This study (n=18) used psilocybin administration in order to investigate the neuropharmacology of schizophrenia. The authors suggest that 5-HT2A and NMDA receptors may be involved in the cognitive deficits observed in schizophrenic individuals.
Previously the NMDA (N-methyl-D-aspartate) receptor (NMDAR) antagonist ketamine was shown to disrupt generation of the auditory event-related potential (ERP) mismatch negativity (MMN) and the performance of an 'AX'-type continuous performance test (AX-CPT)--measures of auditory and visual context-dependent information processing--in a similar manner as observed in schizophrenia. This placebo-controlled study investigated effects of the 5-HT(2A) receptor agonist psilocybin on the same measures in 18 healthy volunteers. Psilocybin administration induced significant performance deficits in the AX-CPT, but failed to reduce MMN generation significantly. These results indirectly support evidence that deficient MMN generation in schizophrenia may be a relatively distinct manifestation of deficient NMDAR functioning. In contrast, secondary pharmacological effects shared by NMDAR antagonists and the 5-HT(2A) agonist (ie disruption of glutamatergic neurotransmission) may be the mechanism underlying impairments in AX-CPT performance observed during both psilocybin and ketamine administration. Comparable deficits in schizophrenia may result from independent dysfunctions of 5-HT(2A) and NMDAR-related neurotransmission.
Neurocognitive impairments are a core feature of schizophrenia and include both higher-order deficits (attention, executive function, working memory) and more basic sensory memory impairments. Umbricht and colleagues describe mismatch negativity (MMN) as an auditory event-related potential (ERP) that indexes echoic sensory memory and context-sensitive preattentive processing, and note that MMN is reduced in most studies of schizophrenia. They contrast MMN with performance on an AX-type continuous performance task (AX-CPT), which taxes use of contextual information and is sensitive to prefrontal dysfunction; schizophrenic patients characteristically make excess BX errors, reflecting failure to use preceding cues to inhibit a prepotent response to a target stimulus. Against this background, previous pharmacological work has implicated NMDA receptor (NMDAR) dysfunction in both MMN and AX-CPT abnormalities: NMDAR antagonists such as ketamine reduce MMN and produce AX-CPT deficits in healthy volunteers that resemble schizophrenia. At the same time, evidence suggests that 5-HT2A receptor dysfunction may contribute to psychotic and cognitive phenomena, because 5-HT2A agonists (for example psilocybin) induce psychotomimetic effects and impair some cognitive functions. The present study therefore set out to test whether psilocybin (a 5-HT2A agonist) affects MMN generation, sensory ERPs and AX-CPT performance in healthy volunteers using the same procedures used previously with ketamine, with the aim of clarifying whether 5-HT2A-related neurotransmission contributes to the deficits observed in schizophrenia and whether shared downstream effects (for example on glutamate or dopamine systems) could account for overlapping cognitive impairments.
Papers cited by this study that are also in Blossom
Umbricht, A., Schmid, L., Koller, R. · JAMA Psychiatry (2000)
Vollenweider, F. X., Leenders, K. L., Maguire, P. et al. · Neuropsychopharmacology (1997)
Vollenweider, F. X., Vollenweider-Scherpenhuyzen, M. F. I., Bäbler, A. et al. · NeuroReport (1998)
Papers in Blossom that reference this study
Dor-Ziderman, Y., David, J., Berkovich-Ohana, A. · Psychopharmacology (2025)
The study used a within-subject, randomized and counterbalanced design in which 18 healthy, right-handed volunteers (10 men, 8 women; mean age 25.1 ± 4.3 years) each completed a psilocybin and a placebo session. Subjects were screened with structured clinical interview, physical examination, ECG and laboratory tests; exclusion criteria included past or present Axis I disorders, substance dependence or abuse, family history of Axis I disorders to second-degree relatives, and medical disorders. Intelligence and handedness were assessed; none of the female participants was pregnant. Psilocybin was administered orally at 0.28 mg/kg in 1- and 5-mg capsules prepared by the hospital pharmacy. Subjects were blind to drug order; sessions started around 09:00 after an overnight fast. Baseline ERP recordings were obtained, then psilocybin or placebo was given, and a second ERP recording took place 70 minutes after ingestion. Behavioural ratings (Brief Psychiatric Rating Scale, BPRS) and orientation items were collected at the end of each ERP recording. Participants remained under