Delta phase reset predicts conflict-related changes in P3 amplitude and behavior

When multiple competing responses are activated, we respond more slowly than if only one response is activated (response conflict). Conflict-induced slowing is reduced for consecutive high-conflict stimuli, an effect known as conflict adaptation. Verguts and Notebaert's (2009) adaptation by binding theory suggests this is due to Hebbian learning of cognitive control, potentiated by the response of the locus coeruleus norepinephrine (NE) system. Phasic activity of the NE system can potentially be measured non-invasively in humans by recording the P3 component of the event-related potential (ERP), and the P3 is sensitive to conflict adaptation. Bouret and Sara's (2005) network reset theory suggests that phasic NE might functionally reset ongoing large-scale network activity, generating synchronous neural population activity like the P3. To examine the possibility that network reset contributes to conflict effects in the P3, we recorded high-density EEG data while subjects performed a flanker task. As expected, conflict and conflict adaptation modulated P3 amplitudes. Brain-behavior correlation analyses indicated that activity during the rise of the P3 was related to RT and predicted RT differences due to conflict. More importantly, phase of delta oscillations not only predicted reaction time differences between low-conflict and high-conflict conditions, but delta phase reset also predicted the amplitude of the P3. Delta oscillations exhibited dominant peaks both pre and post-stimulus, and delta at stimulus onset predicted the post-stimulus ERP, in particular the N2 and P3. This result bridges human EEG with basic mechanisms suggested by computational neural models and invasive patient recordings, namely that salient cognitive events might reset ongoing oscillations leading to the generation of the phase-locked evoked potential. We conclude that partial phase reset is a cortical mechanism involved in monitoring the environment for unexpected events, and this response contributes to conflict effects in the ERP. These results are in line with theories that phasic NE release might reset ongoing cortical activity, leading to the generation of ERP components like the P3.