg/kg) induced region-dependent alterations in glutamate, which predicted distortions in the subjective experience of one’s self (ego dissolution). Whereas higher levels of medial prefrontal cortical glutamate were associated with negatively experienced ego dissolution, lower levels in hippocampal glutamate were associated with positively experienced ego dissolution. Such findings provide further insights into the underlying neurobiological mechanisms of the psychedelic, as well as the baseline, state. Importantly, they may also provide a neurochemical basis for therapeutic effects as witnessed in ongoing clinical trials.
Psychedelics induce pronounced alterations of consciousness, including transient distortions in self-experience commonly described as ego dissolution, in which self-referential awareness is reduced and self–world boundaries are blurred. Earlier research links the hallucinogenic effects of classical psychedelics such as psilocybin to agonism of cortical 5-HT2A receptors, and preclinical work further implicates glutamatergic signalling downstream of 5-HT2A activation as a potential pathway mediating acute neural and behavioural effects. Functional imaging studies have also associated alterations in default mode network (DMN) function with ego-dissolution experiences, and both the medial prefrontal cortex (mPFC) and hippocampus are candidate regions due to their 5-HT2A receptor density and roles in self-referential processing. Mason and colleagues set out to test, in humans, whether acute psilocybin alters glutamate concentrations in key brain regions and whether such changes relate to subjective ego-dissolution and resting-state network functional connectivity (FC). Using ultra-high field proton magnetic resonance spectroscopy (7T MRS) targeted at the mPFC and right hippocampus, together with resting-state fMRI and validated questionnaires of altered states and ego dissolution, the study aimed to characterise region-specific neurometabolic changes during peak drug effects and assess their association with both network-level connectivity and subjective experience.
Papers cited by this study that are also in Blossom
Nour, M. R., Evans, J., Nutt, D. J. et al. · Frontiers in Human Neuroscience (2016)
The investigators employed a randomised, double-blind, placebo-controlled, parallel-group design. Sixty healthy adults with prior but not recent (within 3 months) psychedelic experience were allocated to oral psilocybin (0.17 mg/kg) or placebo, with groups matched on age, sex and education. Ethical approvals and informed consent procedures were completed in line with relevant regulations. Neuroimaging and subjective assessments were timed to capture peak effects. Structural MRI was acquired at 50 minutes post administration, single-voxel MRS at the mPFC (65 min) and right hippocampus (95 min), and resting-state fMRI at 102 min, all on a 7T scanner. MRS voxels measured glutamate, GABA, N-acetyl-aspartate (tNAA) and myo-inositol (mI) relative to total creatine (tCr) to correct for common acquisition variabilities. MRS data were analysed using LCModel. Resting-state data processing used the CONN toolbox with group independent component analysis (ICA) restricted to 20 components; within-network and between-network FC were assessed with voxel-wise and ROI-based approaches, respectively. Subjective state was measured retrospectively at 360 minutes post dosing using the 5-Dimensions of Altered States of Consciousness (5D-ASC) scale and the Ego Dissolution Inventory (EDI). Venous blood samples at 80, 150 and 360 minutes assessed psilocin concentrations. Statistical tests included non-parametric Mann–Whitney U tests for metabolite and questionnaire comparisons, two-sample t-tests for voxel-wise and ROI FC contrasts (voxel p < 0.001 uncorrected, cluster p < 0.05 FDR-corrected), and canonical correlation analysis to relate biological predictors (relative glutamate in mPFC and hippocampus plus extracted within-network FC metrics) to subjective measures of ego dissolution. Missing data were handled with iterative imputation where applicable, and significance was set at p < 0.05.