supervision until effects subsided. Auditory ERPs were elicited by a fixed sequence of 100-ms 1000 Hz standards, interspersed with 100-ms 1500 Hz frequency deviants and 250-ms 1000 Hz duration deviants (SOA 300 ms; 1517 stimuli across four blocks). EEG was recorded from 28 scalp sites with nose reference, sampled at 500 Hz and band-pass filtered at 0.1–100 Hz during acquisition; epochs comprised a 100-ms prestimulus baseline and 500-ms poststimulus interval. After ocular correction and artifact rejection, epochs were averaged and low-pass filtered at 15 Hz. Analyses concentrated on N1 and P2 to standards (at Fz) and MMN to frequency and duration deviants (at FCz); MMN waveforms were computed by subtracting standards from deviants. Due to an insufficient number of sweeps in one subject, MMN analyses included 17 subjects. During auditory stimulation subjects performed a visual AX-CPT presented in four blocks of 280 stimuli each. Letters were shown for 250 ms; subjects pressed a button when X followed A (AX). Sequences were 70% AX, 10% each of BX, AY, BY. Within blocks, 50% of cue-target pairs had short ISI (0.8 s) and 50% long ISI (4 s). One subject ceased task performance during psilocybin; a second had response registration failure, so AX-CPT analyses were based on 16 subjects. Primary dependent measures were N1/P2 amplitudes and latencies, MMN amplitudes and latencies, AX-CPT hit rates, false alarm rates (BX, AY, BY), discrimination index d' and response bias Br. Statistical evaluation used repeated-measures ANOVAs with session (psilocybin vs placebo) and time (baseline vs infusion) as within-subject factors; MMN type and false alarm type were included where appropriate, and paired t-tests were used for post hoc contrasts. Alpha was set at 0.05.
Behavioural effects: Psilocybin produced robust subjective and behavioural changes on the BPRS. The total BPRS score increased from 18.9 ± 1.5 at baseline to 28.1 ± 9.9 during psilocybin (session × time interaction F1,17 = 16.00, p = 0.001). The psychosis factor rose (baseline 4.0 ± 0.0 to 7.5 ± 2.9; F1,17 = 24.79, p < 0.001) and smaller but significant increases were seen on anergia, activation and hostility factors. Orientation (autobiographic, temporal, spatial) was not affected. Auditory ERPs: For sensory ERPs, psilocybin significantly decreased N1 peak amplitude at Fz (session × time interaction F1,17 = 6.03, p < 0.05); post hoc paired t-test showed a smaller N1 during psilocybin versus its baseline (t = −2.09, df = 17, p = 0.05). N1 latency was unchanged. Topographic analysis confirmed a general N1 amplitude reduction across electrode sites (infusion × time interaction F1,17 = 6.14, p = 0.03). Psilocybin did not significantly affect P2 measures as reported. Mismatch negativity (MMN): Robust MMN to both frequency and duration deviants was present at baseline, with maxima at FCz and larger responses to frequency deviants. Although MMN amplitudes decreased slightly during both placebo and psilocybin phases and the decrease was numerically more marked for frequency deviants under psilocybin, repeated-measures ANOVA did not show a significant effect of psilocybin on MMN peak amplitudes (session × time interaction F1,16 = 2.22, p = 0.16; session × time × MMN type interaction F1,16 = 0.14, p = 0.7). Separate analyses showed a trend for greater reduction in the frequency condition (session × time F1,16 = 3.20, p = 0.09) but no effect in the duration condition (F1,16 = 0.36, p = 0.6). MMN peak latencies were unaffected. Note that MMN analyses excluded one subject because of insufficient sweeps (n = 17); sweep counts were slightly reduced during psilocybin for some conditions but remained adequate for signal-to-noise. AX-CPT performance: Psilocybin impaired AX-CPT performance markedly. Hit rates declined at both ISIs (session × time interaction F1,15 = 23.92, p < 0.001), with no significant interaction with ISI. False alarms increased, predominately for BX sequences; a three-way infusion × time × false alarm type interaction was significant (F2,14 = 13.51, p = 0.001). Contrasts showed a significantly greater increase of BX errors than AY (F1,15 = 16.03, p = 0.001) and BY (F1,15 = 28.30, p < 0.001) errors when comparing psilocybin to placebo and baseline. Paired t-tests confirmed higher BX error rates during psilocybin versus baseline for both short ISI (t = 5.95, df = 15, p < 0.001) and long ISI (t = 5.23, df = 15, p < 0.001). Discrimination index d' decreased significantly under psilocybin (session × phase F1,16 = 52.49, p < 0.001); response bias Br decreased non-significantly (F1,16 = 2.34, p = 0.13). AX-CPT analyses were based on 16 subjects due to task non-completion or technical failure in two participants.
