It is a prominent idea that cognitive control mediates conflict adaptation, in that response conflict in a previous trial triggers control adjustments that reduce conflict in a current trial. In the present EEG study, we investigated the dynamics of cognitive control in a response-priming task by examining the effects of previous trial conflict on intertrial and current trial oscillatory brain activities, both on the electrode and the source level. Behavioral results showed conflict adaptation effects for RTs and response accuracy. Physiological results showed sustained intertrial effects in left parietal theta power, originating in the left inferior parietal cortex, and midcentral beta power, originating in the left and right (pre)motor cortex. Moreover, physiological analysis revealed a current trial conflict adaptation effect in midfrontal theta power, originating in the ACC. Correlational analyses showed that intertrial effects predicted conflict-induced midfrontal theta power in currently incongruent trials. In addition, conflict adaptation effects in midfrontal theta power and RTs were positively related. Together, these findings point to a dynamic cognitive control system that, as a function of previous trial type, up- and down-regulates attention and preparatory motor activities in anticipation of the next trial.

Although it is widely accepted that serotonin plays a pivotal role in the modulation of anxiety- and depression-related personality traits as well as in the pathogenesis of anxiety disorders and depression, the role of serotonin in cognition is less clear. In the present study, we investigated the involvement of serotonin in cognitive behaviors by examining the impact of genetic variation in key regulators of serotonergic neurotransmission on behavioral measures in a cognitive control task. Eighty-five healthy participants performed a cued continuous performance task (the AX Continuous Performance Task [AXCPT]) and were genotyped for polymorphisms in the transcriptional control regions of the tryptophan hydroxylase 2 gene (TPH2 G-703T; rs4570625) and the serotonin transporter gene (5-HTTLPR). The core result was that individuals lacking the rare TPH2 T allele were not faster than T allele carriers, but committed fewer errors and were less variable in responding. These findings parallel those of a recent study where an enhancement of executive control in individuals without the rare TPH2 T/T genotype was observed. Together with recent evidence that individuals without the T allele exhibit higher scores in anxiety- and depression-related personality traits, our results underscore the role of the TPH2 G-703T polymorphism in the modulation of behavior and raise the intriguing possibility that genetic variants associated with higher negative emotionality may have beneficial effects on some cognitive functions.