This open-label fMRI study (n=20) investigated amygdala responses to emotional stimuli in patients with treatment-resistant depression following psilocybin therapy. Unlike SSRIs which typically blunt amygdala responses, psilocybin increased responsiveness to fearful and happy faces, suggesting a therapeutic mechanism involving the reconnection with, rather than suppression of, emotions.
Papers cited by this study that are also in Blossom
Bogenschutz, M. P., Johnson, M. W. · Progress in Neuro-Psychopharmacology and Biological Psychiatry (2016)
Recent evidence indicates that psilocybin with psychological support may be effective for treating depression. Some studies have found that patients with depression show heightened amygdala responses to fearful faces and there is reliable evidence that treatment with SSRIs attenuates amygdala responses (Ma, 2015). We hypothesised that amygdala responses to emotional faces would be altered post-treatment with psilocybin. In this open-label study, 20 individuals diagnosed with moderate to severe, treatment-resistant depression, underwent two separate dosing sessions with psilocybin. Psychological support was provided before, during and after these sessions and 19 completed fMRI scans one week prior to the first session and one day after the second and last. Neutral, fearful and happy faces were presented in the scanner and analyses focused on the amygdala. Group results revealed rapid and enduring improvements in depressive symptoms post-psilocybin. Increased responses to fearful and happy faces were observed in the right amygdala post-treatment, and right amygdala increases to fearful versus neutral faces were predictive of clinical improvements at 1-week. Psilocybin with psychological support was associated with increased amygdala responses to emotional stimuli, an opposite effect to previous findings with SSRIs. This suggests fundamental differences in these treatments’ therapeutic actions, with SSRIs mitigating negative emotions and psilocybin allowing patients to confront and work through them. Based on the present results, we propose that psilocybin with psychological support is a treatment approach that potentially revives emotional responsiveness in depression, enabling patients to reconnect with their emotions.:
Roseman and colleagues situate their work in the recent renaissance of clinical research on classic psychedelics, noting growing evidence that psilocybin combined with psychological support can produce rapid reductions in depressive and anxiety symptoms. They outline a neurobiological rationale focused on the amygdala, a subcortical structure sensitive to emotionally salient stimuli that has been implicated in depression. Previous functional MRI studies in untreated depressed patients have often reported amygdala hyper-reactivity to negative stimuli, and conventional antidepressants such as SSRIs tend to attenuate amygdala responses early in treatment. The study aimed to test whether amygdala responses to emotional faces are altered after psilocybin treatment in people with treatment-resistant depression (TRD). Using a validated emotional faces fMRI paradigm, the investigators predicted that post-treatment amygdala reactivity would change relative to baseline and that such changes would relate to clinical measures of depressive symptoms. They paid particular attention to the fearful versus neutral contrast because prior SSRI work has emphasised attenuation to negative stimuli, and they also anticipated that aspects of the acute psychedelic experience might relate to subsequent changes in amygdala function.
This was an open-label interventional study of psilocybin with psychological support in patients with moderate to severe treatment-resistant major depression. Ethical approval was obtained from the relevant UK bodies and all participants provided written informed consent. Twenty patients were enrolled; 19 completed both pre- and post-treatment fMRI scans. Demographics for the scanned sample were six females, mean age 44.7 years (SD 10.9, range 27–64). Inclusion required a Hamilton Depression Rating Scale (HAM-D) score ≥16 and failure to improve after at least two adequate antidepressant courses. Participants were asked to be free of antidepressant medication for at least two weeks prior to study procedures. Exclusion criteria included current or past psychotic disorder, first-degree relative with psychosis, significant medical illness contraindicating participation, history of serious suicidal attempts requiring hospitalisation, history of mania, blood/needle phobia, pregnancy, and current drug or alcohol dependence. The intervention comprised preparatory psychological sessions (about 4 hours) followed by two psilocybin-assisted therapy sessions one week apart. The first session was a low ‘‘test’’ dose of 10 mg p.o. and the second a higher therapeutic dose of 25 mg p.o. During dosing, participants lay with eyes closed listening to music while two therapists provided nondirective supportive care. Baseline fMRI scanning occurred prior to any psychological or pharmacological intervention; the post-treatment scan was performed the morning