In a double-blind, placebo-controlled cross-over study using spectral dynamic causal modelling of resting-state fMRI, the authors show that LSD alters effective connectivity within cortico–striato–thalamo–cortical circuits by increasing thalamus→posterior cingulate connectivity via serotonin 2A (5‑HT2A) receptor activation and decreasing ventral striatum→thalamus connectivity independently of 5‑HT2A. These results support the thalamic filter model of psychedelic action and advance mechanistic understanding relevant to therapeutic development.
Psychedelics exert unique effects on human consciousness. The thalamic filter model suggests that core effects of psychedelics may result from gating deficits, based on a disintegration of information processing within cortico–striato–thalamo-cortical (CSTC) feedback loops. To test this hypothesis, we characterized changes in directed (effective) connectivity between selected CTSC regions after acute administration of lysergic acid diethylamide (LSD), and after pretreatment with Ketanserin (a selective serotonin 2A receptor antagonist) plus LSD in a double-blind, randomized, placebo-controlled, cross-over study in 25 healthy participants. We used spectral dynamic causal modeling (DCM) for resting-state fMRI data. Fully connected DCM models were specified for each treatment condition to investigate the connectivity between the following areas: thalamus, ventral striatum, posterior cingulate cortex, and temporal cortex. Our results confirm major predictions proposed in the CSTC model and provide evidence that LSD alters effective connectivity within CSTC pathways that have been implicated in the gating of sensory and sensorimotor information to the cortex. In particular, LSD increased effective connectivity from the thalamus to the posterior cingulate cortex in a way that depended on serotonin 2A receptor activation, and decreased effective connectivity from the ventral striatum to the thalamus independently of serotonin 2A receptor activation. Together, these results advance our mechanistic understanding of the action of psychedelics in health and disease. This is important for the development of new pharmacological therapeutics and also increases our understanding of the mechanisms underlying the potential clinical efficacy of psychedelics.
Papers cited by this study that are also in Blossom
Preller, K. H., Vollenweider, F. X. · Behavioral Neurobiology of Psychedelic Drugs (2016)
Classic psychedelics produce profound alterations in mood, perception, cognition, and the sense of self, yet the neural mechanisms that give rise to these altered states remain incompletely understood. One influential account, the cortico‑striato‑thalamo‑cortical (CSTC) or thalamic‑filter model, proposes that psychedelics disrupt the thalamus’s capacity to gate sensory and sensorimotor information to the cortex, producing ‘‘sensory flooding’’ and cognitive disintegration. Neurotransmitter systems implicated in this model include serotonergic (notably 5‑HT2A), dopaminergic and glutamatergic pathways, but direct tests of the model’s predictions in humans have been lacking. Preller and colleagues set out to test the CSTC gating hypothesis by characterising directed (effective) connectivity among key CSTC nodes after acute administration of lysergic acid diethylamide (LSD), and after pretreatment with the selective 5‑HT2A antagonist ketanserin (Ket). Using spectral dynamic causal modelling (DCM) applied to resting‑state fMRI in a double‑blind, randomised, placebo‑controlled, crossover sample of healthy participants, the study tested two primary predictions: LSD would increase thalamus→cortex effective connectivity and reduce striatal (ventral striatum, VS) influence on the thalamus, and many of these LSD effects would depend on 5‑HT2A receptor stimulation.
