Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action
This paper (1998) was one of the first to identify psilocybin/psilocin as working on the serotonin (5-HT2A) receptor and not only on the dopaminergic system. The direct comparisons as mentioned in the article are nowadays a bit more nuanced.
Abstract
Psilocybin, an indoleamine hallucinogen, produces a psychosis-like syndrome in humans that resembles first episodes of schizophrenia. In healthy human volunteers, the psychotomimetic effects of psilocybin were blocked dose-dependently by the serotonin-2A antagonist ketanserin or the atypical antipsychotic risperidone but were increased by the dopamine antagonist and typical antipsychotic haloperidol. These data are consistent with animal studies and provide the first evidence in humans that psilocybin-induced psychosis is due to serotonin-2A receptor activation, independently of dopamine stimulation. Thus, serotonin-2A overactivity may be involved in the pathophysiology of schizophrenia and serotonin-2A antagonism may contribute to therapeutic effects of antipsychotics.
Research Summary of 'Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action'
βBlossom's Take
Introduction
Earlier research has emphasised dopaminergic dysfunction in schizophrenia, but accumulating evidence implicates serotonin (5-HT) systems as well. Clinical observations include altered cortical serotonin receptor binding in schizophrenia, potent 5-HT2 antagonism among atypical antipsychotics, and the fact that classic indoleamine hallucinogens such as psilocybin and LSD can elicit syndromes in healthy people that resemble early stages of schizophrenia, including ego disturbances, affective changes, loosened associations and perceptual alterations. Animal studies suggest that hallucinogens act via 5-HT2 receptors, yet extrapolation to humans is uncertain and some hallucinogens also affect dopaminergic systems, leaving open whether human effects are mediated directly by 5-HT2 receptors, indirectly via dopamine, or both. To address this gap, Vollenweider and colleagues tested whether psilocybin’s psychotomimetic and cognitive effects in healthy volunteers are mediated by 5-HT2 and/or dopamine D2 receptors. Using a placebo-controlled, within-subject design, they examined how pretreatment with a selective 5-HT2 antagonist (ketanserin), a D2 antagonist typical antipsychotic (haloperidol), or a mixed 5-HT2/D2 antagonist atypical antipsychotic (risperidone) altered psilocybin-induced psychological and working memory effects, assessed chiefly with the Altered State of Consciousness (APZ-OAV) rating scale and a delayed response task (DRT).
Methods
The study enrolled 25 healthy university-affiliated volunteers screened by psychiatric interview and medical assessment; individuals with personal or first‑degree family histories of major psychiatric disorder or with a history of illicit drug abuse were excluded. Ethical approval and regulatory authorisation for psilocybin were obtained. Psilocybin (0.25 mg/kg, oral) was chosen to produce robust psychological effects lasting roughly 120–180 minutes after a 20–30 minute onset. Antagonists were ketanserin (20 and 40 mg, oral), haloperidol (0.021 mg/kg, intravenous), and risperidone (0.5 and 1.0 mg, oral); the haloperidol and risperidone doses were expected to occupy roughly 55–65% of D2 receptors. Experiment 1 used a within-subject design in 15 subjects (eight male, seven female; mean age 29.7 ± 5.3) split into three groups of five, each group tested at monthly intervals for one antagonist series (ketanserin, haloperidol, or risperidone). For ketanserin and haloperidol pretreatments, antagonist or placebo was given and 75 minutes later subjects received psilocybin (or placebo); for risperidone, pretreatment preceded psilocybin by 90 minutes for kinetic reasons. Psychological state was measured with the APZ-OAV scale and working memory with a visual-manual delayed response task (DRT) immediately prior to treatment and again approximately 80 minutes after, coinciding with peak psilocybin effects. Experiment 2 comprised a separate cohort of 10 subjects (five male, five female; mean age 28.4 ± 4.0) to replicate the ketanserin 40 mg pretreatment finding; the protocol matched Experiment 1 but included APZ-OAV ratings only. The APZ-OAV yields three dimensions: OSE (oceanic boundlessness), VUS (visionary restructuralization), and AIA (dread of ego-dissolution). The DRT involved 32 trials in which participants recalled target positions after a 10 s delay while performing a concurrent category-shift task; response times on correct trials were recorded. Statistical analysis used two-way repeated-measures ANOVAs with pretreatment and drug as within-subject factors, Tukey post hoc tests where indicated, non-parametric Friedman ANOVAs for certain comparisons, and Spearman correlations for associations between reaction-time changes and psychopathology. Significance was set at p < 0.05.
