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Raposo, I.

Publications and source records attributed to Raposo, I..

3 recordsLinked to original sources

Volitional stopping is preceded by a transient beta oscillation

Human motor cortex EEG beta (15-30 Hz) oscillations undergo transient power modulations (bursts) during volitional control of movements. They are a potential control signal for brain-machine interfaces and are a therapeutic target in Parkinsons disease. The prevailing view is that EEG beta bursts increase during stopping and immobility, but do not precede stopping. In contrast to prior work in humans and animals that used a latent and unobservable stopping time in the stop-signal task, we developed a translational animal model to align EEG with overt action stopping. We recorded 32-electrode EEG along with the angular velocity of a treadmill while head-fixed rats stopped in-progress running on a freely-rotating, non-motorized treadmill. Contrasting prior work, motor cortex beta bursts increased before stopping and not during stopping or immobility. Using information theoretic measures, we show that beta power was informative about treadmill velocity 200 msec in the future, but only during planning to stop. By introducing artificial temporal jitter to mimic the estimation of stopping time used in prior work, we show that this predictive brain-action relationship fails with even small jitter. Finally, we use a variety of machine learning methods to show that, despite EEG beta oscillations being a clear neural correlate preceding stopping, it has limited utility for real-time action decoding. Our work suggests a new conceptual model for neural control of action stopping.

neuroscience↗

Periodic neglect after frontoparietal lesions provides causal evidence for rhythmic attention sampling

Contemporary models conceptualize spatial attention as a blinking spotlight that sequentially samples visual space. Hence, behavior fluctuates over time even in states of presumed sustained attention. Recent evidence suggested that rhythmic neural activity in the frontoparietal network constitutes the functional basis of rhythmic attentional sampling. However, causal evidence to support this notion remains absent. Using a lateralized spatial attention task, we addressed this issue in patients with focal lesions in the frontoparietal attention network. Our results uncovered that frontoparietal lesions introduce periodic neglect, i.e., temporally-specific behavioral deficits that were aligned with the underlying neural oscillations. Attention-guided perceptual sensitivity was on par with healthy controls during optimal phases but attenuated during the less excitable sub-cycles. Theta-dependent sampling (3 - 8 Hz) was causally dependent on prefrontal cortex, while alpha-band sampling (8 - 14 Hz) emerged from parietal areas. Collectively, our findings reveal that lesion-induced high amplitude, low frequency brain activity is not epiphenomenal, but has immediate behavioral consequences. More generally, these results provide causal evidence for the hypothesis that the functional architecture of attention is inherently rhythmic.

neuroscience↗

Brightness illusions evoke pupil constriction and a visual cortex response in rats

The mind affects the body via central nervous system (CNS) control of the autonomic nervous system (ANS). In humans, one striking illustration of the mind-body connection is that illusions, subjectively perceived as bright, drive constriction of the eyes pupil by activating the sympathetic arm of the ANS. How the CNS is involved in this pupil response is unknown and requires an animal model for intracerebral investigation of potential regions, cell types, and neuronal projections. However, the physiological response to this illusion has long been thought to occur only in humans. Here, we report that the same brightness illusion that evokes pupil constriction in humans also does so in rats. Cortex-wide EEG recordings revealed that, compared to a luminance-matched control stimulus, the illusion (which appears subjectively brighter to humans) evoked a larger response only in primary visual cortex (V1). This cortical response preceded pupil constriction by ~335 msec suggesting a potential causal role for V1 on the pupil. Our results establish a new animal model of importance for studying how the CNS response involved in sensing a brightness illusion drives a physiological reaction in the body. We provide objective evidence that complex mind-body connections are not confined to humans and that V1 may be part of a shared, mammalian, neural network for bodily reactions to illusions.

neuroscience↗