Twenty‑five healthy volunteers (19 males, 6 females; mean age 25.24 years, SD 3.72, range 20–34) were screened to exclude psychiatric, neurological, cardiovascular, substance‑use and MRI contraindications. Participants provided informed consent and were asked to abstain from drugs, alcohol and caffeine for specified intervals before sessions; urine testing and other checks were used to verify compliance. A double‑blind, randomised, crossover design comprised three sessions per participant separated by two weeks: placebo pretreatment + placebo (Pla+Pla), placebo pretreatment + LSD 100 μg (Pla+LSD), and ketanserin 40 mg pretreatment + LSD 100 μg (Ket+LSD). Pretreatment occurred 60 minutes before LSD to allow ketanserin to reach peak plasma levels. Resting‑state fMRI scans (10 minutes) were acquired twice per session (approximately 75 min and 300 min after treatment); because main drug effects did not differ across sessions the analyses focussed on the earlier session. Subjective effects were assessed with the 5‑Dimensions Altered States of Consciousness (5D‑ASC) questionnaire administered 720 min after dosing. MRI data were acquired at 3T using standard EPI parameters and preprocessed with slice timing correction, realignment, spatial normalisation to MNI space and 6‑mm smoothing; motion did not exceed 3 mm for any participant. Regions of interest (ROIs) selected for effective connectivity analyses were the thalamus, ventral striatum (VS), posterior cingulate cortex (PCC), and superior temporal gyrus (Temp). Each ROI was defined as an 8‑mm radius sphere centred on MNI coordinates derived from prior task‑based contrasts in the same cohort (thalamus: −15, −8, 1; VS: 9, 8, −8; PCC: −3, −46, 31; Temp: −56, −54, 8). Nuisance regressors (six motion parameters, CSF and white matter signals) and a 128‑s high‑pass filter were applied before time‑series extraction. Spectral DCM (DCM12 within SPM12) was used to estimate fully connected models for each condition and session. To improve efficiency the investigators concatenated time series over subjects per region and condition, yielding cross‑spectral density (CSD) estimates; this step, however, precluded analyses of between‑subject correlations (for example, linking connectivity to subjective effects). Between‑condition effects were modelled using parametric empirical Bayes (PEB) with two orthogonal contrasts: Pla < [LSD + (Ket + LSD)] to assess drug effects, and (Ket + LSD) < LSD to assess 5‑HT2A blockade. Effects were reported only when posterior probability exceeded 0.95 based on Bayesian model comparison (free energy). The team also extracted signed connectivity parameters to determine putative excitatory or inhibitory influences. The authors note that the extracted ROI time series and statistics are deposited in Bitbucket.
Subjective effects assessed with the 5D‑ASC showed that ketanserin blocked LSD’s subjective effects: Ket+LSD did not differ significantly from placebo, while LSD alone produced robust subjective changes (detailed results reported elsewhere). For effective connectivity, the drug‑versus‑placebo contrast [Pla < (LSD + (Ket + LSD))] revealed multiple directed changes. Increased effective connectivity was observed from the thalamus to the ventral striatum and from the PCC to the ventral striatum. Decreases were reported for thalamus→Temp, VS→thalamus, VS→PCC and VS→Temp. Regarding intrinsic self‑connections, the PCC showed reduced self‑inhibition (interpreted as disinhibition or increased excitability) under drug. The ketanserin‑related contrast [(Ket + LSD) < LSD], isolating effects dependent on 5‑HT2A activation, showed increased effective connectivity from the thalamus to the VS and from the thalamus to the PCC, and from the VS to the Temp when ketanserin preceded LSD; decreased effective connectivity was observed from the PCC to the thalamus, and an increase in self‑inhibition of the Temp was found. Using signed parameter estimates, the analyses indicated that LSD increased thalamus→PCC effective connectivity while reducing PCC→thalamus coupling; these particular changes were blocked by ketanserin and thus attributed to 5‑HT2A receptor stimulation. The Temp region showed decreased excitability (increased self‑inhibition) and reduced thalamus→Temp coupling, also reported as 5‑HT2A‑dependent. By contrast, several LSD‑induced changes involving the ventral striatum were not blocked by ketanserin: decreased VS→thalamus and VS→PCC, decreased thalamus→Temp, increased PCC→VS, and reduced self‑inhibition of the PCC. The paper reports that only effects with posterior probability >0.95 were considered significant and that tables and supplementary material contain the detailed signed parameter estimates and variances.