Results
Oral psilocybin (0.25 mg/kg) produced a transient psychosis-like syndrome in healthy volunteers, with effects emerging 20–30 minutes after ingestion, peaking after an additional 30–50 minutes and lasting around 1–2 hours. On the APZ-OAV, psilocybin significantly increased scores on all three dimensions (OSE, VUS, AIA) across the antagonist experiments, reflecting derealisation and exalted mood (OSE), visual/perceptual alterations including hallucinations and synaesthesia (VUS), and anxious ego-dissolution with thought disorder and suspiciousness (AIA). Pretreatment with the 5-HT2 antagonist ketanserin dose-dependently attenuated these effects: two-way ANOVAs showed significant drug × pretreatment interactions for OSE (F(2,8) = 12.2, p < 0.004), VUS (F(2,8) = 26.3, p < 0.0003) and AIA (F(2,8) = 21.7, p < 0.0006). Specifically, 20 mg ketanserin reduced psilocybin-induced APZ-OAV scores by about 50–70%, while 40 mg largely prevented the effects in four of five subjects (98–100% reduction) and substantially reduced scores in the remaining subject (75–87%). A separate replication cohort confirmed that 40 mg ketanserin blocked psilocybin effects by 87–96% with highly significant interactions (OSE F ≈ 51.7, p < 0.0001; VUS F ≈ 111.7, p < 0.00001; AIA F ≈ 16.2, p < 0.003). Risperidone, a mixed 5-HT2/D2 antagonist, produced dose-dependent attenuation as well: 0.5 mg reduced APZ-OAV scores by about 69–78% and 1.0 mg nearly abolished the psilocybin-induced syndrome (98–99%), with significant drug × pretreatment interactions (OSE F(2,8) = 7.4, p < 0.02; VUS F(2,8) = 8.2, p < 0.01; AIA F(2,8) = 8.5, p < 0.01). By themselves, neither ketanserin nor risperidone altered APZ-OAV scores. In contrast, haloperidol had a limited and differential effect: it reduced the OSE scale by about 54% (drug × pretreatment interaction for OSE F(1,4) = 20.4, p < 0.01) but did not reduce VUS scores (main drug effect F(1,4) = 52.3, p < 0.002; no significant pretreatment or interaction). Unexpectedly, haloperidol amplified AIA scores by 148% when combined with psilocybin; statistical tests showed significant main effects (drug F(1,4) = 14.4, p < 0.02; pretreatment F(1,4) = 8.7, p < 0.04) though no significant interaction in the two-way ANOVA, and confirmatory Friedman tests indicated the increase was greater than with psilocybin alone (p < 0.025). Item analysis suggested this increase reflected increased thought disorder and anxiety. On the DRT, psilocybin lengthened reaction times without reducing accuracy. Ketanserin and risperidone, but not haloperidol, dose-dependently blocked the psilocybin-induced reaction-time increases (ketanserin F(2,8) = 6.0, p < 0.03; risperidone F(2,8) = 4.8, p < 0.04). Antagonists alone did not affect reaction times, and changes in reaction time did not correlate significantly with APZ-OAV psychopathology measures.
