Cortical excitability is assumed to depend on cortical arousal level in an inverted U-shaped fashion: Largest (optimal) excitability is usually associated with medium levels of arousal. It has been proposed that under conditions of low arousal, compensatory effort is exerted if attentional demands persist. People tend to avoid this resource-consuming top–down compensation by creating or selecting environmental conditions that provide sufficient bottom–up stimulation. These assumptions were tested in an attention-demanding dual-task situation: We combined a simulated driving task to induce three different arousal levels by varying stimulation (high vs. low vs. self-chosen) with a visual two-stimulus paradigm to assess cortical excitability by the initial contingent negative variation (iCNV) component of the event-related potential. Additionally, we analyzed the oscillatory power of the beta2 band of the electroencephalogram at anterior frontal sites, which is assumed to reflect low-arousal compensatory activity. The iCNV amplitude differed in all three arousal conditions as expected: It was highest in the condition of self-chosen stimulation and lowest in the low- and high-arousal conditions. Additionally, in the low-arousal condition, anterior frontal beta2 power was found to be significantly higher than in the other two conditions and correlated positively with subjective strain. This pattern of results suggests that subjects select medium levels of stimulation which optimize cortical excitability under attentional demand conditions. The elevated fronto-central beta2 power in the low-stimulation condition may indicate the involvement of the anterior cingulate cortex in compensating for reduced arousal by top–down stimulation of the noradrenergic arousal system.

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.