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Kirschner, H.

Publications and source records attributed to Kirschner, H..

5 recordsLinked to original sources

Transcranial ultrasound stimulation of the aMCC transiently improves performance, modulates N2 and conflict monitoring dynamics

Conflict monitoring and error processing are fundamental mechanisms underlying cognitive control and adaptive behavior and have been consistently associated with increased activity in the anterior midcingulate cortex (aMCC). Here, we used transcranial ultrasound stimulation (TUS), an emerging technique that enables non-invasive, deep, and focal neuromodulation, and EEG to investigate the causal role of the aMCC in cognitive control. Our findings demonstrate that TUS of aMCC improved performance, modulated the relationship between conflict monitoring and the stimulus-locked N2, and strengthened the suppression of distracting flankers as revealed by drift-diffusion model analyses. This suggests that TUS of aMCC enhances proactive control. Interestingly, TUS did not affect the error-related negativity as a measure of error monitoring. Finally, the TUS effects were observed during early compared with later task blocks corroborating previous findings which suggested that TUS effects are temporally dynamic and characterized by a limited post-stimulation window. HIGHLIGHTSO_LIaMCC-TUS and PCC-TUS both increase behavioral accuracy during the early stages of task performance. C_LIO_LIaMCC-TUS transiently reduces the effect of incongruence on the stimulus-locked N2 suggesting reduced response conflict. C_LIO_LIExploratory DDM analyses suggest that aMCC-TUS improves suppression of conflict- inducing distractors. C_LIO_LIaMCC thus selectively enhances proactive control, thereby reducing response conflict. C_LIO_LITUS effects show a transient temporal profile, peaking 17-27 minutes after stimulation and declining after [~]37 minutes. C_LI

neuroscience↗

Sleep deprivation disrupts error awareness and subsequent behavioural regulation

Sleep deprivation is known to impair cognitive performance, yet its effects on error awareness and subsequent behavioral adjustments remain incompletely understood. Here, we investigated how sleep loss affects the use of subjective performance evaluation to guide post-error adaptations. Thirty healthy adults completed a novel, gamified error awareness multi-rule Simon task once while well rested and once after 24 h of total sleep deprivation. On each trial, participants reported both their task response and subjective evaluation of response accuracy. This design allowed us to dissociate objective performance from subjective error awareness and to examine their influence on subsequent behavior over time. Sleep deprivation slowed responses, reduced accuracy, increased missed responses, and decreased the proportion of consciously detected errors. These effects increased with time on task and were accompanied by greater instability in sustained attention. Critically, post-error adjustments were driven by subjective error awareness rather than factual error commission. Reaction times slowed most strongly after subjectively perceived errors, including instances in which the preceding response had been objectively correct. Accuracy showed post-error decreases that were most pronounced following unaware errors. Sleep deprivation further altered these awareness-dependent control processes, particularly in later task phases. Together, these findings indicate that sleep deprivation disrupts both error awareness and the effective use of awareness signals for behavioral regulation. Statement of significanceOne night of total sleep deprivation reduces behavioral error awareness and disrupts post-error adjustments in a time-dependent manner. Crucially, our findings show that adaptive cognitive control is strongly shaped by subjective error awareness--even when that awareness is inaccurate. By identifying conscious performance evaluation as a key mechanism linking sustained attention, sleep loss, and behavioral regulation, this work highlights the importance of considering subjective awareness when studying adaptive control under fatigue.

neuroscience↗

Methamphetamine-induced adaptation of learning rate dynamics depend on baseline performance.

The ability to calibrate learning according to new information is a fundamental component of an organisms ability to adapt to changing conditions. Yet, the exact neural mechanisms guiding dynamic learning rate adjustments remain unclear. Catecholamines appear to play a critical role in adjusting the degree to which we use new information over time, but individuals vary widely in the manner in which they adjust to changes. Here, we studied the effects of a low dose of methamphetamine (MA), and individual differences in these effects, on probabilistic reversal learning dynamics in a within-subject, double-blind, randomized design. Participants first completed a reversal learning task during a drug-free baseline session to provide a measure of baseline performance. Then they completed the task during two sessions, one with MA (20 mg oral) and one with placebo (PL). First, we showed that, relative to PL, MA modulates the ability to dynamically adjust learning from prediction errors. Second, this effect was more pronounced in participants who performed moderately low at baseline. These results present novel evidence for the involvement of catecholaminergic transmission on learning flexibility and highlights that baseline performance modulates the effect of the drug.

neuroscience↗

Cortical beta power reflects a neural implementation of decision boundary collapse in a speeded flanker task

A prominent account of decision-making assumes that information is accumulated until a fixed response threshold is crossed. However, many decisions require weighting of information appropriately against time. Collapsing response thresholds are a mathematically optimal solution to this decision problem. However, our understanding of the neurocomputational mechanisms that underly dynamic response thresholds remains very incomplete. To investigate this issue, we used a multistage drift diffusion model (DDM) and also analysed EEG beta power lateralization (BPL). The latter served as a neural proxy for decision signals. We analysed a large dataset (n=863) from a speeded flanker task and data from an independent confirmation sample (n=119). We show that a DDM with collapsing decision thresholds, a process where the decision boundary reduces over time, captured participants time-dependent decision policy better than a model with fixed thresholds. Previous research suggests that BPL over motor cortices reflects features of a decision signal and that its peak may serve as a neural proxy for the decision threshold. Our findings offer compelling evidence for the existence of collapsing decision thresholds in decision-making processes.

neuroscience↗

Feedback-related EEG dynamics separately reflect decision parameters, biases, and future choices

Optimal decision making in complex environments requires dynamic learning from unexpected events. To speed up learning, we should heavily weight information that indicates state-action-outcome contingency changes and ignore uninformative fluctuations in the environment. Often, however, unrelated information is hard to ignore and can potentially bias our learning. Here we used computational modelling and EEG to investigate learning behaviour in a modified probabilistic choice task that introduced two types of unexpected events that were irrelevant for optimal task performance, but nevertheless could potentially bias learning: pay-out magnitudes were varied randomly and, occasionally, feedback presentation was enhanced by visual surprise. We found that participants overall good learning performance was biased by distinct effects of these non-normative factors. On the neural level, these parameters are represented in a dynamic and spatiotemporally dissociable sequence of EEG activity. Later in feedback processing the different streams converged on a central to centroparietal positivity reflecting a final pathway of adaptation that governs future behaviour.

neuroscience↗