Discussion
Vollenweider and colleagues interpret their results as strong evidence that psilocybin’s psychotomimetic effects in humans are mediated specifically by activation of 5-HT2 receptors, and in particular the 5-HT2A subtype. The finding that a selective 5-HT2 antagonist (ketanserin) and the mixed 5-HT2/D2 antagonist risperidone nearly abolished both the subjective psychosis-like syndrome and the working-memory impairment implicates 5-HT2A agonism as the principal mechanism, validating prior animal data linking hallucinogenic effects to 5-HT2 receptors. The pattern of symptom changes—prominent derealisation and euphoria (OSE), visual hallucinations (VUS), and anxious ego-dissolution and thought disorder (AIA)—is taken to mirror features of early or acute schizophrenia, supporting the notion that serotonergic hyperactivity may contribute to psychotic symptom formation. The selective blockade by ketanserin, which is substantially more potent at 5-HT2A than 5-HT2C receptors, is presented as evidence favouring 5-HT2A over 5-HT2C involvement. By contrast, the typical D2 antagonist haloperidol was substantially less effective at blocking psilocybin-induced phenomena and, notably, increased anxious ego-dissolution (AIA) when combined with psilocybin; this pattern suggests that D2 antagonism alone does not prevent—and may even exacerbate—certain psilocybin-elicited symptoms. The authors note that psilocybin and its active metabolite psilocin do not act directly at D2 receptors, so haloperidol’s partial effects might reflect an indirect modulation of dopaminergic systems; however, the data do not permit inference about whether haloperidol-enhanced AIA arises from serotonergic modulation of dopamine, GABA, or other systems. The demonstration that psilocybin-induced working memory deficits were prevented by 5-HT2 but not D2 antagonism leads the investigators to suggest a possible role for 5-HT2A stimulation in cognitive impairments seen in schizophrenia, consistent with clinical observations that some cognitive deficits respond better to atypical than typical neuroleptics. Finally, the authors propose that psilocybin-induced psychosis could serve as an experimental human model to study aspects of atypical antipsychotic action that are not captured by amphetamine-based (dopamine-centric) models, while acknowledging mechanistic uncertainties that remain.
Conclusion
The study concludes that psilocybin produces schizophrenia-like symptoms and working-memory impairments primarily via stimulation of 5-HT2 receptors, most likely the 5-HT2A subtype. From this, the authors infer that excessive 5-HT2A activity may contribute to psychotic symptom formation and cognitive deficits in at least a subset of patients with schizophrenia, and that selective 5-HT2A antagonists could have therapeutic utility. They further suggest that psilocybin-induced psychosis may provide a useful human model to investigate facets of atypical antipsychotic pharmacology that differ from those revealed by dopaminergic models.
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METHODS
The study was approved by the Ethics Committee of the Psychiatric University Hospital Zürich and the use of psilocybin by the Swiss Federal Health Office (BAG), Department of Pharmacology and Narcotics (DPN), Bern. Psilocybin was obtained from the BAG (DPN), Bern, and prepared as capsules (1 and 5 mg) at the Pharmaceutical Institute of the University of Bern, Switzerland. Twenty-five healthy volunteers were recruited from university staff and screened by psychiatric interview to assure that they had neither personal nor family histories of major psychiatric disorders in first-degree relatives. Subjects with a history of illicit drug abuse were excluded from the study. Subjects were healthy according to physical examination, electrocardiogram, and blood analyses. All subjects gave written informed consent. The psilocybin dose used was high enough (0.25 mg/kg, p.o.) to induce robust psychological alterations over a period of 120-180 min.The doses of haloperidol (0.021 mg/kg, i.v.) and risperidone (1 mg, p.o.) chosen were expected to occupy about 55-65% of dopamine D2 receptors.
RESULTS
