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Neural activity during repeated presentations of a sensory stimulus exhibits considerable trial-by-trial variability. Previous studies have reported that trial-by-trial neural variability is reduced (quenched) by the presentation of a stimulus. However, the functional significance and behavioral relevance of variability quenching and the potential physiological mechanisms that may drive it have been studied only rarely. Here, we recorded neural activity with EEG as subjects performed a two-interval forced-choice contrast discrimination task. Trial-by-trial neural variability was quenched by ϳ40% after the presentation of the stimulus relative to the variability apparent before stimulus presentation, yet there were large differences in the magnitude of variability quenching across subjects. Individual magnitudes of quenching predicted individual discrimination capabilities such that subjects who exhibited larger quenching had smaller contrast discrimination thresholds and steeper psychometric function slopes. Furthermore, the magnitude of variability quenching was strongly correlated with a reduction in broadband EEG power after stimulus presentation. Our results suggest that neural variability quenching is achieved by reducing the amplitude of broadband neural oscillations after sensory input, which yields relatively more reproducible cortical activity across trials and enables superior perceptual abilities in individuals who quench more.

Neural activity during repeated presentations of a sensory stimulus exhibits considerable trial-by-trial variability. Previous studies have reported that trial-by-trial neural variability is reduced (quenched) by the presentation of a stimulus. However, the functional significance and behavioral relevance of variability quenching and the potential physiological mechanisms that may drive it have been studied only rarely. Here, we recorded neural activity with EEG as subjects performed a two-interval forced-choice contrast discrimination task. Trial-by-trial neural variability was quenched by ϳ40% after the presentation of the stimulus relative to the variability apparent before stimulus presentation, yet there were large differences in the magnitude of variability quenching across subjects. Individual magnitudes of quenching predicted individual discrimination capabilities such that subjects who exhibited larger quenching had smaller contrast discrimination thresholds and steeper psychometric function slopes. Furthermore, the magnitude of variability quenching was strongly correlated with a reduction in broadband EEG power after stimulus presentation. Our results suggest that neural variability quenching is achieved by reducing the amplitude of broadband neural oscillations after sensory input, which yields relatively more reproducible cortical activity across trials and enables superior perceptual abilities in individuals who quench more.

Numerous studies have shown that neural activity in sensory cortices is remarkably variable over time and across trials even when subjects are presented with an identical repeating stimulus or task. This trial-by-trial neural variability is relatively large in the prestimulus period and considerably smaller (quenched) following stimulus presentation. Previous studies have suggested that the magnitude of neural variability affects behavior such that perceptual performance is better on trials and in individuals where variability quenching is larger. To what degree are neural variability magnitudes of individual subjects flexible or static? Here, we used EEG recordings from adult humans to demonstrate that neural variability magnitudes in visual cortex are remarkably consistent across different tasks and recording sessions. While magnitudes of neural variability differed dramatically across individual subjects, they were surprisingly stable across four tasks with different stimuli, temporal structures, and attentional/cognitive demands as well as across experimental sessions separated by one year. These experiments reveal that, in adults, neural variability magnitudes are mostly solidified individual characteristics that change little with task or time, and are likely to predispose individual subjects to exhibit distinct behavioral capabilities.

Study Objectives Sleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow-wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD. Methods In this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children. Results Children with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow-wave sleep in comparison to controls. This difference was largest during the first 2 hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents. Conclusions These results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD.

Attention can be subdivided into several components, including alertness and spatial attention. It is believed that the behavioral benefits of attention, such as increased accuracy and faster reaction times, are generated by an increase in neural activity and a decrease in neural variability, which enhance the signal-to-noise ratio of task-relevant neural populations. However, empirical evidence regarding attention-related changes in neural variability in humans is extremely rare. Here we used EEG to demonstrate that trial-by-trial neural variability was reduced by visual cues that modulated alertness and spatial attention. Reductions in neural variability were specific to the visual system and larger in the contralateral hemisphere of the attended visual field. Subjects with higher initial levels of neural variability and larger decreases in variability exhibited greater behavioral benefits from attentional cues. These findings demonstrate that both alertness and spatial attention modulate neural variability and highlight the importance of reducing/quenching neural variability for attaining the behavioral benefits of attention.

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Neural activity fluctuates over time, creating considerable variability across trials. This trial-by-trial neural variability is dramatically reduced (“quenched”) after the presentation of sensory stimuli. Likewise, the power of neural oscillations, primarily in the alpha-beta band, is also reduced after stimulus onset. Despite their similarity, these phenomena have so far been studied and discussed independently. We hypothesized that the two phenomena are tightly coupled in electrophysiological recordings of large cortical neural populations. To test this, we examined magnetoencephalography (MEG) recordings of healthy subjects viewing repeated presentations of a visual stimulus. The timing, amplitude, and spatial topography of variability-quenching and power-suppression were remarkably similar. Neural variability quenching was eliminated by excluding the alpha-beta band from the recordings, but not by excluding other frequency-bands. Moreover, individual magnitudes of alpha-beta band-power explained 86% of between-subject differences in variability quenching. An alternative mechanism that may generate variability quenching is increased phase alignment across trials. However, changes in inter-trial-phase-coherence (ITPC) exhibited distinct timing and no correlations with the magnitude of variability quenching in individual participants. These results reveal that neural variability quenching is tightly coupled with stimulus-induced changes in the power of alpha-beta band oscillations, associating two phenomena that have so far been studied in isolation.