The investigators interpret their findings as supporting key predictions of the CSTC thalamic‑filter model. In particular, LSD increased effective connectivity from the thalamus to cortical targets (notably the PCC) via a mechanism dependent on 5‑HT2A receptor stimulation, while LSD decreased the influence of the ventral striatum on the thalamus independent of 5‑HT2A blockade. Together, these changes are taken to indicate a partial ‘‘opening’’ of the thalamic filter that is selective across cortical targets rather than a global cortical inundation. Increased thalamus→PCC coupling and concurrent disinhibition of the PCC are discussed in relation to predictive coding accounts, where gating is implemented by modulating the precision of ascending prediction errors. The PCC’s role in arousal, awareness and the balance between internal and external cognition is highlighted, and the current results are related to prior reports of thalamo‑cortical and PCC‑related alterations after psychedelic administration, decreased alpha power and changes in default mode network connectivity. The authors suggest that decreased thalamus→Temp coupling and increased Temp self‑inhibition may bear on emotional and social information processing and might be relevant to psychedelics’ potential antidepressant effects, while noting that the present data are acute and cannot speak to long‑term therapeutic outcomes. Regarding pharmacology, the pattern that ketanserin blocked thalamus‑PCC effects but did not block several VS‑related changes leads the authors to hypothesise that non‑5‑HT2A mechanisms—potentially dopaminergic pathways acting on the striatum—may contribute to some LSD effects. They emphasise, however, that the present study cannot conclusively determine contributions from other receptor systems and recommend follow‑up studies, for example using dopamine antagonists or different LSD doses. The authors acknowledge several limitations: ROI selection was restricted to nodes implicated by the CSTC model and the current cohort, so distributed effects outside these regions were not tested; concatenating time series across subjects precluded subject‑level correlations between connectivity and subjective reports (an issue they plan to address using hierarchical PEB); and the absence of a ketanserin‑only (Ket+Pla) condition prevents characterising ketanserin’s standalone effects on connectivity. They also propose methodological extensions such as smaller, subregion‑level ROIs and inclusion of additional CSTC hubs like medial prefrontal cortex. Finally, the study is presented as a demonstration of spectral DCM combined with PEB for group‑level pharmacological resting‑state fMRI, with the authors arguing that the results advance mechanistic understanding of LSD’s action in the human brain and have implications for developing novel therapeutics and for theories of altered conscious states.
Subjective Drug Effects. Subjective drug effects were assessed using the 5-Dimensions Altered States of Consciousness (5D-ASC) questionnaire. Detailed results are reported elsewhere. In brief, all LSD-induced subjective drug effects were blocked by Ket. No significant differences were found between the placebo (Pla) and the Ket + LSD conditions (SI Appendix, Fig.). Drugs vs. Placebo. The contrast drug vs. placebo [Pla < (LSD + [Ket + LSD])] resulted in increased effective connectivity from the thalamus to the VS and the PCC to the VS. Furthermore, decreases in effective connectivity were found: from the thalamus to the Temp, the VS to thalamus, the VS to PCC, and the VS to Temp. Regarding inhibitory self-connections, which control the regions' gain or sensitivity to inputs, there was reduced self-inhibition (i.e., disinhibition) of PCC due to the drug. These results are shown in Fig.. 5-HT2A Blockade. The contrast Ket + LSD < LSD revealed increased effective connectivity from the thalamus to the VS and PCC, and from the VS to the Temp. Decreased effective connectivity was found from the PCC to the thalamus. Furthermore, we found an increase in self-inhibition of the Temp. These results are shown in Fig.. An additional advantage of DCM is the possibility to determine the valence of the connections: that is, define whether they are excitatory or inhibitory in nature. See Tablefor the summary of the signed connectivity parameters and SI Appendix, Tablefor parameter estimates (mean and variance). In sum, our analyses showed that LSD increased effective connectivity from the thalamus to the PCC, whereas the reciprocal connection from the PCC to the thalamus had reduced effective connectivity. Furthermore, we also found decreased excitability (i.e., increased self-inhibition) in the Temp. These alterations seem to be driven by 5-HT 2A receptor stimulation by LSD because they were blocked by Ket. Furthermore, we found that LSD decreased effective connectivity from the VS to the thalamus and the PCC, from the thalamus to the Temp, increased effective connectivity from the PCC to the VS, and reduced self-inhibition of the PCC. These LSD-induced changes were not blocked by Ket.