Umbricht and colleagues interpret the pattern of findings as evidence that psilocybin—acting as a 5-HT2A agonist—selectively reduces N1 amplitude and impairs context-dependent use of information on the AX-CPT (notably producing increased BX errors), but does not produce the marked MMN reductions previously observed with NMDAR antagonism. The dissociation between effects on N1 and MMN differs from the ketamine profile (ketamine reduced MMN but left N1 intact) while the AX-CPT deficits are similar for both drugs and resemble deficits seen in schizophrenia. From this, the investigators infer that MMN generation depends strongly on NMDAR functioning, whereas 5-HT2A receptor signalling is less important for MMN. Conversely, overlapping AX-CPT impairments after ketamine and psilocybin may arise from shared downstream pharmacological effects on glutamatergic and dopaminergic dynamics rather than from identical primary receptor actions. The discussion highlights mechanistic evidence supporting these claims: both NMDAR antagonists and 5-HT2A agonists can increase dopamine release in humans and induce excessive glutamate release in animals, and group II metabotropic receptor agonists or agents that inhibit glutamate release (for example lamotrigine) can attenuate cognitive effects of NMDAR antagonists. The authors note differences in pharmacological modulation—ketamine-induced deficits can be ameliorated by haloperidol and lamotrigine, whereas psilocybin-induced deficits are reversed by 5-HT2A antagonists but not by D2 blockers—yet both drug classes may converge on abnormal glutamatergic tone as a common denominator. Several limitations and alternative explanations are acknowledged. The authors consider the possibility that the study lacked power to detect a small psilocybin effect on MMN, but argue that subject numbers and the presence of a significant N1 effect make a strong MMN reduction unlikely. They also note that MMN elicited by frequency deviants can be confounded with an N1 to the deviant and that the modest numerical change in frequency MMN may reflect the N1 reduction. Dose comparability to the prior ketamine study is discussed: although behavioural and cognitive effects were similar in magnitude, the processes underlying MMN may be more resistant to disruption by 5-HT2A agonism or might require higher doses. Finally, the authors draw clinical implications cautiously. They suggest that MMN and other early ERP markers may provide indices closer to specific receptor-related abnormalities (notably NMDAR dysfunction), while deficits in tasks like AX-CPT may arise from heterogeneous pathophysiology converging on similar network-level disturbances. This distinction has potential treatment relevance: atypical antipsychotics (with 5-HT2A antagonism) might ameliorate cognitive deficits related to altered glutamatergic dynamics, but would not be expected to correct deficits that are a direct consequence of NMDAR hypofunction such as MMN reduction. The investigators present these conclusions as supportive but circumspect—pointing to independent abnormalities of NMDAR and 5-HT2A systems as contributors to cognitive deficits in schizophrenia, with disrupted glutamatergic signalling a plausible shared mechanism underlying overlapping effects.
The study was approved by the ethics committee of the Psychiatric University Hospital Zurich and conducted in the Research Department of the Psychiatric University Hospital Zurich in accordance with the Helsinki declaration. The use of psilocybin was approved by the Swiss Federal Health Office (BAG), Department of Pharmacology and Narcotics (DPN), Bern, Switzerland. Psilocybin was obtained from the BAG-DPN and was prepared as capsules (1 and 5 mg) at the pharmacy of the Kantonsspital Luzern, Switzerland.