Psilocybin (0.25 mg/kg, p.o.) produced a psychotic syndrome including changes in mood, disturbances of sensory perception and thought processes, and impaired ego-functioning. The drug effects began 20-30 min after administration, peaked after another 30-50 min, and lasted 1-2 h. Thus psychological measurements and neuropsychological testing were undertaken during the peak drug effects. The APZ-OAV scores for placebo, psilocybin, and psilocybin plus the different doses of antagonists for experiment 1 are summarized in Fig.. Two-way ANOVA's and Tukey's post hoc comparisons revealed that psilocybin significantly increased the OSE, VUS and AIA scores in the ketanserin, risperidone and haloperidol groups (Fig.). The increase in the OSE score was due to a prominent increase in derealization associated with euphoria, exaltation or grandiosity, and an altered sense of time and space. The increase in the VUS score was attributable to perceptual alterations including visual disturbances ranging from illusions to complex scenery hallucinations, synaesthesias, and changed meaning of percepts. The increase in AIA scores was mainly due to an anxiously experienced loss of ego-boundaries, thought disorder, and moderate suspiciousness and paranoid ideation. As shown in Fig., pretreatment with the 5-HT 2 antagonist ketanserin dose-dependently blocked psilocybininduced psychosis, as revealed by two-way ANOVAs and significant drug x pretreatment interactions (OSE (F(2,8) = 12.2, p < 0.004); VUS (F(2,8) = 26.3, p < 0.0003); AIA (F(2,8) = 21.7, p < 0.0006)). Specifically, 20 mg ketanserin reduced the psilocybin-induced APZ-OAV scores by about 50-70%, while 40 mg ketanserin completely prevented the development of psilocybin effects in four of five subjects (98-100%). In the remaining subject, the mean APZ-OAV scores were also markedly reduced (75-87%), but the subject still reported discrete distortions in the experience of time and space, and impaired body control. Similarly, 0.5 mg of the mixed 5-HT 2/D2 antagonist risperidone attenuated the effects of psilocybin on all three APZ-OAV scales (69-78%), while 1 mg risperidone effectively blocked the development of psilocybin-induced psychosis (98-99%). Two-way ANOVAs yielded again significant drug x pretreatment interactions (OSE (F(2,8) = 7.4, p < 0.02); VUS (F(2,8) = 8.2, p < 0.01); AIA (F(2,8) = 8.5, p < 0.01)). By themselves, neither ketanserin nor risperidone (0.5 and 1.0 mg) had any effects on any APZ-OAV scores. In contrast, pretreatment with haloperidol (0.021 mg/kg, i.v.) reduced the effect of psilocybin only on the OSE scale (54% reduction; drug x pretreatment interaction for OSE (F(1,4) = 20.4, p < 0.01). Tukey's post hoc analysis revealed that this reduction was significant (Fig.). Haloperidol had no influence on psilocybininduced visual illusions and hallucinations as measured by the VUS scale (main effect of drug (F(1,4) = 52.3, p < 0.002)) and pretreatment (F(1,4) = 0.51, p < 0.5), and drug x pretreatment interaction (F(1,4) = 0.4, p < 0.5)). Surprisingly, haloperidol uniformly increased the AIA scores in all of the subjects treated with psilocybin (148% increase). A two-way ANOVA revealed significant main effect of drug (F(1,4) = 14.4, p < 0.02) and pretreatment (F(1,4) = 8.7, p < 0.04), but no significant drug x pretreatment interaction (F(1,4) = 2.1, p < 0.22). Additional non-parametric Friedman ANOVAs showed that this psilocybin-induced increase in AIA scores after haloperidol was significantly greater than psilocybin alone (p < 0.025) and that haloperidol by itself slightly (9.6%), but not significantly, increased the AIA scores as compared to placebo. Furthermore, itembased analysis of the AIA scores revealed that psilocybin mainly increased thought disorder and anxiety after pretreatment with haloperidol. As seen in Figure, psilocybin also increased the reaction time on the memory-guided delayed response task during the peak effects of the drug. Again, ketanserin and risperidone, but not haloperidol, dose-dependently blocked the increase in reaction time on the DRT, as revealed by significant drug x pretreatment interactions (ketanserin (F(2.8) = 6.0, p < 0.03); risperidone (F(2.8) = 4.8, p < 0.04)). Additional Friedman ANOVAs showed that ketanserin, risperidone and haloperidol by themselves did not have any significant effects on reaction times. Performance as measured by the rate of correct responses did not differ significantly between the various conditions. Interestingly, the impairment in reaction time did not correlate significantly with changes in the APZ-OAV scores. Given the importance of the ketanserin findings obtained in experiment 1, a second group of 10 subjects was tested to corroborate the results obtained with 40 mg ketanserin. Once again, pretreatment with 40 mg ketanserin effectively blocked the effects of psilocybin on all APZ-OAV measures by 87-96%. Two-way ANOVAs yielded significant drug x pretreatment interactions for OSE (F(1.9) = 51.7, p < 0.0001), VUS (F(1.9) = 111.7, p < 0.00001), and AIA (F(1.9) = 16.2, p < 0.003) and Tukey's post hoc comparisons confirmed that these effects were significant (Fig.).