after the high-dose session (both scans at approximately 10:00am). The sample size for imaging analyses was 19 (one of 20 did not complete scans). Imaging was performed on a 3T Siemens Tim Trio with a 12-channel head coil. Anatomical MPRAGE and T2*-weighted echo-planar images were acquired; functional scans used 3 mm isotropic voxels, TR 2000 ms, TE 31 ms. The emotional faces task was an 8-minute block design presenting fearful, happy and neutral expressions from the Karolinska Directed Emotional Faces set. Five faces (3 s each) of the same expression were shown per 15 s block, interleaved with 15 s rest blocks; two task versions (reverse block order) were counterbalanced across visits. Participants passively viewed faces and pressed a button with each new face to confirm attention. Preprocessing combined tools from FSL, AFNI, Freesurfer and ANTS and included motion correction, brain extraction, rigid and non-linear registration to MNI space, scrubbing using a framewise displacement threshold of 0.90 mm, spatial smoothing (6 mm FWHM), high-pass filtering (0.01 Hz) and regression of six motion parameters. Mean framewise displacement did not differ before versus after treatment and the proportion of scrubbed volumes was low (mean 2.3% before and after). Region-of-interest (ROI) and voxelwise analyses focused on the amygdala. Two complementary approaches were used: mean signal within left and right amygdala ROIs and voxelwise testing inside a bilateral amygdala mask (Harvard–Oxford atlas, probability > 50%). First-level GLMs (FEAT, FSL) modelled fearful, happy and neutral onsets convolved with a haemodynamic response, with contrasts for each emotion versus baseline and contrasts of fearful > neutral and happy > neutral (five contrasts total). Group-level mixed-effects analyses (FLAME 1+2) compared before versus after treatment. Voxelwise results used a cluster-forming threshold Z > 2.3 with cluster correction at p < .05. To examine associations with clinical outcome, voxelwise analyses within a right amygdala mask used clinical measures as regressors; the primary clinical outcomes pre-specified for this imaging analysis were Beck Depression Inventory (BDI) at 1 week and in-scanner state depression ratings (0–20) comparing baseline with one day post-treatment. The Quick Inventory of Depressive Symptomatology (QIDS) was added post-hoc to allow assessment across multiple time points (1 day, 1, 2, 3 and 5 weeks). State and trait anxiety measures (in-scanner rating and STAI at 1 week) were also explored.
Nineteen patients completed both fMRI sessions and were included in the imaging analyses. ROI analyses showed increased BOLD responses in the right amygdala after treatment for fearful faces (p = .001) and for happy faces (p = .022), with a trend for neutral faces (p = .066). After correcting for multiple tests (five contrasts × two ROIs), only the fearful-face increase in the right amygdala remained statistically significant. No significant pre–post changes were observed in the left amygdala for fearful, happy or neutral faces (p = .11, p = .95 and p = .2, respectively). Voxelwise analysis within the amygdala mask revealed significantly greater right amygdala responses post-treatment for fearful, happy and neutral faces, and for the fearful > neutral contrast. These increases localised to a consistent region of the right amygdala. Whole-brain exploratory analysis indicated additional post-treatment increases in visual cortical areas for the fearful, happy and neutral contrasts; the fearful > neutral whole-brain effect was more restricted, appearing primarily in the right amygdala and right middle temporal gyrus. Clinical outcomes showed substantial early improvement: one day after psilocybin, 15 of 19 patients (79%) had a clinically meaningful state-response (≥50% reduction in in-scanner depressed-mood rating). Changes in right amygdala activation for fearful > neutral faces were positively associated with better clinical outcomes. Specifically, greater post-treatment right amygdala reactivity to fearful > neutral predicted larger reductions in in-scanner state depression and in trait depression measured by BDI at 1 week. At 1 week the mean BDI change reported in the extracted text was 10.2 ± 5.3, with response and remission rates of 63.2% and 57.9% respectively; these clinical improvements were related to increased right amygdala responses to fearful > neutral. Using QIDS, response rates at 1 day (68.4%), 1 week (63.2%) and 3 weeks (63.2%) were associated with greater post-treatment right amygdala reactivity for fearful > neutral. QIDS response at 2 weeks (57.9%) and 5 weeks (47.3%) did not show a relationship with amygdala changes. The authors also report that responders and remitters tended to show increased amygdala reactivity while non-responders and non-remitters showed decreased reactivity for fearful > neutral. Regarding relapse, 13 subjects were responders at 1 day and 9 maintained response at 5 weeks; comparison between the 4 who relapsed and 9 who did not showed no difference in amygdala activation. The extracted text does not provide detailed adverse-event data or other safety outcomes.