For ERP analyses, the primary dependent measures consisted of (a) amplitude and latency of N1 and P2 at Fz to the standard stimulus, and (b) amplitude and latency of frequency and duration MMN at FCz. Effects of psilocybin were evaluated using repeated-measures ANOVAs with session (psilocybin vs placebo) and time (baseline vs psilocybin/placebo administration) as repeated measures. For the analysis of MMN, an additional within-subject twolevel factor denoting MMN type (frequency vs duration condition) was included. Paired t-tests were performed for post hoc analysis if indicated. For the analyses of performance of AX-CPT, dependent measures consisted of hit rate (correct detection of AX sequences) and false alarm rates to BX, AY, or BY sequences. Effects of psilocybin on hit rate were evaluated with 2 Â 3 Â 2 factorial repeated-measures ANOVAs with session (psilocybin vs placebo), time (baseline vs psilocybin/ placebo administration), and ISI (short vs long) as repeated measures. For analyses of false alarm rates, an additional within-subject factor with three levels denoting false alarm type (BX vs AY vs BY) was included. Differences between rates of BX errors and AY and BY errors, respectively, during the two phases of both sessions were evaluated with simple within-subject contrasts involving session (contrast: psilocybin vs placebo), time (contrast: baseline vs psilocybin/placebo administration), and false alarm type (contrast: BX vs AY; BX vs BY). Post hoc paired t-tests were used to assess specific differences if indicated. Furthermore, the discrimination index d 0 and response bias B r were calculated using hit rates and total false alarm rates for the long and short ISI condition. Effects of psilocybin administration were evaluated with repeated-measures ANOVAs similarly as outlined above. For behavioral analyses, we used the BPRS total score and five factors that can be derived from the BPRS items: Alpha levels of 0.05 were considered significant throughout.
In a previous study, we have shown that the NMDAR antagonist ketamine reduced MMN generation and AX-CPT performance in a fashion similar to the deficits observed in schizophrenic patients, thus providing supporting evidence for the NMDA/glutamate hypothesis of schizophrenia. The present study investigated the effects of the 5-HT 2A agonist psilocybin on these measures, to explore the potential role of 5-HT 2A receptor dysfunction in such deficits and to address the question of whether abnormalities in 5-HT 2A receptor-dependent neurotransmission might also contribute to similar deficits in schizophrenia. Administration of the 5-HT 2A agonist psilocybin induced a significant reduction of the sensory ERP N1, but was not associated with significant decreases of MMN to frequency and duration deviants. In contrast, psilocybin administration was associated with deficits in AX-CPT performance that were particularly characterized by a failure to use contextual information (BX errors), whereas the rates of other possible errors where contextual information is not important were not significantly altered. Furthermore, the absence of a delay effect indicates that psilocybin did not adversely affect the maintenance of contextual information. The significant reduction of N1, but not of MMN, during administration of psilocybin differs from the pattern of effects (significant reductions of MMN, but not of N1) during ketamine administration. In contrast, the profile of psilocybin-induced deficits in AX-CPT performance is remarkably similar to the deficits observed in healthy volunteers during ketamine administration and in schizophrenic patients. To the extent that these differences and similarities reflect the underlying mechanisms, our results indicate that the pharmacological properties unique to ketamine and psilocybin (ie the NMDAR antagonist and 5-HT 2A receptor agonist action, respectively) are the important factor determining their effects on MMN and N1 generation. Thus, together with the findings of our previous study, the results of this investigation support the conclusion that the generation of MMN indeed depends strongly on NMDAR functioning, whereas the 5-HT 2A receptor plays a lesser role. Conversely, deficits in AX-CPT performance induced by both ketamine and psilocybin may result not only from their direct antagonist and agonist actions at their respective receptor sites, but also from secondary pharmacological effects that appear to be similar in nature for both drugs and take place downstream to these receptor sites in dopamine and glutamate systems. Both NMDA and 5-HT 2A receptors exert strong modulatory effects on dopaminergic and glutamatergic systems in rodents and humans. The blockade or activation, respectively, of these receptors leads to changes that seem to affect the dynamic properties of these neurotransmitter systems. In animals, the administration of NMDAR antagonists leads to target-specific disruption of