Demographics and pharmacokinetics: The psilocybin (n = 30) and placebo (n = 30) groups did not differ on reported demographic variables. Mean serum psilocin peaked at 80 minutes post dose (15.61 ± 1.66 ng/mL) and declined by 360 minutes (4.85 ± 0.54 ng/mL), consistent with the administered oral dose. Subjective effects: Psilocybin produced robust subjective effects. Scores increased on all 5D-ASC dimensions (U = 13.5–225; p ≤ 0.001; effect sizes 0.43–0.84) and on the EDI (U = 91.5, p < 0.001, effect size = 0.67), indicating both positively and negatively valenced ego-dissolution experiences relative to placebo. MRS findings: Spectral quality and exclusions were reported but specific numbers were given in tables referenced in the text. In the mPFC, relative glutamate (glutamate/tCr) was higher after psilocybin than placebo (psilocybin 1.23 ± 0.02 vs placebo 1.14 ± 0.02; U = 200.50, p = 0.01; effect size = 0.80). The mPFC also showed higher tNAA/tCr (1.41 ± 0.03 vs 1.31 ± 0.02; U = 210.0, p = 0.02; effect size = 0.72) and higher GABA/tCr (0.17 ± 0.01 vs 0.14 ± 0.01; U = 66.0, p = 0.01; effect size = 0.99) under psilocybin. By contrast, hippocampal glutamate/tCr was lower after psilocybin versus placebo (0.77 ± 0.03 vs 0.88 ± 0.03; U = 163.50, p = 0.03; effect size = 0.69). No other significant group differences in hippocampal GABA, tNAA, mI or total creatine were observed, and the authors note that reliable hippocampal GABA quantification was not achievable in this dataset. Resting-state networks: After quality control the rsfMRI sample was reduced to 22 psilocybin and 26 placebo participants. ICA identified multiple canonical networks, though the DMN and sensorimotor networks were split into subcomponents; anterior and posterior DMN components were included in analyses. Within-network coactivation was significantly reduced under psilocybin in visual networks 1 and 2, both DMN subcomponents (anterior and posterior), and the auditory network. Between-network FC showed widespread increases under psilocybin relative to placebo, affecting all investigated networks except the lateral motor network. Brain–behaviour relationships: A canonical correlation analysis examined four biological predictors (mPFC and hippocampal glutamate plus selected within-network FC measures) against three ego-dissolution variables (anxious ego dissolution (AED), oceanic boundlessness (OB), and EDI scores). The full model was significant (F(12,61.14) = 2.47, p = 0.008) and explained 65.9% of variance. The first two canonical functions were noteworthy (squared canonical correlations R_c^2 = 0.363 and 0.282). Function 1 was dominated by AED and was principally predicted by increased mPFC glutamate with a secondary contribution from anterior DMN FC, indicating that higher frontal glutamate most strongly related to negatively experienced ego dissolution. Function 2 was dominated by EDI and OB and was primarily predicted by decreased hippocampal glutamate with secondary contribution from posterior DMN FC, implicating hippocampal glutamate decreases in positively valenced ego-dissolution experiences.