Roseman and colleagues interpret their main finding—an increase in right amygdala responses to emotional faces one day after psilocybin treatment—as fundamentally different from the commonly reported SSRI effect of reduced amygdala reactivity to negative stimuli. They argue that whereas SSRIs have been proposed to exert therapeutic effects in part by attenuating amygdala responses (potentially blunting emotional reactivity), psilocybin with psychological support may instead revive or amplify emotional responsiveness, enabling patients to confront and work through difficult emotions. The observed association between increased right amygdala responses to fearful > neutral faces and subsequent clinical improvement at one week is presented as consistent with this interpretation. The authors position their results relative to prior studies, noting a discrepancy with an earlier report of reduced amygdala responses during the acute psilocybin experience in healthy volunteers. They caution that acute effects during intoxication may differ from post‑acute changes and that apparent attenuations in imaging studies can sometimes reflect reduced task engagement rather than true functional downregulation. Qualitative data from the same clinical trial are cited to support the notion that patients commonly describe greater emotional acceptance and the ability to undergo cathartic emotional processing after psilocybin. Limitations acknowledged by the investigators include the open-label, uncontrolled design, which prevents disentangling the specific contribution of psilocybin from psychological support or non-specific factors. They note the restricted imaging time‑point (one day post-treatment) and the absence of acute-phase imaging in this sample. Additional limitations discussed are the lack of a healthy control group and the absence of active comparator arms such as psilocybin without psychological support or a pharmacological control (e.g. SSRI). The authors recommend future studies with longer follow-up imaging, acute and post-acute imaging, multimodal approaches combining PET and fMRI to relate receptor changes to function, and controlled designs to test replicability and specificity of the effects. In concluding remarks within the Discussion, the authors characterise psilocybin as a potentially rapid-acting, low-abuse-potential intervention for major depression that may operate through a distinct neurobiological mechanism from SSRIs by enhancing emotional connectedness. They present selected patient quotations describing emotional release and increased acceptance as illustrative of the phenomenological changes that may accompany the observed neurobiological effects. The investigators call for replication and further work to determine whether enhanced amygdala responsiveness is causally linked to enduring antidepressant benefits.
This trial received a favourable opinion from the National Research Ethics Service LondondWest London, was sponsored and approved by Imperial College London and by the UK MHRA. All participants provided written informed consent.
Increased amygdala responses to emotional faces were observed one day after treatment with psilocybin for treatment-resistant depression. Post-treatment increases in amygdala responses to fearful versus neutral faces were related to a successful clinical outcome one week later. Importantly, the present findings are in contrast to observations of decreased amygdala responses after treatment with conventional antidepressants and particularly with SSRIs. It has been proposed that decreased amygdala responsiveness to negative emotional stimuli under SSRIs is a key component of their therapeutic action, but the present study's findings suggest that this model does not extend to the therapeutic action of psilocybin for TRD. Observations of reduced amygdala responses to negative emotional stimuliand reduced behavioural response biases to negative stimuli with conventional antidepressantshave been interpreted as evidence of a functional remediation, linked to the correcting of negative cognitive biases in depression. However, it is suggested that chronically-used antidepressants have a more generalised effect on emotional processing, moderating not just responsiveness to negative emotional stimuli, but emotional stimuli more broadly. Focusing specifically on the amygdala, this structure is known to be generally sensitive to emotional salience, regardless of the emotional valence of the stimuliTableRelationship between BOLD changes (after > before therapy; fearful > neutral) within the right amygdala and clinical outcomes. To avoid multiple comparisons, we hypothesized that amygdala changes would be related to two main clinical outcomes BDI at 1 week and in-scanner depression ratings. Other comparisons should be considered exploratory (QIDS, STAI and in-scanner state anxiety). The "Type of score" column describes how the test was done: Remission (BDI 9) and Response (>50% reduction) were used to split the group for remitters/non-remitters or responders/non-responders. The differences between responders and non-responders and remitters and nonremitters are presented in the Max column which describe the z score in the Max voxel of difference, and the z scores of these categories separately are also reported in separate columns for the same voxel as in Max. The "Type of score" "Change" is the difference in the rating for After-Before. The "Change" in BDI and the change in amygdala response were entered to a GLM. Note that clusters close to MNI_152 coordinates (x,y,z) of 18,0,-20 are reliable as they survived cluster correction for few of the clinical outcomes. Furthermore, note that the significant clusters had reduced response for non-responders and non-remitters and enhanced response for responders and remitters. Real cluster sizes may be larger as the clusters in this table are constrained by the amygdala mask. N . It is possible that the notion that SSRIs have a selective action on amygdala responses to negative stimuli is fallible, and rather, SSRIs and related antidepressants have a more generalised muting influence on amygdala responses to emotionally salient