Psychedelics induce an altered state of consciousness that, on the one hand, mimics predominantly positive symptoms of schizophrenia, but on the other hand, may have beneficial therapeutic effects in mood and anxiety disorders. The history of research on psychedelics is also intertwined with the investigation of the role of the serotonergic system in cognition and behavior in health and psychiatric disorders (3). However, the neurobiology and pharmacology of psychedelics, in particular LSD, is still poorly understood in humans. Geyer and Vollenweider (3) proposed that key effects of psychedelics may result from the disintegration of information processing of internal and external stimuli within CSTC feedback loops. In this work we sought to mechanistically test this hypothesis by leveraging the recent advances in modeling endogenous activity using DCM for restingstate fMRIwith the administration of LSD and Ket, a 5-HT 2A receptor antagonist. Investigating effective (restingstate) connectivity in LSD-induced states, the present study closes critical knowledge gaps by showing that LSD alters connectivity within CSTC pathways. In particular, LSD increases effective connectivity from the thalamus to cortical areas, via agonistic activity on the 5-HT 2A receptor, and decreases effective connectivity from the VS to the thalamus independently of 5-HT 2A receptor stimulation. At the core of the CSTC model by Geyer and Vollenweider (3) is the hypothesis that psychedelics alter the capacity of the thalamus to control or gate the flow of information to the cortex. The thalamus is the central part of the diencephalon containing relay cells that project to the cortex. The thalamus also gates the main input to the cortex from subcortical areas and likely all regions of the cortex receive input from the thalamus. It also plays a key role in various neurobiological theories of consciousness, suggesting that neural activity in thalamo-cortical loops gives rise to conscious experience. During sleep, sedation, and anesthesia, thalamo-cortical connectivity is decreased, while information transfer from the thalamus to the cortex is highest during states requiring high levels of sustained attention. Alterations in thalamo-cortical connectivity are also crucial features of various psychiatric disorders, predominantly schizophrenia, and also depression and obsessive-compulsive disorder. Here, we show that, in line with the CSTC model, LSD increased the excitatory connection from the thalamus to the PCC. This finding is particularly interesting in light of predictive coding formulations of the CSTC model, where filtering or gating is implemented via changes in the precision of ascending prediction errors. Much neurobiological evidence points to the thalamus as a key source of the requisite neuromodulation. This result is also consistent with a previous study showing increased functional thalamo-cortical connectivity after LSD administration. Furthermore, LSD increased excitability of the PCC and reduced effective connectivity from the PCC to the thalamus. The PCC has repeatedly been shown to be involved in the effects of psychedelics. For example, decreased functional connectivity between the PCC and frontal brain areas has been reported after psilocybin and LSD administration, as well as decreased global brain connectivity after LSD administration. Furthermore, at a postacute assessment 24 h after ayahuasca intake, functional connectivity was increased between the PCC and the anterior cingulate cortex and reductions in glutamate + glutamine, creatine, and N-acetylaspartate + N-acetylaspartylglutamate in the PCC were measured. Our study showing increased excitability of the PCC is also in line with previous results reporting LSD, psilocybin, and ayahuascainduced decreases in α-power, as decreases in α-oscillations have been reported to reflect a state of enhanced cortical excitability. Specifically, reductions in α-power in the PCC assessed with magnetoencephalography after psilocybin and LSD administration correlated with self-report questionnaire items indicating psilocybin-induced