Biology subjects

Chalkley, N.

Publications and source records attributed to Chalkley, N..

2 recordsLinked to original sources

bioRxiv2026

Cortico-basal ganglia dynamics of global and selective response inhibition in humans

Response inhibition is an important cognitive control mechanism, which enables flexible behavior by stopping inappropriate actions. Intracranial recordings across species have identified a neural circuit that implements response inhibition via the subthalamic nucleus of the basal ganglia. However, this work has been limited to simple tasks, in which unequivocal, salient "stop"-signals require the inhibition of all ongoing responses. Notably, response inhibition in the real world is substantially different. Real-world response inhibition is selective: it occurs only after specific salient signals ( stimulus-selectivity) and stops only specific movements, while others continue ( response-selectivity). If and how the fronto-subthalamic system implements selective inhibition is largely unknown. Here, we recorded subthalamic local field potentials and scalp-EEG in humans performing a novel, selective inhibition task. Salient signals either required stopping all initiated responses (global inhibition), stopping only some responses (response-selective inhibition), or continuing all responses - i.e., ignoring the signal (which ensures stimulus-selectivity). All three signals initially triggered a common fronto-subthalamic inhibitory process, signified by a rapid increase in {beta}-burst activity. During global inhibition, subthalamic {beta}-bursting subsequently increased above baseline, persisting for over a second. During response-selective inhibition, this activity was delayed, which enabled a second bout of disinhibition and allowed appropriate responses to continue. Throughout this period, frontal cortical and subthalamic {beta}-band activity was tightly coupled. This shows that selective inhibition is implemented through rapid, context-dependent engagement and release of fronto-subthalamic inhibition. Moreover, subthalamic activity lasted substantially longer than assumed by classic behavioral-computational models. This supports recent theoretical models that assume protracted response inhibition during action-stopping.

neuroscience↗

bioRxiv2025

Pupil dilation indexes - but does not causally influence - conscious error detection: a double-blind, placebo-controlled investigation of performance-monitoring using atomoxetine.

BackgroundConscious error detection is accompanied by error-related changes in phasic autonomic activity. This autonomic response is diminished in older age - accompanied by impairments in the conscious detection of action errors - i.e., increased error blindness. Indeed, the degree to which the autonomic response to errors declines across the lifespan is correlated with the increase in error blindness. However, the direction of causality - whether changes in autonomic reactivity are a consequence or cause of increased error blindness - is still debated. In the present study, we experimentally modulated the phasic autonomic response to action errors in healthy older adults while measuring their conscious error detection. MethodsAcross two sessions, thirty healthy older adults (60-80 years old) were given the sNRI atomoxetine or placebo in a double-blind fashion. In each session, they performed an anti-saccade task, which is commonly used to test conscious error detection. The autonomic response to errors was measured via changes in pupil dilation. A novelty-oddball task was also employed as a manipulation check. ResultsAtomoxetine reduced phasic pupil dilation to both novel stimuli in the novelty-oddball task and to action errors in the anti-saccade task. However, despite this blunting of the phasic autonomic response to errors, there were no significant differences in conscious error awareness between atomoxetine and placebo. Primary task performance was also unaffected. ConclusionsDespite its effects on phasic autonomic activity after errors, atomoxetine had no effect on conscious error detection in healthy older adults. This suggests that phasic autonomic activity is a consequence, rather than a contributing factor, to conscious error awareness. It also suggests that changes to phasic autonomic activity is unlikely to explain increased error blindness in older age.

neuroscience↗