stimuli. Relatedly, negative stimuli may be processed as especially salient, and thus be associated with greater amygdala responses e which are subsequently hyper-sensitive to intervention-led change. Reduced amygdala responses to emotional stimuli after chronic antidepressant medication has been linked with activation of postsynaptic serotonin 1A receptors (5-HT1ARs), which have an inhibitory action on pyramidal cell firingand are densely expressed in the amygdala. While this mechanism has a solid empirical basis, there is no known mechanism to explain how 5-HT1AR-induced attenuation of amygdala responsiveness can selectively apply to negative stimuli, without simultaneously affecting the processing of positive stimuli of an equivalent salience. Indeed, there is evidence of blunting of positive mood with SSRIs. Moreover the relative ineffectiveness of conventional serotonergic antidepressant medications to alleviate anhedonia may be explained by a generalised moderation of emotional responsiveness with these drugs. We recently carried out a qualitative analysis of patient experiences from this clinical trial, asking patients whether psilocybin with psychological support has been effective for them, and if so, how? Since the majority of patients reported improvements with the treatment, most answered in the affirmative and described a greater willingness to accept all emotions post-treatment (including negative ones). These effects were often contrasted with those of their previous depression treatments which they described as working to reinforce emotional avoidance and disconnection. Conversely, psilocybin was said to make emotional 'confrontation' more likely, and the accompanying psychological support helped patients achieve an emotional breakthrough (catharsis) and resolution. Consistently, recent work has suggested that overcoming challenging emotional phenomena under a psychedelic is predictive of better long-term mental health outcomes. It is important to highlight an important discrepancy between the present results, observed post acutely in patients treated with psilocybin for major depression viewing emotional faces and those from a previous study in which amygdala responses to emotional stimuli (not faces) were assessed during the acute psilocybin 'high' in healthy individuals. This latter study reported unspecific decreases in right amygdala responses to negative and neutral stimuli under psilocybin, which, based on the aforementioned similarities with the action of conventional antidepressants, the authors interpreted as supporting an antidepressant action for psilocybin. We advise caution with this interpretation however, not least because our pre versus post resting-state fMRI findings suggest that post-acute changes in spontaneous brain function are very different if not antithetical to psilocybin's acute brain effects. Moreover, findings of 'attenuated responses' with potent interventions may be explained by compromised task engagement. A consistent explanation has been used to account for apparent functional impairments in imaging studies of pathological states such as schizophrenia, i.e. impoverished responses are observed because patients do not properly engage with the task and its stimuli. It is important to acknowledge the limitations of the present study. It would be interesting to collect longer-term imaging data than the 1-day post treatment scanning point chosen here (e.g. one week and one month after treatment with psilocybin). If feasible, it would also be interesting to collect imaging data during the acute experience to see how this relates to post treatment brain changes. Future work may look to combine PET and fMRI to systematically address potential relationships between receptor densities and functional brain measures before and after treatment with psilocybin. The recruitment of a healthy control group, receiving the same interventions would also add value, as would the inclusion of a meaningful comparator condition such as psilocybin alone versus psilocybin in combination with psychological support, plus the same for placebo and perhaps an active pharmacological control, such as an SSRI and/or methylphenidate. As this study was not placebo controlled, the contribution of psilocybin with psychological support cannot be differentiated from psychological support and other aspects of the therapy. It would also be worthwhile to see if the present results extend to a less severe population of depressed patients, including those with less extensive histories of exposure to psychiatric medication. Psilocybin represents a novel intervention for major depression that appears to be safe, rapid and potentially enduring in its antidepressant action. Furthermore, it is important to note that psilocybin's abuse potential is low. The original rationale for using psychedelic ('mind-revealing') drugs as aides to psychotherapy was that they serve to dismantle psychological defences, allowing suppressed emotional material to surface, sometimes with cathartic effect. The present findings of increased amygdala responsiveness post psilocybin resonate with patients' descriptions of feeling emotionally re-connected and accepting after the treatment. The finding of a relationship between increased right amygdala responses to fearful > neutral faces post treatment and subsequent clinical improvements adds further endorsement to this interpretation. Future work is required to test the replicability of these findings and test whether enhanced amygdala responsiveness is related to the potentially enduring positive mood effects of psychedelics. If confirmed, this would suggest an alternative neurobiological basis to the alleviation of depressive symptoms distinct from that of the SSRI antidepressants. ""I felt so much lighter, like something had been released, it was an emotional purging, the weight and anxiety and depression had been lifted." ""I have felt a sense of acceptance; more acceptance of agony, boredom, loneliness. [A] willingness to try to accept the negative times -but also an appreciation of the wonderful times." (Two patients' testimonies from recent psilocybin for TRD trial).