alterations in selfprocessing and ego-integration. This is in line with current theories of the role of the PCC in cognitive functioning, which associate the PCC with arousal and awareness as well as the control of the balance between internally and externally directed thought. The interaction of the PCC with other brain networks is therefore considered to be important for conscious awareness and the failure to suppress PCC activity to be associated with the intrusion of internal mentation. Previous effective connectivity studies using the spectral DCM have consistently shown the PCC, which is a core region in the default mode network (DMN), to be a robustly driven hub receiving information from other core regions of the DMN: that is, the medial prefrontal cortex and bilateral angular gyrus. The CSTC model also proposes that the gating capacities of the thalamus are controlled by the striatum (4). Vollenweider and Geyer hypothesized that increasing serotonergic activation by psychedelics reduces the influence of the striatum on the thalamus, which leads to opening the thalamic filter. The present data show that LSD indeed reduces effective connectivity from the VS to the thalamus, therefore corroborating the assumption that alterations in striatal-thalamic interaction are important mechanisms underlying psychedelic states. In contrast to LSD-induced increases in effective connectivity from the thalamus to the PCC, excitatory connectivity from the thalamus to the Temp was decreased and the inhibitory selfconnection of the Temp was increased by LSD. Previous studies showed that: (i) decreases in functional connectivity between the Temp and other cortical regions after LSD and psilocybin administration, and (ii) alterations in lagged phase synchronization of δ-oscillations after psilocybin administration, both correlating with subjective drug-induced effects. The temporal lobe is associated with processing emotional and social information, both of which are altered in psychedelic statesand is implicated in the pathophysiology of schizophrenia. Because it has been reported that patients suffering from major depression disorder show increased thalamo-temporal connectivity, attenuating effective connectivity from the thalamus to the Temp might additionally represent a neurobiological mechanism by which psychedelics potentially exert their antidepressive potential. However, because the present study investigated acute alterations in connectivity, further studies are needed to clarify whether these results translate into long-term therapeutic effects. The present results therefore show that while the thalamus indeed decreases information gating and therefore increases "bottom-up" information flow to certain cortical areas as well as the VS in accordance with the CSTC model, LSD does not cause an undifferentiated cortical inundation as first hypothesized in the model, but rather leads to a pattern of increased information flow to particular areas of the cortex while thalamic connectivity with other cortical areas is reduced in resting state. This might explain the seemingly paradoxical subjective effects often reported in psychedelic-induced altered states of consciousness that are characterized by increased arousal as well as a dreamlike experience, impaired cognition but at the same time reported perceived mental clarity, and psychosis-like effects combined with blissful experiences. Therefore, psychedelics states differ from previously investigated states like anesthesia, sleep, or cognitively demanding situations. The design of the present study also involved the pretreatment of LSD with the 5-HT 2A receptor antagonist Ket and therefore allowed for investigation of the role of this specific receptor system in LSD-induced alterations in effective connectivity. While we have previously shown that Ket blocked all subjective and most neural effects of LSD, the present analysis showed particular alterations in the thalamus-PCC connections, dependent on the 5-HT 2A receptor. This is in line with a previous study showing that PCC desynchronization under the influence of psilocybin