Macià Buades-Rotger

Individuals with hostile expectations (HEX) anticipate harm from seemingly neutral or ambiguous stimuli, and this can trigger antisocial behaviour. However, it is unclear how HEX are acquired, how the level of environmental threat affects the learning process, and to what extent HEX acquisition predicts real-world measures of antisocial thought, conduct, and personality. In an online sample of healthy young individuals (n=256, 70% women), we administered a virtual shooting task and employed computational modelling of behaviour to investigate HEX learning under high and low threat, respectively. We found that HEX acquisition was best explained by a two-level hierarchical Bayesian model of reinforcement learning, and that a threatening context facilitated HEX. The tendency to shoot under threat was correlated with hostile appraisals of angry faces in a separate task, which speaks for a general hostility bias across learning and perception. Crucially, we also examined whether computati...

Social interactions can be stressful, especially if they involve provocation or ambiguity. At the same time, such interactions necessitate social cognition. The question thus arises how stress affects social cognition and how personality attributes modulate this effect. The aim of the current study was to investigate the link between emotional reactivity, physical exercise, and social cognition under stress. As a measure of social cognition, we used spontaneous perspective taking, i.e., the degree to which participants represented the mental state of another agent. Studying young female participants, we investigated how physiological regulation, measured through resting heart-rate variability, is related to spontaneous social perspective taking under stress, and to predicted anger in an ambiguous social scenario. When controlling for resting heart rate, vagally mediated heart-rate variability was negatively correlated with the effect of stress on perspective taking, indicating that good physiological regulation supports social cognition under stress. Further, participants who reported to exercise at least once a week showed higher perspective taking under stress than less active participants. Finally, we found tentative evidence for participants who exercised regularly to show reduced predicted anger in response to an ambiguous provocation. Our findings suggest that good physiological regulation and regular physical exercise support social cognition under stress.

Social cognition allows humans to understand and predict other people’s behavior by inferring or sharing their emotions, intentions and beliefs. Few studies have investigated the impact of one’s own emotional state on understanding others. Here, we tested the effect of being in an angry state on empathy and theory of mind (ToM). In a between-groups design we manipulated anger status with different paradigms in three studies (autobiographical recall (N = 45), negative feedback (N = 49), frustration (N = 46)) and checked how this manipulation affected empathic accuracy and performance in the EmpaToM. All paradigms were successful in inducing mild anger. We did not find the expected effect of anger on empathy or ToM performance but observed small behavioral changes. Together, our results validate the use of three different anger induction paradigms and speak for rather weak behavioral effects of mild state anger on empathy and ToM.

Implicit measures of aggressiveness are able to circumvent response biases that plague self-reports, but it is unclear how they link to neural activation during aggressive interactions and to aggression-related endocrine function. Here, we tested whether an implicit attentional bias toward antisocial semantic information was associated with endogenous testosterone (T) and cortisol (C) levels, as well as with aggressive behavior and amygdala reactivity to angry faces in a separate competitive paradigm. On Day one, participants (39 healthy young women) completed an emotional word Stroop task in which they had to indicate the font color of antisocial, prosocial, or neutral words. On Day two, we measured subjects' brain activity during a competitive reaction time task in which the female opponent displayed angry or neutral facial expressions at the start of each trial and provoked participants with increasingly strong sound blasts. T and C were measured in saliva during a regular weekday as well as before and after scanning. We previously showed that aggression was associated with enhanced amygdala reactivity to angry faces in this sample. The present analyses revealed that subjects were slower to identify the font color of antisocial relative to neutral words, and that this attentional bias predicted higher aggression. T and C were uncorrelated with Stroop scores. Crucially, the relationship between implicit attention to antisocial words and aggression was mediated by amygdala reactivity to angry faces. Our data indicate that a tendency to dwell on implicit hostile cues reflects enhanced responsivity to overt anger displays.

Cultural differences in aggression are still poorly understood. The purpose of this article is to assess whether a tool for measuring aggression has the same meaning across cultures. Analyzing samples from Spain (n=262), US (n=344) and Hong-Kong (n=645), we used confirmatory factor analysis to investigate measurement invariance of the refined version of the Aggression-Questionnaire (Bryant & Smith, 2001). The measurement of aggression was more equivalent between the Chinese and Spanish versions than between these two and the American version. Aggression does not show invariance at the culture level. Cultural variables such as affective autonomy or individualism may influence the meaning of aggression. Aggressive behavior models can be improved by incorporating cultural variables.