Mason and colleagues interpret their findings as the first human demonstration that psilocybin acutely induces region-dependent alterations in glutamate, with increases in the mPFC and decreases in the hippocampus, and that these differential changes correlate with distinct dimensions of ego dissolution. The observed mPFC glutamatergic increase aligns with preclinical evidence that 5-HT2A receptor activation elevates cortical glutamate release and with human imaging reports of increased frontal cerebral blood flow after psychedelics. The concurrent mPFC increase in GABA and tNAA suggests a complex local response involving both excitatory and inhibitory elements and a potential change in neuronal metabolic state; tNAA is noted as a marker often interpreted as reflecting neuronal viability or function. Regarding the hippocampal glutamate decrease, the researchers discuss possible mechanisms including indirect inhibition via 5-HT2A receptor effects on interneurons and direct activation of inhibitory 5-HT1A receptors, which are relatively dense in limbic regions; however, the study cannot distinguish these mechanisms. The authors link hippocampal glutamate decrements and posterior DMN decoupling to hypotheses that loss of access to autobiographical semantic information underlies positively experienced ego dissolution, and they cite parallels with prior findings that decoupling between medial temporal lobe structures and other networks correlates with ego-dissolution ratings. The canonical correlation results are interpreted to suggest that increased mPFC glutamate is the strongest predictor of negatively valenced ego-dissolution (anxious, loss-of-control experiences), whereas reduced hippocampal glutamate predicts positively experienced ego-dissolution (feelings of unity and boundary dissolution). The authors note the apparent paradox that acute psychedelic administration can increase anxiety while longer-term clinical trials report reductions in anxiety, and they propose speculative mechanisms such as acute glutamate-driven hyperfrontality versus longer-term receptor downregulation and plasticity; they link the glutamatergic pathway to putative downstream increases in BDNF and neuroplasticity described in preclinical models. Limitations acknowledged by the study team include the moderate dose chosen to maintain participant tolerance in the scanner, which may not produce maximal ego dissolution, and technical constraints of ultra-high field fMRI such as increased geometric distortions and relatively short scan duration for test–retest reliability. The authors also highlight methodological limits in reliably quantifying hippocampal GABA in this dataset and the difficulty of maintaining blinding due to the overt subjective effects of psychedelics, suggesting active placebo or cross-psychotropic controls in future work. Finally, they emphasise that while the findings offer a neurochemical correlate for aspects of ego dissolution and a potential mechanistic link to therapeutic effects, causal pathways and long-term changes remain to be established in further research.
A detailed description of the experimental procedure, image acquisition, MRS quantification, and rsfMRI analysis is provided in the Supplementary methods, and briefly summarized here. The present study employed a randomized, placebo-controlled, double-blind, parallel group design. Sixty healthy participants, with previous experience with a psychedelic drug but not within the past 3 months, were allocated to a treatment condition (0.17 mg/kg psilocybin or placebo, p.o.). Groups were matched for age, sex, and education level. This study was conducted according to the code of ethics on human experimentation established by the declaration of Helsinki (1964) and amended in Fortaleza (Brazil, October 2013) and in accordance with the Medical Research Involving Human Subjects Act (WMO) and was approved by the Academic Hospital and University's Medical Ethics committee. All participants were fully informed of all procedures, possible adverse reactions, legal rights and responsibilities, expected benefits, and their right for voluntary termination without consequences.
Statistical analysis of metabolite concentration levels and questionnaire responses were conducted in IBM SPSS Statistics 24 using nonparametric Mann-Whitney U tests. For the assessment of within-network FC, the unthresholded, binarized ICA component images were compared between placebo and drug conditions (two-sample t-test). Parametric statistics were used (voxel threshold p < 0.001 uncorrected, cluster threshold p < 0.05 cluster-size, false discovery rate (FDR) corrected, two-sided). For the assessment of between-network FC, unthresholded, binarized maps of RSNs obtained from the ICA analysis were imported as ROIs and the weighted sums of the time series were extracted. Time courses between all RSNs were then compared for both conditions using bivariate correlations. The resulting correlation coefficients were compared between placebo and drug conditions (two-sample t-test). Results were corrected for multiple comparisons using FDR. Canonical correlationswere conducted to evaluate the association between psilocybin-induced changes in (i) relative glutamate concentration levels in the mPFC and hippocampus, (ii) ratings of ego dissolution, including two dimensions of the 5D-ASC (oceanic boundlessness and anxious ego dissolution) and scores on the EDI, and (iii) within-network resting state FC, using extracted connectivity strength (beta) values. Variables were separated into two sets; set 1 included biological variables as predictors [(i) and (iii)] and set 2 included the subjective variables as criterion (ii). An iterative imputation approach was performed to fill in missing data points, when applicable. The alpha criterion of significance of all tests was assumed at p < 0.05.