can be explained by increased excitability of 5-HT2A receptor-rich deep-layer pyramidal neurons. In our study, Ket blocked increased effective connectivity from the thalamus to the PCC and reduced connectivity from the PCC to the thalamus, as well as increased inhibition of the Temp. On the other hand, mostly connections involving the VS were not blocked by Ket: decreased effective connectivity from the VS to the thalamus and the PCC, from the thalamus to the Temp, increased effective connectivity from the PCC to the VS, and reduced inhibition of the PCC, suggesting that these LSD-induced alterations are probably not attributable to LSD's agonistic action on the 5-HT 2A receptor. Previous animal studies suggested that, in addition to, 5-HT2A receptors, dopamine D2 receptors play a role in the effects of LSD. Considering that the effects not blocked by Ket mostly involve the VS and that the striatum is a key structure in dopaminergic pathways, the involvement of the dopamine system in LSD-induced alterations in brain connectivity seems likely. However, the present study cannot conclusively answer questions regarding the role of other receptor systems beyond the 5-HT 2A system in the neurobiological effects of LSD, and therefore further studies are warranted to test the specific contributions of other receptors, for example, by pretreatment with dopamine-antagonists. However, considering that Ket normalized all subjective effects, it is, on the one hand, possible that alterations induced by LSD's action on other receptors only provoke noticeable subjective effects when 5-HT 2A receptors are stimulated concurrently. On the other hand, it is possible that higher doses of LSD are needed to produce noticeable subjective effects even when the 5-HT 2A receptor is blocked. Future studies could therefore test the effects of multiple (and higher) doses of LSD. Beyond the CSTC model, several authors have proposed additional theories to explain the biological underpinnings of alterations in consciousness experienced following the administration of psychedelics. An early psychophysiological model by Fischer proposed that shifts in the ratio of sensory-to-motor activity could explain subjective symptoms. More recent evidence from human studies suggests that psychedelic-induced alterations in consciousness are related to increased entropy in the brain, leading to disorganization of brain activity and more flexible cognition (entropic brain hypothesis). This model has been corroborated with studies showing that psilocybin produces an increase in blood-oxygen level-dependent (BOLD) signal variance and decreased connectivity within the DMN. These models are not mutually exclusive, and focus on complementary correlates of altered states of consciousness. While this is beyond the scope of the present study, a unifying framework should be developed and tested in future studies. This study was limited to brain regions implicated by the CSTC model, which have been shown empirically to be sensitive to the effects of psychedelics in previous studies, as well as within the current participants. Clearly, testing additional models in future studies has the potential to extend our knowledge about the effects of LSD on effective connectivity among more distributed brain regions, in particular, additional hubs of the CSTC model such as the medial prefrontal cortex. Furthermore, future analyses using smaller regions-of-interest (ROIs) could reveal differential effects of subregions of the current ROIs. Additionally, to focus on drug effects using efficient estimates of the cross-spectral density (CSD), we concatenated time-series data over subjects. This precluded analysis between subject effects; for example, we were unable to relate connectivity parameters to subjective effects. We will address this limitation in the future using (hierarchical) PEB. Although a previous study has shown that Ket does not induce an altered state of consciousness or affect sensorimotor gating, the lack of a Ket + Pla condition represents a further limitation of this study. This suggests that future studies will be