the normal functioning of ascending dopaminergic pathways. Both activation and blockade of 5-HT 2A receptors have been demonstrated to exert strong modulatory effects on dopaminergic neurotransmission. In humans, ketamine administration increases spontaneous and amphetamineinduced dopamine release. Similarly, administration of psilocybin in healthy volunteers is associated with increased dopamine release. In addition, both NMDAR antagonists and 5-HT 2A agonists induce excessive release of glutamate in rodents, an effect that can be blocked in both cases by group II metabotropic receptor agonists. Consistently, in human volunteers lamotrigine, a drug that inhibits glutamate release, attenuates the cognitive effects of ketamine. Thus, NMDAR antagonists and 5-HT 2A agonists share some secondary pharmacological effects. Besides these similar effects, 5-HT 2A receptors have been shown to modulate NMDAR-dependent effects, and even antagonize effects of NMDAR antagonists. In healthy volunteers, ketamine-induced cognitive deficits are ameliorated by haloperidol (a dopamine D 2 receptor blocker) and lamotrigine. In contrast, psilocybin-induced cognitive deficits are only ameliorated by 5-HT 2A antagonists, but not by dopamine D 2 antagonists. Hence, increased glutamatergic tone (ie, abnormal dynamics of this system) may be the common denominator underlying overlapping aspects of the cognitive effects of dissociative NMDAR antagonists and hallucinogenic 5-HT 2A agonists in humans. To the extent that deficits induced by acute drug challenges in healthy volunteers inform us about pathophysiological mechanisms underlying comparable deficits in schizophrenia, the findings of this and our previous studyhave several implications for the investigation, pathophysiology, and treatment of cognitive deficits in schizophrenia. First of all, they suggest that deficits of long-latency ERPs such as N1 and MMN may provide potentially useful markers of specific receptorrelated abnormalities, whereas abnormal performance in tasks such as the AX-CPT may be similar in patients whose primary abnormality lies within quite different receptor systems (such as independent abnormalities in both NMDA receptor and 5-HT 2A receptor-dependent neurotransmission). Thus, profiling patients with regard to their performance on neuropsychological tests may not permit specifying etiologically heterogeneous subgroups. Conversely, using markers of early information processing such as ERPs may provide indices that are closer to suspected abnormalities in NMDAR and 5-HT 2A receptor-dependent neurotransmission. Second, neurocognitive deficits have become a major treatment focus in recent years, with the growing realization that they constitute an important limiting factor for rehabilitation and outcome. If indeed excessive glutamate release (ie abnormal dynamics of the glutamate system, whether as a result of NMDA receptor hypofunction or excessive signaling through the 5-HT 2A receptor) plays a role in these deficits, then 5-HT 2A receptor antagonists, but not dopamine D 2 receptor antagonists, would be expected to exert beneficial effects: In the scenario of a primary deficit in NMDAR-dependent neurotransmission, 5-HT 2A antagonists may counteract its secondary effects on the glutamate system, whereas in the case of 5-HT 2A receptor-related dysfunction their effect may be direct. Both scenarios would predict that atypical but not typical antipsychotic drugs improve cognitive deficits that result from secondary disturbances due to NMDAR hypofunction, such as deficits in AX-CPT and possibly other cognitive tasks that tax attention and working memory. In contrast, neither atypical nor typical antipsychotics would be expected to affect those deficits hypothesized to be a direct manifestation of NMDAR hypofunction such as deficient MMN generation. Indeed, there is accumulating evidence that atypical antipsychotics, in contrast to typical compounds, improve deficits in tasks assessing verbal memory, immediate recall, and attention. In addition, we and others have previously reported exactly such effects of clozapine and, to a lesser extent, risperidone in studies evaluating their effects on MMN and the attentiondependent ERP P3. Clozapine and risperidone, but not typical antipsychotics, significantly improved the deficient generation of P3 (an attention-dependent ERP) in schizophrenia; like typical antipsychotics, however, clozapine and risperidone failed to affect MMN deficits. Consistent with these observations, we have found that both ketamine and psilocybin significantly reduce auditory P3 generation. The finding of a significant decrease of N1 amplitude during psilocybin administration is consistent with studies demonstrating a tight modulation of the so-called N1 intensity dependence by the serotonergic system. N1 intensity dependence refers to the increase of N1 amplitude with increasing stimulus intensity. There is considerable evidence