The present study demonstrates the first attempt to assess the acute effects of psilocybin on glutamate levels in key areas of the human brain, which may play a major role in the actions of serotonergic psychedelics. Using an ultra-high field multimodal MRI approach, we demonstrated that, compared with placebo, psilocybin-induced region-dependent alterations in neurometabolite concentrations. Specifically, participants who received psilocybin demonstrated higher relative glutamate concentration levels in the mPFC, and lower relative glutamate concentration levels in the hippocampus. Analyses indicated that regiondependent alterations in glutamate were also correlated with different dimensions of ego dissolution. Whereas changes in mPFC glutamate were found to be the strongest predictor of negatively experienced ego dissolution, changes in hippocampal glutamate were found to be the strongest predictor of positively experienced ego dissolution. Previous studies have demonstrated that the mPFC is highly enriched with 5-HT 2A receptors located primarily on layer V pyramidal neurons, and modulate excitatory transmission in cortical circuits. Preclinical studies have demonstrated that activation of such receptors via serotonergic psychedelics results in a predominantly excitatory responsevia an increase in glutamate release, as observed in humans for the first time in this study. A glutamatergic increase in this area is also in accordance with human functional imaging studies which have demonstrated a hyperfrontal regional cerebral blood flow (CBF) pattern after psilocybin, and similar 5-HT 2A agonist psychedelics. However, we also found that psilocybin administration was associated with higher levels of GABA in this area, results in line with findings that 5-HT 2A receptors are also located on GABAergic interneurons. Taken together, findings suggest that activation of 5-HT 2A receptors in the mPFC results in both excitation and inhibition of cortical pyramidal cells, potentially resulting in an increased metabolic rate in this area, but not necessarily increased neural input or output. In contrast to the mPFC, the present study demonstrated that participants who received psilocybin demonstrated lower relative glutamate concentrations in the hippocampus, suggesting that psilocybin decreases glutamate in this area. Such a decrease is in line with data from a recent functional imaging study with psilocybin, demonstrating reduced absolute CBF in the hippocampus compared with placebo, of which the authors proposed two potential mechanisms. Namely, decrements could be due to agonism of 5-HT 2A receptors located on GABAergic interneurons, which can indirectly inhibit pyramidal neurons, decreasing activation in this area. Conversely, it has also been established that, along with the 5-HT 2A receptor, psilocin also has a high affinity for the 5-HT 1A receptor. Referred to as serotonin's principal inhibitory receptor, the 5-HT 1A receptors highest density is found in the limbic regions of the brain such as the hippocampuswhere it is expressed on neurons that are postsynaptic to the serotonergic input. Thus lower levels in glutamate as seen in this study, as well as regional decreases reflected in others, could be due to activation of postsynaptic inhibitory 5-HT 1A receptors. Nevertheless, due to methodological limitations, this study is not able to delineate which mechanism is contributing to the lower levels in glutamate. Further information could have been potentially gained from quantification of GABA in the hippocampus, however we were unable to reliably do so, due to inherent quantification challenges when assessing GABA levels, arising from low brain concentration levels, metabolite signal overlap, and low signal-to-noise in the hippocampus. Future studies with sequences developed