Studies in both pathological and healthy samples have suggested altered functional connectivity between orbitofrontal cortex (OFC) and amygdala as a possible cause of anger and aggression. In patient populations presenting with pathological aggression, there is also evidence for changes in structural connectivity between OFC and amygdala. In healthy samples, however, the relationship between white matter integrity and aggression has not been studied to date. Here, we investigated the relationship between trait aggressiveness and structural OFC-amygdala connectivity in a large sample (n = 93) of healthy young men. Using diffusion tensor imaging, we measured the distribution of fractional anisotropy and mean diffusivity along the uncinate fascicle bilaterally. We found no differences in either measure between participants high and low in physical aggressiveness, or between those high and low in trait anger. Our results therefore argue against a direct relationship between structural OFC-amygdala connectivity and normal-range trait aggressiveness.

To examine the reproducibility of the Stroop effect, behavioral data from 22 healthy female individuals were repeatedly (three-month interval between two separate measurement sessions) obtained while performing a color-choice Stroop task under realistic magnetic resonance imaging (MRI) and electroencephalography (EEG) laboratory conditions. At the group statistical level, the Stroop effect, indicated by longer response times for incongruent than for congruent stimulus conditions, was consistently present for almost all examined measurement levels. However, differential effects of laboratory contexts on retest reproducibility were observed across repeated measurement levels, both within and between sessions. These results challenge existing theories about the underlying nature of Stroop interference processing. It appears necessary to apply a multitheoretical approach, because intraindividual variability within and across measurement sessions suggests potential fluctuations in the individual mental strategies applied, recruitment of varying memory resources, the influence of mediator variables such as working memory capacity and/or attention, and many more possible variations. Single-observation studies run the risk of favoring a single theoretical concept and therefore underestimating the individual factor. We further conclude that dependent analysis-of-variance statistics are a more fit test for reproducibility than are correlative reliability estimations.

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Many studies point toward volume reductions in the amygdala as a potential neurostructural marker for trait aggression. However, most of these findings stem from clinical samples, rendering unclear whether the findings generalize to non-clinical populations. Furthermore, the notion of neural networks suggests that interregional correlations in grey matter volume (i.e., structural covariance) can explain individual differences in aggressive behavior beyond local univariate associations. Here, we tested whether structural covariance between amygdala subregions and the rest of the brain is associated with self-reported aggression in a large sample of healthy young students (n=263; 51% women). Salivary testosterone concentrations were measured for a subset of n=76 participants (45% women), allowing us to investigate the influence of endogenous testosterone on structural covariance. Aggressive individuals showed enhanced covariance between superficial amygdala (SFA) and dorsal anterior insula (dAI), but lower covariance between laterobasal amygdala (LBA) and dorsolateral prefrontal cortex (dlPFC). These structural patterns overlap with functional networks involved in the genesis and regulation of aggressive behavior, respectively. With increasing endogenous testosterone, we observed stronger structural covariance between centromedial amygdala (CMA) and medial prefrontal cortex in men and between CMA and orbitofrontal cortex in women. These results speak for structural covariance of amygdala subregions as a robust correlate of trait aggression in healthy individuals. Moreover, regions that showed structural covariance with the amygdala modulated by either testosterone or aggression did not overlap, speaking for a more complex role of testosterone in human social behavior rather than the simple assumption that testosterone only increases aggressiveness.

Appropriate social behavior in aggressive-provocative interactions is a prerequisite for a peaceful life. In previous research, the dysfunctions of the control of aggression were suggested to be modulated by enhanced bottom-up (sub-cortically driven) and reduced top-down (iso-cortical frontal) processing capability. In the present study, two groups of individuals with enhanced (EG) and normal (NG) experiences of violent acts during their socialization made binary behavioral decisions in quasi-realistic social interactions. These interactions were presented in short video clips taken from a first-person perspective. The video clips showed social interaction scenarios oriented on realistic everyday life situations. The behavioral data supported the distinct affective qualities of three categories of social interactions. These categories were labeled as aggressive–provocative, social–positive, and neutral–social interactions. Functional neuroimaging data showed extended activation patterns and higher signal intensity for the NG compared to the EG in the lateral inferior frontal brain regions for the aggressive provocative interactions. Furthermore, the peri-aqueductal gray (PAG) produced enhanced activations for the affective interaction scenarios (i.e., aggressive-provocative and social-positive) in both groups and as a trend with the medium effect size for the neutral interactions in the EG. As the individuals in the EG did not show open aggression during the functional MRIA (fMRI) investigation, we concluded that they applied individual self-control strategies to regulate their aggressive impulses immediately. These strategies appeared to be top-down regulated through the dorsal frontal brain areas. The predominant recruitment of the heteromodal cortices during the neural processing of complex social interactions pointed to the important role of the learning history of individuals and their socialization with differing levels of violent experiences as crucial modulators in convicts. Our data suggest that building or strengthening the association between prototypical social contexts (e.g., aggressive-provocative interactions) and appropriate behaviors as a response to it provides a promising approach to successfully re-socialize people with a delinquent history.