Hallucinogenic psilocybin is known to alter the subjective experience of time. However, there is no study that systematically investigated objective measures of time perception under psilocybin. Therefore, we studied dose-dependent effects of the serotonin (5-HT)2A/1A receptor agonist psilocybin (4-phosphoryloxy-N, N-dimethyltryptamine) on temporal processing, employing tasks of temporal reproduction, sensorimotor synchronization and tapping tempo. To control for cognitive and subjective changes, we assessed spatial working memory and conscious experience. Twelve healthy human volunteers were tested under placebo, medium (115 microg/kg), and high (250 microg/kg) dose conditions, in a double-blind experimental design. Psilocybin was found to significantly impair subjects' ability to (1) reproduce interval durations longer than 2.5 sec, (2) to synchronize to inter-beat intervals longer than 2 sec and (3) caused subjects to be slower in their preferred tapping rate. These objective effects on timing performance were accompanied by working-memory deficits and subjective changes in conscious state, namely increased reports of 'depersonalization' and 'derealization' phenomena including disturbances in subjective 'time sense.' Our study is the first to systematically assess the impact of psilocybin on timing performance on standardized measures of temporal processing. Results indicate that the serotonin system is selectively involved in duration processing of intervals longer than 2 to 3 seconds and in the voluntary control of the speed of movement. We speculate that psilocybin's selective disruption of longer intervals is likely to be a product of interactions with cognitive dimensions of temporal processing -presumably via 5-HT2A receptor stimulation.
In an antisaccade task, subjects are instructed to inhibit a reflexive saccade towards a peripheral stimulus flash and to generate a saccade in the opposite direction. It has been shown recently that normal subjects will generate a high number of incorrect prosaccades in an antisaccade task if the fixation point is extinguished 200 ms before the stimulus appears and if a valid cue for the subsequent antisaccade is given during this gap period. In the present study we recorded cerebral event-related potentials from 19 scalp electrodes from normal subjects prior to correct and incorrect responses in a cued antisaccade task to investigate the neural processes associated with correct antisaccades and incorrect prosaccades in this task. Correct antisaccades and incorrect prosaccades were associated with a negative potential with a maximal amplitude around stimulus onset over the dorsomedial frontal cortex. This potential was higher prior to correct antisaccades than prior to incorrect prosaccades. The execution of a correct antisaccade was preceded by a shift of a negative potential from the parietal hemisphere contralateral to the visual stimulus towards the parietal hemisphere ipsilateral to the stimulus. These results support the view that the supplementary eye fields participate in the inhibition of incorrect saccades in a cued antisaccade task and show that the parietal cortex participates in generating a neural representation of the visual stimulus in the hemifield ipsilateral to the stimulus before generating a motor response.
Recent experimental observations indicate that pathways interconnecting the bilateral vestibular nuclei (VN) may provide positive-feedback loops for signals across the midline. The implications of such positive feedback are considered in the context of vestibular compensation. A simple conceptual model of the interconnected VN is studied analytically, based on the hypothesis that the restoration of central symmetry is achieved via changes of neural gain in closed commissural loops. A wide variety of experimental conditions related to vestibular compensation are investigated. Analytic model predictions are compared to behavioral and neurophysiological findings in the literature. The results show that organized control over commissural gains in closed loops coupling the bilateral VN is fully compatible with all phenomena cited in the article. In particular, such a mechanism for vestibular compensation can reconcile observations such as the fact that Bechterew phenomena and decompensation can both be elicited from the compensated state. Placing the site of vestibular compensation in pathways linking the VN has many implications. Other forms of central neural plasticity (e.g., vestibuloocular reflex (VOR) gain plasticity) may rely on a similar principle, since modulation of transmidline coupling can be a very powerful means of altering responses in a bilateral nervous system.
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