to specifically quantify GABA in low signal-to-noise areas should make further attempts to do so, given recent research implicating hippocampal GABA in the pathology of disorders that psychedelics are being investigated to treat. In the current study, psilocybin induced previously established key features of a psychedelic experience: increases in feelings of ego dissolution, and disrupted RSN activity. Psilocybin increased scores on all dimensions of the 5D-ASC, as well as on the EDI. In addition, psilocybin altered within-network FC similarly as has been shown with LSD, including decrements in coactivation within the DMN, visual network 1, and the auditory network. Finally, we demonstrated higher between-network FC across all networks, which is similar with previous studies assessing the same after psilocybinand LSD. Finally, we assessed the relationship between psilocybininduced changes in the brain, and the subjective experience of sense of self. Canonical correlations were conducted to predict increases in ratings of AED, the dimension encompassing the loss of autonomy and self-control of thought processes, intentionality, decision making, and spontaneous movements. Our data support the conclusion that increasing levels of mPFC glutamate were the strongest predictor in regards to feelings of AED, with decreasing anterior DMN FC and hippocampal glutamate being secondary predictors. These findings are in line with previous work, implicating increased frontal metabolism in feelings of AED after psilocybinand ego pathology in the ketamine model of psychosis. Interestingly, AED-associated changes in mood include paranoia, heightened arousal and attention to the surroundings, and anxiety. A paradoxical effect of serotonergic psychedelics is that acutely they have been found to increase feelings of anxiety, whereas clinical trials with psychedelic drugs suggest long-term anxiety relief in patients. Accordingly, there is a wide range of animal and human pharmacological evidence supporting the role of the glutamatergic system in anxiety, with increases in glutamate in the frontal cortex associated with high versus low state-trait anxiety, and reductions corresponding to anxiety-related symptomatic relief. Taken together, the finding that mPFC glutamate was by far the strongest predictor of increased feelings of anxiety, one could propose that acute psychedelic-induced anxiety may be due to localized glutamate-induced hyperfrontality, whereas longterm reductions could be due to agonist-induced 5-HT 2A receptor downregulation in this area. Nonetheless, future studies should assess long-term changes in 5-HT 2A receptor function in the mPFC, and their relation with subjective effects. We also assessed the relationship between psilocybin-induced brain changes and feelings of positively experienced ego dissolution, including ratings on the EDI, and scores of OB on the 5D-ASC. We found that the primary predictor of positively experienced ego dissolution was a decrement in hippocampal glutamate, with secondary contributions of mPFC glutamate and posterior DMN integrity. Previous work has implicated both the MTL (containing the hippocampus) and DMN circuitry in the neural correlates of the self. Namely, abnormal function of MTL regions have been implicated in psychotic statesand feelings of depersonalizationand ego-disturbances. Similarly, studies of drug-induced ego dissolution have found that the decoupling of MTL regions such as the parahippocampus and the DMN correlate positively with feelings of ego dissolution, with this decoupling being hypothesized to be one of the main underlying mechanisms of the subjective experience. In regards to why this gives rise to ego dissolution, it has been suggested that psychedelic drug-induced decoupling of these regions results in a temporary loss