As many paths lead to aggression, understanding which situations and which person-specific traits facilitate or impede aggressive behavior is crucial. Provocation is among one of the most frequently reported predictors of aggressive behavior. However, it remains unclear whether the reaction to provocation is universal across different forms of aggression and whether individuals differ in their reactivity to such signals. Using the Taylor Aggression Paradigm (TAP), we investigated the influence of individual and contextual factors on physical and non-physical aggression in healthy men and women. The impact of trait aggression, sex, provocation, and the success of a competition against a fictitious opponent on aggressive behavior was examined in three different versions of the TAP. While equal provocation and punishment modalities were used in the first two versions, monetary deductions in the first and heat stimulus in the second study, the third experiment used non-physical provocation to trigger physical punishment. Trial-by-trial analyses revealed that provocation, independent of its specific nature, is a strong predictor for aggressive behavior, especially in highly aggressive participants. Although women initially showed less aggression than men, sex differences were diminished under prolonged, increasing provocation when provocation and punishment modality were identical. Only when modalities diverged, women, compared with men, were more hesitant to punish their opponent. These results, thus, extend evidence that women show lower levels of aggression under low provocation. However, high levels of provocation have similar effects on males’ and females’ reactive aggressive behavior across different forms of aggression. When competing for money, losing against the fictitious opponent was functioning as an additional provocative signal stimulating aggressive responses. Differences in aggressive responding have to be interpreted in the context of the specific type of provocation and aggression that is investigated since these modalities are shown to interact with individual characteristics.

Increased aggression and impulsivity represent a key component of several psychiatric disorders, including substance use disorder, which is often associated with deficient prefrontal brain activation. Thus, innovative tools to increase cognitive control are highly warranted. The current study investigates the potential of transcranial direct current stimulation (tDCS), a tool to modulate cortical activation, to increase cognitive control in individuals with a high potential for impulsive and aggressive behavior. In a double-blind, sham-controlled study, we applied anodal tDCS over the right dorsolateral prefrontal cortex in an all-male sample of alcohol dependent patients (AD), tobacco users (TU) and healthy controls (HC) who completed the Taylor Aggression Paradigm and Stop Signal Task twice. While there were no observable effects of tDCS in controls, results revealed altered aggressive behavior in AD following active stimulation. Specifically, these individuals did not show the standard increase in aggression over time seen in the other groups. Furthermore, improved response inhibition was found in AD and TU following active but not sham stimulation. Our study demonstrates that prefrontal tDCS improves our laboratory measure of impulse control in at-risk groups, illustrating the importance of sample characteristics such as nicotine intake and personality traits for understanding the effects of brain stimulation.

Aggression and psychopathy are multifaceted conditions determined interpersonal and antisocial factors. Only a few studies analyze the link between these separate factors and specific brain morphology distinctively. A voxel-based morphometry (VBM) analysis was performed on 27 violent offenders and 27 controls aiming to associate sub-features of aggressive and psychopathic behavior with specific gray matter volumes. Trait aggression was assessed using two self-report tests (Aggression Questionnaire, AQ, and Reactive-Proactive-Aggression Questionnaire, RPQ) and psychopathy with the Psychopathy Checklist-Revised (PCL-R). Total and sub-scale scores of these tests were correlated to the brain morphometry of the offenders group in separate analyses. It was found that psychopathic behavior was negatively correlated with prefrontal gray matter volume and that this result was primarily driven by the antisocial behavior sub-scale of the PCL-R. Furthermore, less gray matter in right superior frontal and left inferior parietal regions with increasing antisocial behavior could be observed. One cluster comprising the right middle and superior temporal gyrus was negatively correlated with both, reactive aggression and antisocial behavior. These results outline (1) the importance of distinctively analyzing sub-features that contribute to aggressive and psychopathic behavior, given that the negative correlation of psychopathy global scores with prefrontal volume was driven by one single facet of the PCL-R scale (antisocial behavior). Moreover, these results indicate (2) frontotemporo-parietal network deficits in antisocial, criminal offenders, with a particular strong effect in the temporal lobe.

Opioid addiction is a chronic, relapsing disorder associated with persistent changes in brain plasticity. Reconfiguration of neuronal connectivity may explain heightened abuse liability in individuals with a history of chronic drug exposure. To characterize network-level changes in neuronal activity induced by chronic opiate exposure, we compared FOS expression in mice that are morphine-naïve, morphine-dependent, or have undergone 4 wk of withdrawal from chronic morphine exposure, relative to saline-exposed controls. Pairwise interregional correlations in FOS expression data were used to construct network models that reveal a persistent reduction in connectivity strength following opiate dependence. Further, we demonstrate that basal gene expression patterns are predictive of changes in FOS correlation networks in the morphine-dependent state. Finally, we determine that regions of the hippocampus, striatum, and midbrain are most influential in driving transitions between opiate-naïve and opiate-dependent brain states using a control theoretic approach. This study provides a framework for predicting the influence of specific therapeutic interventions on the state of the opiate-dependent brain.

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Elevated levels of risk‐taking behavior as well as affective instability are both cardinal features of Borderline Personality Disorder (BPD). To our knowledge, there are no studies which directly investigate underlying affective processes of risk‐taking behavior in BPD, despite the centrality of affect in BPD symptomatology, and indications of affective dysregulation contributing to increased risk‐taking behavior in BPD. Here, we examined risk‐taking behavior in BPD and its underlying affective processes, using skin conductance responses (SCRs) as a proxy. Twenty‐three individuals with BPD and 24 healthy controls performed a modified version of the Balloon Analogue Risk Task, where decisions take place over a time scale of several seconds, enabling us to investigate a continuous integral of SCRs in anticipation of decisions. We used trial‐by‐trial mixed model analyses to account for within‐ and between‐participant effects, as well as large variability that are often observed in SCRs. In contrast to healthy controls, who showed elevated SCRs in response to high risk, individuals with BPD did not show differential physiological sensitivity towards different risk levels. In addition, increased SCRs––under low risk––were related to more cautious risk‐taking behavior in HCs. However, increased SCRs under low risk in BPD were related to greater risk‐taking behavior. Alterations in the processing of affective signals, such as SCRs in the context of risk, may impair adaptation to environmental demands and may lead to increased risk‐taking behavior in BPD.