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Bächinger, M.

Publications and source records attributed to Bächinger, M..

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Pupil self-regulation modulates markers of cortical excitability and cortical arousal

The brains arousal state (i.e., central arousal) is regulated by multiple neuromodulatory nuclei in the brainstem and significantly influences high-level cognitive processes. By exploiting the mechanistic connection between the locus coeruleus (LC), a key regulator of central arousal, and pupil dynamics, we recently demonstrated that participants can gain volitional control over arousal-regulating centers including the LC using a pupil-based biofeedback approach. Here, we test whether pupil-based biofeedback modulates electrophysiological markers of cortical excitability, cortical arousal, and phasic LC activity. Combining pupil-based biofeedback with single-pulse TMS, EEG recordings, and an auditory oddball task revealed three main results: pupil self-regulation significantly modulates (i) cortical excitability, (ii) the EEG spectral slope, a marker of cortical arousal, and (iii) the P300 response to target tones, an event-related potential suggested to be tightly linked to phasic LC activity. Interestingly, pupil self-regulation strength was linearly linked to the modulation of the spectral slope, suggesting a common physiological mechanism. Here, we have shown that pupil-based biofeedback modulates fundamental aspects of brain function. Whether this method could further be used to modulate these aspects in case of disturbances associated with neurological and psychiatric disorders needs to be investigated in future studies.

neuroscience↗

Dynamic Causal Modelling Highlights the Importance of Decreased Self-Inhibition of the Sensorimotor Cortex in Motor Fatigability

Motor fatigability emerges when challenging motor tasks must be maintained over an extended period of time. It is a frequently observed phenomenon in everyday life which affects patients as well as healthy individuals. Motor fatigability can be measured using simple tasks like finger tapping at maximum speed for 30s. This typically results in a rapid decrease of tapping frequency, a phenomenon called motor slowing. In a previous study (Bachinger et al. 2019), we showed that motor slowing goes hand in hand with a gradual increase of activation in the primary sensorimotor cortex (SM1), supplementary motor area (SMA), and dorsal premotor cortex (PMd). Previous electrophysiological measurements further suggested that the increase in SM1 activity might reflect a breakdown of inhibition and, particularly, a breakdown of surround inhibition which might have led to heightened coactivation of antagonistic muscles. It is unclear what drives the activity increase in SM1 caused by motor slowing and whether motor fatigability affects the dynamic interactions between SM1 and upstream motor areas like SMA and PMd. Here, we performed dynamic causal modelling to answer this question. Our main findings revealed that motor slowing was associated with a significant reduction in SM1 self-inhibition which is in line with previous electrophysiological results. Additionally, the model revealed a significant decrease in the driving input to premotor areas suggesting that structures other than cortical motor areas might cause motor fatigability.

neuroscience↗