of access of semantic autobiographical information, resulting in a breakdown of one's personal identity. Our data add to this hypothesis, suggesting that modulations of hippocampal glutamate in particular may be a key mediator in the decoupling underlying feelings of (positive) ego dissolution. Interestingly, although the DMN has been the most implicated RSN in this process, Lebedev et al.found that increases in ego dissolution correlated with decreased FC between the parahippocampal formation and other major networks, such as the salience, frontoparietal, and sensorimotor network; suggesting a key role in this area in particular, as our data also demonstrate. However future research should further assess the contribution of other areas to this experience, such as the posterior cingulate cortex. Implications of these findings also extend far beyond understanding the neurobiology of the acute psychedelic experience and drug-induced ego dissolution. There is growing evidence that psychedelics can provide therapeutic relief for individuals suffering from increasingly common and difficult to treat disorders such as depression, anxiety, addiction, and post-traumatic stress disorders. Thus understanding the mechanisms by which psychedelics provide symptomatic relief may identify novel therapeutic targets. Interestingly, the degree of ego dissolution has been found to correlate with long-term clinical outcomesand increases in well-being. In addition, a hypothetical (neurobiological) model has been proposed to explain the long-term effects witnessed in clinical trials. It has been suggested that indirect activation of glutamate networks via 5-HT 2A receptor agonism increases BDNF, and ultimately enhances neuroplasticity. In line with this, it has been shown in preclinical models that psychedelics increase functional and structural neuroplasticity, however evidence in humans is limited, due to restrictions of methodological techniques. Our data provide indirect evidence that psychedelics might have the potential to increase neuroplasticity in the human cortex via increased glutamatergic activity, but not in the hippocampus; findings that are in accordance with previous 5-HT 2A receptor activation studies. In addition, psilocybin administration was associated with higher levels of mPFC NAA, a compound regarded as a measure of neuronal viability and function, and decreased in disorders associated with regional neuronal loss and disrupted neuronal function. Of note, compared to previous psychedelic studies, the dose administered was low to moderate, and thus not high enough to induce total ego dissolution. However, the aim of this study was not to assess maximal effects of psilocybin, but rather an effective dose that would induce a relevant psychedelic state that participants could endure in the MRI scanner. Our data demonstrate that the dose was effective, inducing significantly higher levels of both positively and negatively experienced ego dissolution compared with placebo, as well as the other subjective effects representative of a psychedelic state (Figs.). Furthermore, although BOLD sensitivity is increased by the use of ultra-high magnetic fields, geometric distortions become more prominent, which could have affected our BOLD signal in inferior brain regions, and our scan time was arguably short from a test-retest reliability standpoint. Nevertheless, our results are similar to aforementioned studieswho acquired their data at a lower field strength, with varying scanning lengths. Finally, an inherent difficulty of studying substances with such salient subjective effects is maintaining the treatment blind. Thus, it could be suggested that participant recognition of the treatment condition could affect neural and subjective results, emphasizing the importance of active placebo