CONCLUSION
The present results provide compelling evidence that the model psychosis induced by psilocybin in healthy human volunteers is the result of a specific activation of the 5-HT 2 subtype of serotonin receptors. These findings validate the many studies in animals indicating that the behavioral effects of hallucinogens are attributable to 5-HT 2 agonist actions. This study corroborates the several previous suggestions of similarities between the early and acute stages of schizophrenia and the psychological effects of indoleamine-derived hallucinogens such as psilocybin and LSD.In particular, the finding that psilocybin produced derealization and depersonalization associated with heightened mood, euphoria and/or grandiosity (OSE) and visual hallucinations (VUS) is consistent with the observation that the earliest affective changes in incipient schizophrenia are often pleasurable and that visual, as opposed to auditory, hallucinations occur with higher prevalence in first-break than chronic schizophrenics. Anxious ego-dissolution, loss of body and thought control, and ideas of reference (AIA), however, are not only common features of both psilocybin-induced psychosis and early schizophrenic stages, but also occur in chronic schizophrenics in acute episodes. Indeed, a recent study demonstrated that schizophrenics during both first episodes and relapse had similar prominent OSE and AIA scores as seen in this study in psilocybin subjects.The most novel aspect of the present findings is the demonstration that psilocybin-induced psychosis could be completely prevented by either the atypical neuroleptic and mixed 5-HT 2/D2 antagonist risperidone or by the 5-HT 2 antagonist ketanserin, but not by the typical neuroleptic and D2 antagonist haloperidol. This finding adds substantial evidence to the view that 5-HT 2 agonism is responsible for the psychological effects of psilocybin and, presumably, other indoleamine hallucinogens. Furthermore, the soma rights re-served 7 since 29.06.2015 atfinding that ketanserin, with about 100-fold greater potency at the 5-HT 2A vs 5-HT 2C receptor, completely blocked psilocybin-induced psychosis strongly indicates that the effects of psilocybin are mediated by 5-HT 2A rather than 5-HT 2C receptor activation. This interpretation is corroborated by recent findings demonstrating that the highly selective 5-HT 2A receptor antagonist M100,907 (formerly MDL 100,907), but not 5-HT 2C antagonists, completely antagonized the disruptive effect of the hallucinogenic 5-HT 2A/C agonist DOI on prepulse inhibition (PPI) of startle in rats.Insofar that PPI deficits and 5-HT 2A receptor alterations were recently found in schizophrenic patients,the present data are consistent with the hypothesis that serotonergic hyperactivity may also contribute to the pathophysiology of schizophrenia. To the extent that the effects of psilocybin studied here are relevant to the symptoms of acute schizophrenia, the blockade of these effects by a 5-HT 2 antagonist supports the notion that 5-HT 2 antagonism may contribute significantly to the antipsychotic actions of atypical neuroleptics.In this regard, it is particularly interesting to note that the typical antipsychotic haloperidol was substantially less effective than risperidone in blocking the psychosis-like symptoms produced by psilocybin, despite the fact that the doses of haloperidol and risperidone were selected to have comparable effects on dopamine D2 receptors.In contrast, haloperidol even increased psilocybin-induced AIA scores. This finding might be somewhat surprising, but is consistent with single case reports indicating that classic neuroleptics do enhance, rather than ameliorate, LSD-induced psychosis.Whether psilocybin increases the AIA scores after pretreatment with haloperidol through a serotonergic modulation of dopamine or other neurotransmitter systems, such as GABA,or both, cannot be inferred from the present data. Nevertheless, despite the fact that psilocybin and psilocin do not act directly upon D2 receptorshaloperidol partially ameliorated psilocybin-induced OSE scores. This finding could indicate that psilocybin has an indirect influence on dopaminergic systems which is then antagonized by haloperidol. Finally, haloperidol, in contrast to ketanserin and risperidone, had no effects on psilocybininduced perceptual disturbances and hallucinatory phenomena (VUS) indicating that these symptoms are specifically attributable to direct activation of 5-HT 2A receptors and do not depend upon the dopaminergic system. The second important result was that psilocybin produced spatial working memory deficits comparable to those seen in schizophrenic patientsand that these deficits could be completely prevented by 5-HT 2 , but not D2 antagonism. This finding strongly suggests that 5-HT, and particularly 5-HT 2A receptor stimulation, may also contribute to cognitive impairments in schizophrenia. This interpretation is consistent with the since 29.06.2015 atobservation that schizophrenic patients with cognitive deficits respond better to atypical than typical neuroleptics.Furthermore, the observation that psilocybin-induced working memory deficits did not correlate with psychopathological measures is in line with the notion that cognitive deficits in schizophrenia appear to occur independent of positive and negative symptoms of schizophrenia.
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Study Details
- Study Typeindividual
- Populationhumans
- Characteristicsplacebo controlledsingle blindrandomizedcrossover
- Journal
- Compound
- Topics
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