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Disruption of auditory event-related evoked potentials (ERPs) P300 and mismatch negativity (MMN), electrophysiological markers of attentive and pre-attentive cognitive processing, is repeatedly described in psychosis and schizophrenia. Similar findings were observed in a glutamatergic model of psychosis, but the role of serotonergic 5-HT2A receptors in information processing is less clear. We studied ERPs in a serotonergic model of psychosis, induced by psilocybin, a psychedelic with 5-HT2A/C agonistic properties, in healthy volunteers. Twenty subjects (10M/10F) were given 0.26 mg/kg of psilocybin orally in a placebo-controlled, double-blind, cross-over design. ERPs (P300, MMN) were registered during the peak of intoxication. Correlations between measured electrophysiological variables and psilocin serum levels and neuropsychological effects were also analyzed. Psilocybin induced robust psychedelic effects and psychotic-like symptoms, decreased P300 amplitude (p = 0.009) but did not affect the MMN. Psilocybin’s disruptive effect on P300 correlated with the intensity of the psychedelic state, which was dependent on the psilocin serum levels. We also observed a decrease in N100 amplitude (p = 0.039) in the P300 paradigm and a negative correlation between P300 and MMN amplitude (p = 0.014). Even though pre-attentive cognition (MMN) was not affected, processing at the early perceptual level (N100) and in higher-order cognition (P300) was significantly disrupted by psilocybin. Our results have implications for the role of 5-HT2A receptors in altered information processing in psychosis and schizophrenia.

Serotonergic agonist psilocybin is a psychedelic with antidepressant potential. Sleep may interact with psilocybin’s antidepressant properties like other antidepressant drugs via induction of neuroplasticity. The main aim of the study was to evaluate the effect of psilocybin on sleep architecture on the night after psilocybin administration. Regarding the potential antidepressant properties, we hypothesized that psilocybin, similar to other classical antidepressants, would reduce rapid eye movement (REM) sleep and prolong REM sleep latency. Moreover, we also hypothesized that psilocybin would promote slow-wave activity (SWA) expression in the first sleep cycle, a marker of sleep-related neuroplasticity. Twenty healthy volunteers (10 women, age 28–53) underwent two drug administration sessions, psilocybin or placebo, in a randomized, double-blinded design. Changes in sleep macrostructure, SWA during the first sleep cycle, whole night EEG spectral power across frequencies in non-rapid eye movement (NREM) and REM sleep, and changes in subjective sleep measures were analyzed. The results revealed prolonged REM sleep latency after psilocybin administration and a trend toward a decrease in overall REM sleep duration. No changes in NREM sleep were observed. Psilocybin did not affect EEG power spectra in NREM or REM sleep when examined across the whole night. However, psilocybin suppressed SWA in the first sleep cycle. No evidence was found for sleep-related neuroplasticity, however, a different dosage, timing, effect on homeostatic regulation of sleep, or other mechanisms related to antidepressant effects may play a role. Overall, this study suggests that potential antidepressant properties of psilocybin might be related to changes in sleep.

Difficulty with emotion perception is a core feature of autism spectrum disorder (ASD) that is also associated with the broader autism phenotype. The current study explored the neural underpinnings of conscious and nonconscious perceptions of affect in typically developing individuals with varying levels of autistic-like traits, as measured by the Autism Quotient (AQ). We investigated the relationship between autistic traits and face processing efficiency using event-related potentials (ERPs). In 20 typically developing adults, we utilized ERPs (the P100, N170, and P300) to measure differences in face processing for emotional faces that were presented either (a) too quickly to reach conscious awareness (16 ms) or (b) slowly enough to be consciously observed (200 ms). All individuals evidenced increased P100 and P300 amplitude and shorter N170 latencies for nonconscious versus consciously presented faces. Individuals with high AQ scores evidenced delayed ERP components. Nonconsciously perceived emotional faces elicited enhanced neural responses regardless of AQ score. Higher levels of autistic traits were associated with inefficient face perception (i.e., longer latency of ERP components). This delay parallels processing delays observed in ASD. These data suggest that inefficient social perception is present in individuals with subclinical levels of social impairment.

Self-report studies indicate that cannabis could increase sexual desire in some users. We hypothesized that intoxication increases activation of brain areas responsive to visual erotica, which could be useful in the treatment of hypoactive sexual desire disorder, a condition marked by a lack of sexual desire. The aim of this study is to assess the aphrodisiacal properties of cannabis. We conducted an open-randomized study with 21 heterosexual casual cannabis users. A 3T MRI was used to measure brain activation in response to erotic pictures. Blood samples were collected to determine the serum levels of cannabinoids, cortisol and prolactin. Participants were grouped according to whether they had ever experienced any aphrodisiacal effects during intoxication (Group A) or not (Group non-A). Intoxication was found to significantly increase activation in the right nucleus accumbens in the Group A while significantly decreasing activation in the Group non-A. There was also a significant interaction between the group and intoxication, with elevated prolactin in the Group non-A during intoxication. No intoxication-related differences in subjective picture evaluations were found. Cannabis intoxication increases activation of the right nucleus accumbens to erotic stimuli. This effect is limited to users whose prolactin is not elevated in response to intoxication. This effect may be useful in the treatment of low sexual desire.

Objective Time-course of ketamine effect was assessed in depressive patients by QEEG to elucidate changes associated with treatment and to assess potential predictors of response. Methods The analysis was completed from data of two double-blind, cross-over, placebo-controlled studies, assessing the effect of ketamine infusion (0.54 mg/kg) in 51 inpatients with MDD. EEG data were analysed during the infusion (10 and 30 min) and 24hours after ketamine administration using eLORETA. Results Ketamine induced immediate decrease of parietooccipital alpha-sources and an increase of gamma-sources in all subjects. Better response to treatment was connected with higher pre-treatment alpha activity in parietooccipital region, lower theta sources in mediofrontal areas and rostral cingulate and with lower lagged-phase alpha synchronization. Responders were also characterized by increase of mediofrontal delta/theta sources immediately after ketamine infusion. The intensity of psychotomimetic symptoms were strong predictor of ketamine antidepressive effect. Conclusion Our results suggest that higher pre-treatment occipital alpha activity together with lower theta activity in anterior cingulate and mediofrontal cortex and lower alpha lagged phase synchronization could serve as moderators of treatment response to ketamine. The antidepressive effect of ketamine seems to be undoubtedly connected with patient‘s psychotomimetic experience. Supported by grant AZV MZCR 15-33250A.

The elucidation of the brain circuitry underlying neural bases of mood and emotion represents the essential aim of modern neuroscience and psychiatric research. The aims of the study was to identify QEEG correlates of autobiographically induced emotionally neutral and emotionally negative situation (sadness) using the QEEG methods sLORETA (standardized low-resolution brain electromagnetic tomography)and eLORETA connectivity in remitted patients with bipolar affective disorder (BAP) ( N = 30), depression ( N = 20) and healthy controls ( N = 30). Within-group comparisons (pairwise t -tests) using log-transformed values of sLORETA images(emotionally neutral vs. negative emotional state) revealed that autobiographical induction of sadness in healthy volunteers led to the increase of neuronal activity (current density in the gamma frequency band) in subgenual and anterior cingulate (Brodmann area 25, 32, 34). Patients with BAP (sadness) showed more pronounced activation of limbic and mediofrontal areas (BA 10, 11, 24, 25, 32, 33, 47). This “hyperactivation” can be considered as a trait marker of BAP, which can be identified even in patients in remission. In contrast, between-group comparisons (in both neutral and negative emotional state) were not associated with any significant changes in brain activity in healthy volunteers compared to patients with BAP.