conditions or crosspsychotropic comparisons in future trials. In conclusion, our data demonstrate that the serotonergic psychedelic, psilocybin, acutely induces region dependent alterations in glutamate that correlate with established behavioral changes during the psychedelic state. Such findings provide further insights into the underlying neurobiological mechanisms of the psychedelic state, and importantly, provide a neurochemical basis for how these substances alter individuals' sense of self, and may be giving rise to therapeutic effects witnessed in ongoing clinical trials.
Create a free account to open full-text PDFs.
Studerus, E., Gamma, A., Vollenweider, F. X. · PLOS ONE (2010)
Nour, M. R., Carhart-Harris, R. L. · British Journal of Psychiatry (2017)
Carhart-Harris, R. L., Bolstridge, M., Rucker, J. et al. · Lancet Psychiatry (2016)
Carhart-Harris, R. L., Goodwin, G. M. · Neuropsychopharmacology (2017)
Griffiths, R. R. · Journal of Psychopharmacology (2008)
Mason, N. L., Mischler, E., Uthaug, M. V. et al. · Journal of Psychoactive Drugs (2019)
Uthaug, M. V., Van Oorsouw, &. K., Kuypers, &. K. P. C. et al. · Psychopharmacology (2018)
Gasser, P., Holstein, D., Michel, Y. et al. · Journal of Nervous and Mental Disease (2014)
Grob, C. S., Danforth, A. L., Chopra, G. S. et al. · JAMA Psychiatry (2011)
Sanches, R. F., Osório, F. L., Dos Santos, R. G. et al. · Journal of Clinical Psychopharmacology (2016)
Vollenweider, F. X., Kometer, M. · Nature Reviews Neuroscience (2010)
Carhart-Harris, R. L., Erritzoe, D., Williams, T. et al. · PNAS (2012)
Smigielski, L., Scheidegger, M., Kometer, M. et al. · NeuroImage (2019)
Müller, F., Dolder, P. C., Schmidt, A. et al. · NeuroImage (2018)
Carhart-Harris, R. L., Muthukumaraswamy, S., Roseman, L. et al. · PNAS (2016)
Palhano-Fontes, F., Andrade, K. C., Tófoli, L.F. et al. · PLOS ONE (2015)
Roseman, L., Leech, R., Feilding, A. et al. · Frontiers in Human Neuroscience (2014)
Lord, L. D., Expert, P., Atasoy, S. et al. · NeuroImage (2019)
Atasoy, S., Leor, R., Kaelen, M. et al. · Scientific Reports (2017)
Tagliazucchi, E., Roseman, L., Kaelen, M. et al. · Current Biology (2016)
Carhart-Harris, R. L., Leech, R., Erritzoe, D. et al. · Schizophrenia Bulletin (2012)
Vollenweider, F. X., Leenders, K. L., Maguire, P. et al. · Neuropsychopharmacology (1997)
Carhart-Harris, R. L., Leech, R., Shanahan, M. et al. · Frontiers in Human Neuroscience (2014)
Carhart-Harris, R. L., Friston, K. J. · Brain (2010)
Lebedev, A. V., L€ Ovd En, M., Rosenthal, G. et al. · Human Brain Mapping (2015)
Brown, R. T., Nicholas, C. R., Cozzi, N. V. et al. · Clinical Pharmacokinetics (2017)
Lewis, C. R., Preller, K. H., Kraehenmann, R. et al. · NeuroImage (2017)
Carhart-Harris, R. L., Nutt, D. J. · Journal of Psychopharmacology (2017)
Carhart-Harris, R. L., Kaelen, M., Bolstridge, M. et al. · Psychological Medicine (2016)
Milliere, R., Carhart-Harris, R. L., Roseman, L. et al. · Frontiers in Psychology (2018)
Oehen, P., Traber, R., Widmer, V. et al. · Journal of Psychopharmacology (2012)
Garcia-Romeu, A., Griffiths, R. R., Johnson, M. W. · Current Drug Abuse Reviews (2015)
Roseman, L., Nutt, D. J., Carhart-Harris, R. L. · Frontiers in Pharmacology (2018)
Ly, C., Greb, A. C., Cameron, L. P. et al. · Cell Reports (2018)
Studerus, E., Kometer, M., Hasler, F. et al. · Journal of Psychopharmacology (2010)
Papers in Blossom that reference this study
Madrid-Gambin, F., Mallaroni, P., Haro, N. et al. · Biomedicine & Pharmacotherapy (2026)
Gubser, L. P., Trippel, A. S., Zoelch, N. et al. · Brain Research Bulletin (2026)
Calder, A. E., Rausch, B., Liechti, M. E. et al. · Journal of Psychopharmacology (2024)
Caspani, G., Ruffell, S. G. D., Tsang, WF. et al. · Pharmacological Research (2024)
Casanova, A. F., Ort, A., Smallridge, J. W. et al. · iScience (2024)
Rieser, N. M. · Biological Psychiatry (2024)