Create a free account to open full-text PDFs.
Carbonaro, T. M., Bradstreet, M. P., Barrett, F. S. et al. · Journal of Psychopharmacology (2016)
Carhart-Harris, R. L., Bolstridge, M., Rucker, J. et al. · Lancet Psychiatry (2016)
Carhart-Harris, R. L., Nutt, D. J. · Journal of Psychopharmacology (2017)
Carhart-Harris, R. L., Roseman, L., Bolstridge, M. et al. · Scientific Reports (2017)
Dos Santos, R. G., Osório, F. L., Crippa, J. A. et al. · Therapeutic Advances in Psychopharmacology (2016)
Gasser, P., Holstein, D., Michel, Y. et al. · Journal of Nervous and Mental Disease (2014)
Kirchner, K. · Journal of Psychopharmacology (2014)
Griffiths, R. R., Johnson, M. W., Richards, W. A. et al. · Psychopharmacology (2011)
Griffiths, R. R., Richards, W. A., Mccann, U. et al. · Journal of Psychopharmacology (2006)
Grob, C. S., Danforth, A. L., Chopra, G. S. et al. · JAMA Psychiatry (2011)
Kraehenmann, R., Preller, K. H., Scheidegger, M. et al. · Biological Psychiatry (2015)
Majic, T., Schmidt, T. T., Gallinat, J. · Journal of Clinical Psychopharmacology (2015)
Grob, C. S., Mithoefer, M. C., Brewerton, T. D. · Lancet Psychiatry (2016)
Moreno, F. A., Wiegand, C. B., Taitano, E. K. et al. · Journal of Clinical Psychiatry (2006)
Osório, F. L., Sanches, R. F., Macedo, L. et al. · brazilian Journal of Psychiatry (2015)
Rucker, J., Young, A. H., Jelen, L. A. et al. · Journal of Psychopharmacology (2016)
Schmid, Y., Liechti, M. E. · Psychopharmacology (2017)
Papers in Blossom that reference this study
Lyons, T., Spriggs, M. J., Kerkelä, L. et al. · Nature Communications (2026)
Cherniak, A. D., Granqvist, P., Mikulincer, M. et al. · Journal of Psychoactive Drugs (2026)
Jacobs, E., Zahid, Z., Hinkle, J. et al. · BMJ (2026)
Goldy, S. P., Sepeda, N. D., Hilbert, S. N. et al. · Psychiatry Research (2026)
Wall, M. B., Demetriou, L., Giribaldi, B. et al. · American Journal of Psychiatry (2025)
Harding, R., Singer, N., Wall, M. B. et al. · Molecular Psychiatry (2025)
Seybert, C., Schimmers, N., Silva, L. et al. · Lancet (2024)
Shinozuka, K., Jerotic, K., Mediano, P. A. M. et al. · Translational Psychiatry (2024)
Stoliker, D., Novelli, L., Vollenweider, F. X. et al. · Biological Psychiatry (2024)
Weiss, B., Leor Roseman, •., Giribaldi, B. et al. · International Journal of Mental Health and Addiction (2024)
Erritzoe, D., Timmermann, C., Godfrey, K. et al. · Nature Mental Health (2024)
Solaja, I., Haldane, K., Mason, N. et al. · Neuroscience and Biobehavioral Reviews (2024)
Wall, M. B., Harding, R., Zafar, R. et al. · Molecular Psychiatry (2023)
Zeifman, R. J., Wagner, A. C., Monson, C. M. et al. · Journal of Affective Disorders (2023)
Wall, M. B., Lam, C., Ertl, N. et al. · Journal of Affective Disorders (2023)
Rossi, G. N., Rocha, J. M., Osório, F. L. et al. · Journal of Clinical Psychopharmacology (2023)
Rudin, D., Areesanan, A., Liechti, M. E. et al. · Frontiers in Psychiatry (2023)
