Catecholaminergic Modulation of Conflict Control Depends on the Source of Conflicts.

ABSTRACT:

Background

To display goal-directed behavior, we must be able to resolve response conflicts that arise from processing various distractors. Such conflicts may be triggered by different kinds of distractor stimuli (e.g., priming and flanker stimuli), but it has remained largely unclear whether the functional and neurobiological underpinnings of both conflict types differ. We therefore investigated the functional relevance of the catecholamines dopamine and norepinephrine, which have been shown to increase the signal-to-noise ratio in neuronal processing and should therefore modulate response conflicts.

Methods

In a double-blind, randomized, placebo-controlled study design, we examined the effect of methylphenidate (0.5 mg/kg) on both flanker-induced and priming-induced response conflicts in a group of n=25 healthy young adults. We used EEG recordings to examine event-related potentials in combination with source localization analyses to identify the cognitive-neurophysiological subprocesses and functional neuroanatomical structures modulated by methylphenidate.

Results

Compared with placebo, methylphenidate decreased flanker conflicts. This was matched by increased congruency effects in the fronto-central N2/P3 event-related potential complex and associated with modulations in the right inferior frontal gyrus. In contrast to this, methylphenidate did not modulate the size of prime-evoked conflicts.

Conclusions

Our results suggest that catecholamine-driven increases in signal-to-noise ratio and neural gain control do not equally benefit differently evoked conflicts. This supports the hypothesis of an at least partly different neurobiological basis for flanker- and prime-evoked response conflicts. As the right inferior frontal gyrus plays an important role in inhibition, the catecholaminergic system may reduce flanker conflicts by supporting the inhibition of distracting information.

SUBMITTER: Bensmann W 

PROVIDER: S-EPMC6165959 | biostudies-literature |

REPOSITORIES: biostudies-literature