that a low serotonergic tone is associated with an increased N1 intensity dependence, an effect mediated in particular through the 5-HT 1A and 5-HT 2A receptor. One would therefore expect a 5-HT 2A agonist to reduce N1 intensity dependence or, with intensity kept constant, to reduce N1 amplitude. The latter is exactly the observation in this study. We note that early ERP studies reported a reduced N1 intensity dependence in schizophrenic patients. This abnormality, if confirmed in studies using modern ERP methodology, might thus relate to dysfunction in 5-HT 2A receptor-dependent neurotransmission. Psilocybin administration was associated with a small but nonsignificant decrease of MMN. It is conceivable that psilocybin reduces MMN, but that our study lacked the power to detect significant changes. In our study on the effects of ketamine, however, a similar number of subjects (20) was investigated and significant effects were observed. Furthermore, a significant effect on N1 was observed in this study. Thus, any reducing effect of 5-HT 2A agonism on MMN generation would be much smaller than the effect of NMDA blockade on MMN or the effect of psilocybin on N1 generation. Furthermore, psilocybin had a more pronounced effect on MMN to frequency deviants. This may actually reflect its reducing effect on N1, given that MMN elicited with the particular paradigm used in this study is confounded with an N1 to the deviant stimulus. Such a confound is not present in the MMN to duration deviants, where the effect of psilocybin was not even close to significance. It is possible that the dose of psilocybin was not comparable to the ketamine dose used in our previous study; however, the cognitive and behavioral effects were of similar magnitude as observed in our previous ketamine study. Thus, at a dose that induced significant deficits in higher cognitive function, psilocybin had no effect on MMN. This could mean that the 5-HT 2A receptor indeed plays no role in MMN generation or, alternatively, that the processes underlying MMN generation may be more impervious to abnormal 5-HT 2A signaling, requiring a much higher dose for their disruption. In conclusion, in healthy volunteers the 5-HT 2A agonist psilocybin was associated with significant deficits in the AX-CPT performance similar to those previously observed during ketamine administration and in schizophrenia, but failed to reduce MMN generation. These findings suggest that deficits in higher cognitive functions in schizophrenia may result from independent abnormalities in both NMDA and 5-HT 2A receptor systems. The disruption of normal glutamatergic signaling may be a candidate mechanism mediating these shared effects. In addition, the results of this study provide further, albeit circumstantial, support for the hypothesis that deficits in MMN generation in schizophrenia may be a relatively direct manifestation of deficient NMDAR functioning. Atypical antipsychotic drugs may affect NMDAR and 5-HT 2A receptor-related dysfunctions similarly through their 5-HT 2A antagonism.
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Casanova, A. F., Ort, A., Smallridge, J. W. et al. · iScience (2024)
Dinkelacker, J., Pop, I. · Journal of Clinical Psychiatry (2023)
Villiger, D. · Frontiers in Psychiatry (2022)
Wießner, I., Falchi, M., Maia, L. O. et al. · Journal of Psychopharmacology (2022)
Vollenweider, F. X., Smallridge, J. W. · Pharmacopsychiatry (2022)
Maia, L. O., Feilding, A., Ribeiro, S. et al. · Psychopharmacology (2021)
Duerler, P., Brem, S., Fraga-González, G. et al. · Cerebral Cortex (2021)
Smigielski, L., Kometer, M., Scheidegger, M. et al. · Human Brain Mapping (2020)
Barrett, F. S., Preller, K. H., Kaelen, M. · International Review of Psychiatry (2018)
Bravermanová, A., Viktorinová, M., Tylš, F. et al. · Psychopharmacology (2018)
Kraehenmann, R. · Current Neuropharmacology (2017)
Preller, K. H., Vollenweider, F. X. · Behavioral Neurobiology of Psychedelic Drugs (2016)
Pokorny, T., Preller, K. H., Kraehenmann, R. et al. · European Neuropsychopharmacology (2016)
McKenna, D., Riba, J. · Current Topics in Behavioral Neurosciences (2016)
Kometer, M., Vollenweider, F. X. · Behavioral Neurobiology of Psychedelic Drugs (2016)
Majic, T., Schmidt, T. T., Gallinat, J. · Journal of Clinical Psychopharmacology (2015)
Tylš, F., Páleníček, T., Horacek, J. · European Neuropsychopharmacology (2013)
Bouso, J. C., Fábregas, J. M., Antonijoan, R. M. et al. · Psychopharmacology (2013)
Bogenschutz, M. P. · Current Drug Abuse Reviews (2013)
Studerus, E., Kometer, M., Hasler, F. et al. · Journal of Psychopharmacology (2010)
Carter, O. L., Hasler, F. ;., Pettigrew, J. D. et al. · Psychopharmacology (2007)
Wittmann, M., Carter, O., Hasler, F. et al. · Journal of Psychopharmacology (2007)
Carter, O., Burr, D. C., Pettigrew, J. D. et al. · Journal of Cognitive Neuroscience (2006)
Gouzoulis-Mayfrank, E., Heekeren, K., Neukirch, A. et al. · Pharmacopsychiatry (2005)