Ortiz Bernal, A. M., Raison, C. L., Lancelotta, R. et al. · Frontiers in Psychiatry (2022)
Wall, M., Nutt, D. J., Kaelen, M. et al. · Journal of Psychopharmacology (2022)
Glazer', J., Murray, C. H., Nusslock', R. et al. · Neuropsychopharmacology (2022)
Bogenschutz, M. P., Ross, S., Bhatt, S. R. et al. · JAMA Psychiatry (2022)
Császár, N., Bob, P., Bókkon, I. · Journal of Integrative Neuroscience (2022)
Jairaj, C., Rucker, J. · Journal of Psychopharmacology (2022)
Gill, H., Puramat, P., Patel, P. et al. · Psychiatry Research (2022)
Aharon-Almagor, A., Barrett, F. S. · Research Square (2022)
Vollenweider, F. X., Smallridge, J. W. · Pharmacopsychiatry (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)
Nygart, V., Pommerencke, L. M., Carhart-Harris, R. L. et al. · Frontiers in Psychology (2021)
Castelhano, J. M., Lima, G. M., Teixeira, M. et al. · Frontiers in Pharmacology (2021)
Healy, C. J., Lee, K. A. · Chronic Stress (2021)
Corrigan, K., Haran, M., Mccandliss, C. et al. · Irish Journal of Medical Science (2021)
Bird, C. I. V., Modlin, N. L., Rucker, J. · International Review of Psychiatry (2021)
Haarsma, J., Harmer, C. J., Tamm, S. · Brain and Neuroscience Advances (2021)
Romeo, B., Hermand, M., Pétillion, A. et al. · Journal of Psychiatric Research (2021)
Rocha, J. M., Rossi, G. N., de Lima Osório, F. et al. · Journal of Clinical Psychopharmacology (2021)
Jobst, B. M., Atasoy, S., Ponce-Alvarez, A. et al. · NeuroImage (2021)
Dos Santos, R. G., Hallak, J. E., Baker, G. et al. · Journal of Psychopharmacology (2021)
Hibicke, M., Gobbi, G. · Journal of Neuroscience (2020)
Ferris, J. A., Nutt, D. J. · Drug Science Policy and Law (2020)
Kelly, J. R., Crockett, M. T., Alexander, L. et al. · Irish Journal of Psychological Medicine (2020)
Aday, J. S., Davoli, C. C., Bloesch, E. K. · Therapeutic Advances in Psychopharmacology (2020)
Zeifman, R. J., Wagner, A. C., Watts, R. et al. · Frontiers in Psychiatry (2020)
Nutt, D. J., Erritzoe, D., Carhart-Harris, R. L. · Cell (2020)
Bershad, A. K., Preller, K. H., Lee, R. et al. · Biological Psychiatry (2020)
Heuschkel, K., Kuypers, K. P. C. · Frontiers in Psychiatry (2020)
Aday, J. S., Mitzkovitz, C. M., Bloesch, E. K. et al. · Neuroscience and Biobehavioral Reviews (2020)
Wolff, M., Evens, R., Mertens, L. J. et al. · Frontiers in Psychiatry (2020)
Barrett, F. S., Doss, M. K., Sepeda, N. D. et al. · Scientific Reports (2020)
Mertens, L. J., Wall, M. B., Roseman, L. et al. · Journal of Psychopharmacology (2020)
Preller, K. H., Vollenweider, F. X. · Frontiers in Psychiatry (2019)
Rocha, J. M., Osório, F. L., Crippa, J. A. et al. · Therapeutic Advances in Psychopharmacology (2019)
Johnson, M. W., Griffiths, R. R., Hendricks, P. S. et al. · Neuropharmacology (2018)
Carhart-Harris, R. L. · Neuropharmacology (2018)
Moroz, M., Carhart-Harris, R. L. · IEEE Explore (2018)