Shinozuka, K., Tewarie, P. K. B., Luppi, A. et al. · Biorxiv (2024)
Tipado, Z., Kuypers, K. P. C., Sorger, B. et al. · European Neuropsychopharmacology (2024)
Weiss, B., Leor Roseman, •., Giribaldi, B. et al. · International Journal of Mental Health and Addiction (2024)
Pasquini, L., Simon, A. J., Gallen, C. L. et al. · Biorxiv (2024)
Pizzi, S. D., Chiacchiaretta, P., Sestieri, C. et al. · NeuroImage (2023)
Mason, N. L., Szabo, A., Kuypers, K. P. C. et al. · Brain Behavior and Immunity - Health (2023)
Buchborn, T., Kettner, H., Kartner, L. et al. · Frontiers in Neuroscience (2023)
Neubert, J. J., Anderson, K., Mason, N. L. · Psyarxiv (2023)
Adamska, I., Finc, K. · Psychopharmacology (2023)
Thal, S. B., Wieberneit, M., Sharbanee, J. M. et al. · Journal of Humanistic Psychology (2023)
Girn, M., Rosas, F. E., Daws, R. E. et al. · Trends in Cognitive Sciences (2023)
Carhart-Harris, R. L., Chandaria, S., Erritzoe, D. E. et al. · Neuropharmacology (2023)
Timmermann, C., Vollenweider, F. X. · Trends in Cognitive Sciences (2023)
Olsen, A. S., Ozenne, B., Madsen, M. K. et al. · NeuroImage (2022)
Aqil, M., Roseman, L. · Neuropharmacology (2022)
Gattuso, J. J., Perkins, D., Ruffell, S. G. D. et al. · International Journal of Neuropsychopharmacology (2022)
Thal, S. B., Wieberneit, M., Sharbanee, J. M. et al. · Journal of Psychopharmacology (2022)
Herrmann, Z., Earleywine, M., De Leo, J. et al. · Journal of Psychoactive Drugs (2022)
Dourron, H. M., Strauss, C., Hendricks, P. S. · Pharmacological Reviews (2022)
Stoliker, D., Egan, G. F., Friston, K. J. et al. · Pharmacological Reviews (2022)
van Elk, M., Yaden, D. B. · Neuroscience and Biobehavioral Reviews (2022)
Wojtas, A., Bysiek, A., Wawrzczak-Bargiela, A. et al. · International Journal of Molecular Sciences (2022)
Doss, M. K., Samaha, J., Barrett, F. S. et al. · Biorxiv (2022)
Pots, W., Chakhssi, F. · Frontiers in Psychology (2022)
Madrid-Gambin, F., Gomez-Gomez, A., Busquets-Garcia, A. et al. · Biomedicine & Pharmacotherapy (2022)
McCulloch, D. E-W., Madsen, M. K., Jensen, P. S. et al. · Frontiers in Pharmacology (2022)
Elman, I., Borsook, D., Pustilink, A. · Neuroscience and Biobehavioral Reviews (2022)
Reckweg, J., Uthaug, M. V., Szabo, A. et al. · Journal of Neurochemistry (2022)
Vollenweider, F. X., Smallridge, J. W. · Pharmacopsychiatry (2022)
Ramaekers, J. G. · Psychopharmacology (2022)
Barrett, F. S., Zhou, Y., Carbonaro, T. M. et al. · Frontiers in Neuroergonomics (2022)
Dursun, S. M., Kelly, J. R., Gillan, C. M. et al. · Frontiers in Psychiatry (2021)
Rieser, N. M., Herdener, M. ;., Preller, K. H. · Current Topics in Behavioral Neurosciences (2021)
Doss, M. K., Madden, M. B., Gaddis, A. et al. · Brain (2021)
Garcia-Romeu, A., Darcy, S., Jackson, H. et al. · Current Topics in Behavioral Neurosciences (2021)
van Oorsouw, K., Uthaug, M. V., Mason, N. L. et al. · Journal of Psychedelic Studies (2021)
Rodríguez Arce, J. M., Winkelman, M. J. · Frontiers in Psychology (2021)
Madsen, M. K., Stenbaek, D. S., Arvidsson, A. et al. · European Neuropsychopharmacology (2021)
Burt, J. B., Preller, K. H., Demirtaş, M. et al. · eLife (2021)
Corrigan, K., Haran, M., Mccandliss, C. et al. · Irish Journal of Medical Science (2021)
Mason, N. L., Kuypers, K. P. C., Reckweg, J. T. et al. · Translational Psychiatry (2021)
Thomas, C. W., Blanco-Duque, C., Breant, B. et al. · Translational Psychiatry (2021)
McCulloch, D. E-W., Madsen, M. K., Stenbæk, D. S. et al. · Journal of Psychopharmacology (2021)
Kadriu, B., Greenwald, M., Ba et al. · International Journal of Neuropsychopharmacology (2020)
Doss, M. K., May, D. G., Johnson, M. W. et al. · Scientific Reports (2020)
Kelly, J. R., Crockett, M. T., Alexander, L. et al. · Irish Journal of Psychological Medicine (2020)
Girn, M., Roseman, L., Bernhardt, B. et al. · Biorxiv (2020)