needed to characterize the influence of Ket alone on effective connectivity. In sum, the present results confirm major predictions proposed in the CSTC model and provide evidence that LSD alters effective connectivity within CSTC pathways that have been implicated in the gating of sensory and sensorimotor information to the cortex: LSD diminishes the influence of the striatum on the thalamus and opens the thalamic filter, but selectively: only to certain areas of the cortex. In particular, the present results pinpoint the role of the thalamus-PCC connection for the effects of psychedelics. Additionally, the present results enhance our knowledge about the contribution of the serotonin system to the functional organization of the brain in LSD-induced states. Finally, the present study showcases the newly developed spectral DCM approach-coupled with modeling using the PEB framework-to testing hypotheses in resting-state pharmacological fMRI at the group level. Taken together, the results deepen our knowledge about the mechanism of action of psychedelics relevant for health and disease and important for the development of new pharmacological therapeutics.
Create a free account to open full-text PDFs.
Kyzar, E. J., Nichols, C. D., Gainetdinov, R. R. et al. · Trends in Pharmacological Sciences (2017)
Geyer, M. A., Vollenweider, F. X. · Trends in Pharmacological Sciences (2008)
Schmid, Y., Enzler, F., Gasser, P. et al. · Biological Psychiatry (2015)
Quednow, B. B., Kometer, M., Geyer, M. A. et al. · Neuropsychopharmacology (2011)
Vollenweider, F. X., Csomor, P. A., Knappe, B. et al. · Neuropsychopharmacology (2007)
Carhart-Harris, R. L., Muthukumaraswamy, S., Roseman, L. et al. · PNAS (2016)
Muthukumaraswamy, S. D., Carhart-Harris, R. L., Moran, R. J. et al. · Journal of Neuroscience (2013)
Carhart-Harris, R. L., Erritzoe, D., Williams, T. et al. · PNAS (2012)
Preller, K. H., Herdener, M., Pokorny, T. et al. · Current Biology (2017)
Preller, K. H., Schilbach, L., Pokorny, T. et al. · Journal of Neuroscience (2018)
Vollenweider, F. X., Kometer, M. · Nature Reviews Neuroscience (2010)
Lenz, C., Dolder, P. C., Lang, U. E. et al. · Acta Psychiatrica Scandinavica (2017)
Sampedro, F., de la Fuente Revenga, M., Valle, M. et al. · International Journal of Neuropsychopharmacology (2017)
Valle, M., Maqueda, A. E., Rabella, M. et al. · European Neuropsychopharmacology (2016)
Kometer, M., Pokorny, T., Seifritz, E. et al. · Psychopharmacology (2015)
Preller, K. H., Pokorny, D., Hock, A. et al. · PNAS (2016)
Kometer, M., Schmidt, A., Bachmann, R. et al. · Biological Psychiatry (2012)
Pokorny, T., Preller, K. H., Kometer, M. et al. · International Journal of Neuropsychopharmacology (2017)
Carhart-Harris, R. L., Kaelen, M., Bolstridge, M. et al. · Psychological Medicine (2016)
Carhart-Harris, R. L., Leech, R., Shanahan, M. et al. · Frontiers in Human Neuroscience (2014)
Tagliazucchi, E., Roseman, L., Kaelen, M. et al. · Current Biology (2016)
Lewis, C. R., Preller, K. H., Kraehenmann, R. et al. · NeuroImage (2017)
Studerus, E., Gamma, A., Vollenweider, F. X. · PLOS ONE (2010)
Papers in Blossom that reference this study
Girn, M., Doss, M. K., Roseman, L. et al. · Nature Medicine (2026)
Stoliker, D., Novelli, L., Khajehnejad, M. et al. · Biorxiv (2025)
Safron, A., Juliani, A., Reggente, N. et al. · Neuroscience of Consciousness (2025)
Caspani, G., Ruffell, S. G. D., Tsang, WF. et al. · Pharmacological Research (2024)
Stoliker, D., Novelli, L., Vollenweider, F. X. et al. · Biological Psychiatry (2024)
Bagdasarian, F. A., Hansen, H. D., Chen, J. et al. · ACS Chemical Neuroscience (2024)
Stoliker, D., Preller, K. H., Novelli, L. et al. · Molecular Psychiatry (2024)
Avram, M., Müller, F., Preller, K. H. et al. · Biological Psychiatry (2024)
Shinozuka, K., Tewarie, P. K. B., Luppi, A. et al. · Biorxiv (2024)
Lewis, E. C., Jaeger, A., Girn, M. et al. · Journal of Psychopharmacology (2024)
Tipado, Z., Kuypers, K. P. C., Sorger, B. et al. · European Neuropsychopharmacology (2024)
Murray, C., Frohlich, J, Haggarty, C. J., Tare, I. et al. · Neuropsychopharmacology (2024)
Pizzi, S. D., Chiacchiaretta, P., Sestieri, C. et al. · NeuroImage (2023)
Buchborn, T., Kettner, H., Kartner, L. et al. · Frontiers in Neuroscience (2023)
Mallaroni, P., Mason, N. L., Kloft, L. et al. · Frontiers in Neuroscience (2023)
Wallach, J., Cao, A. B., Calkins, M. M. et al. · Biorxiv (2023)
Winkelman, M. J., Szabo, A., Frecska, E. · European Neuropsychopharmacology (2023)
Pizzi, S. D., Chiacchiaretta, P., Sestieri, C. et al. · Biological Psychiatry (2023)
Adamska, I., Finc, K. · Psychopharmacology (2023)
Thal, S. B., Wieberneit, M., Sharbanee, J. M. et al. · Journal of Humanistic Psychology (2023)
Ort, A., Smallridge, J. W., Sarasso, S. et al. · iScience (2023)
Sadibolova, R., Murray-Lawson, C., Family, N. et al. · Biorxiv (2023)
Ruffini, G., Damiani, G., Lozano-Soldevilla, D. et al. · PLOS ONE (2023)
Olsen, A. S., Ozenne, B., Madsen, M. K. et al. · NeuroImage (2022)
Bedford, P., Hauke, D. J., Wang, Z. et al. · Neuropsychopharmacology (2022)
Glazer', J., Murray, C. H., Nusslock', R. et al. · Neuropsychopharmacology (2022)
Kwan, A. C., Olson, D. E., Preller, K. H. et al. · Nature Medicine (2022)
Thal, S. B., Wieberneit, M., Sharbanee, J. M. et al. · Journal of Psychopharmacology (2022)
Stoliker, D., Egan, G. F., Friston, K. J. et al. · Pharmacological Reviews (2022)
Császár, N., Bob, P., Bókkon, I. · Journal of Integrative Neuroscience (2022)
van Elk, M., Yaden, D. B. · Neuroscience and Biobehavioral Reviews (2022)
Luppi, A. I., Hansen, J. Y., Adapa, R. et al. · Biorxiv (2022)
Whitney, S., Yaden, D. B., Lipson, J. et al. · Frontiers in Psychology (2022)
McCulloch, D. E-W., Knudsen, G. M., Barrett, F. S. et al. · Neuroscience and Biobehavioral Reviews (2022)
Aharon-Almagor, A., Barrett, F. S. · Research Square (2022)
Lawn, T., Dipasquale, O., Vamvakas, A. et al. · Psychopharmacology (2022)
Ciauncia, A., Safron, A. · Psyarxiv (2022)
Family, N., Hendricks, P. S., Williams, L. T. J. et al. · Journal of Psychopharmacology (2022)
Gaddis, A., Lidstone, D. E., Nebel, M. B. et al. · Biorxiv (2022)
Markopoulos, A., Inserra, A., De Gregorio, D. et al. · Frontiers in Pharmacology (2022)
Vollenweider, F. X., Smallridge, J. W. · Pharmacopsychiatry (2022)
Stoliker, D., Novelli, L., Vollenweider, F. X. et al. · MedRvix (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)
Doss, M. K., Považan, M., Rosenberg, M. D. et al. · Translational Psychiatry (2021)
Avram, M., Rogg, H., Korda, A. et al. · Frontiers in Psychiatry (2021)
Perry, C. M., Malina, M. · Psychopharmacology (2021)
Rodríguez Arce, J. M., Winkelman, M. J. · Frontiers in Psychology (2021)
Zamani, A., Carhart-Harris, R. L., Christoff, K. · Neuropsychopharmacology (2021)
Rodriguiz, R. M., Nadkarni, V., Means, C. R. et al. · Scientific Reports (2021)
Domenico, C., Haggerty, D., Mou, X. et al. · Cell Reports (2021)
Burt, J. B., Preller, K. H., Demirtaş, M. et al. · eLife (2021)
Duerler, P., Brem, S., Fraga-González, G. et al. · Cerebral Cortex (2021)
Savino, A., Nichols, C. D. · Biorxiv (2021)
Bement, W., Banks, M. I., Zahid, Z. et al. · Molecular Biology of the Cell (2021)
Yaden, D. B., Johnson, M. W., Griffiths, R. R. et al. · International Journal of Neuropsychopharmacology (2021)
Jobst, B. M., Atasoy, S., Ponce-Alvarez, A. et al. · NeuroImage (2021)
Nichols, D. E., Walter, H. · Pharmacopsychiatry (2020)
Hibicke, M., Gobbi, G. · Journal of Neuroscience (2020)
Andersen, K. A. A., Carhart-Harris, R. L., Nutt, D. J. et al. · Acta Psychiatrica Scandinavica (2020)
Vollenweider, F. X., Preller, K. H. · Nature Reviews Neuroscience (2020)
Greenway, K. T., Garel, N., Jerome, L. et al. · Expert Review of Clinical Pharmacology (2020)
Girn, M., Roseman, L., Bernhardt, B. et al. · Biorxiv (2020)
Bershad, A. K., Preller, K. H., Lee, R. et al. · Biological Psychiatry (2020)
Agin-Liebes, G. I., Malone, T., Yalch, M. M. et al. · Journal of Psychopharmacology (2020)
Ho, J. T., Preller, K. H., Lenggenhager, B. · Neuroscience and Biobehavioral Reviews (2020)
Family, N., Maillet, E. L., Williams, L. T. J. et al. · Psychopharmacology (2019)
Felix, M., Stefan, B. · Swiss Medical Weekly (2019)
Carhart-Harris, R. L., Friston, K. J. · Pharmacological Reviews (2019)