Short- and long-term treatment with glucocorticoids is widely used in clinical practice and frequently induces features of iatrogenic Cushing syndrome, such as abdominally centered weight gain. Despite decades of glucocorticoids usage, the mechanisms underlying these side effects are still only partly understood. One possibility is that glucocorticoids impact subcortical (hypothalamus, amygdala, insula) and cortical (orbitofrontal and cingulate cortex) brain regions involved in appetite regulation and reward processing. In the present study, we used functional magnetic resonance imaging (fMRI) to study the acute effects of a prednisolone infusion on reactivity of brain reward systems to food stimuli. Twenty healthy normal-weight men were tested in a randomized, double-blind, cross-over study. After an overnight fast and infusion of either 250 mg prednisolone or placebo (always administered between 8 and 9 A M), fMRI scans were taken while presenting food and object pictures in a Go/NoGo (GNG) task. At home, participants were asked to register what they had eaten. On the following morning they came back to the lab and had a supervised ad libitum breakfast at a standardized buffet. Food-Go in contrast to Object-Go pictures yielded increased blood oxygen level dependent (BOLD) activity in hippocampus, amygdala, orbitofrontal cortex, insula and anterior cingulate cortex. Prednisolone increased activation in the bilateral amygdala and right insula for approach-associated food pictures. The buffet test did not reveal significant differences in calorie consumption or preferences of different macronutrients. However, prednisolone-induced insula reactivity to Food-Go images was associated with greater caloric intake, both at home and in the standardized buffet. In sum, we observed a specific effect of prednisolone on the BOLD response of the amygdala and insula to approach-associated food stimuli. As these brain areas have previously been implicated in hedonic eating, the present pattern of results may reflect an increased anticipated reward value of food modulated by glucocorticoids. These effects might potentially drive increased food intake and weight gain under prolonged glucocorticoid treatment.

Exogenous glucocorticoids are known to trigger affective changes, but these are highly variable across individuals. A better understanding of how synthetic glucocorticoids impact the processing of negative emotions in the human brain might help to predict such changes. In the present functional magnetic resonance imaging (fMRI) study, we sought to uncover the slow effects of a synthetic glucocorticoid infusion on the neural response to socio-emotional scenes using a within-participant, double-blind, placebo-controlled design. In two separate sessions, 20 young males were given either an intravenous prednisolone dose (250mg) or placebo in a cross-over, randomized order. Four hours later, they were scanned while viewing drawings of persons in a neutral or negative emotional situation. On the next morning participants provided a blood sample for serum cortisol measurement, which served as a manipulation check. Prednisolone strongly suppressed morning cortisol, and heightened brain reactivity to emotional stimuli in left amygdala, left caudate head, right inferior frontal gyrus, bilateral supplementary motor area, and right somatosensory cortex. Amygdala reactivity was related to lower self-reported fatigue and higher irritability in the prednisolone condition. Moreover, prednisolone blunted inferior frontal and amygdala connectivity with other regions of the emotion-processing neural circuitry. Our results suggest specific brain pathways through which exogenous glucocorticoids may labilize affect.

The steroid hormone testosterone (T) has been suggested to influence reactive aggression upon its action on the basolateral amygdala (BLA), a key brain region for threat detection. However, it is unclear whether T modulates resting-state functional connectivity (rsFC) of the BLA, and whether this predicts subsequent aggressive behavior. Aggressive interactions themselves, which often induce changes in T concentrations, could further alter BLA rsFC, but this too remains untested. Here we investigated the effect of endogenous T on rsFC of the BLA at baseline as well as after an aggressive encounter, and whether this was related to behavioral aggression in healthy young women (n = 39). Pre-scan T was negatively correlated with basal rsFC between BLA and left superior temporal gyrus (STG; p < .001, p < .05 Family-Wise Error [FWE] cluster-level corrected), which in turn was associated with increased aggression (r = .37, p = .020). BLA-STG coupling at rest might thus underlie hostil...

Previous research provided evidence for the critical importance of the PFC and BG for reactive motor inhibition, that is, when actions are cancelled in response to external signals. Less is known about the role of the PFC and BG in proactive motor inhibition, referring to preparation for an upcoming stop signal. In this study, patients with unilateral lesions to the BG or lateral PFC performed in a cued go/no-go task, whereas their EEG was recorded. The paradigm called for cue-based preparation for upcoming, lateralized no-go signals. Based on previous findings, we focused on EEG indices of cognitive control (prefrontal beta), motor preparation (sensorimotor mu/beta, contingent negative variation [CNV]), and preparatory attention (occipital alpha, CNV). On a behavioral level, no differences between patients and controls were found, suggesting an intact ability to proactively prepare for motor inhibition. Patients showed an altered preparatory CNV effect, but no other differences in ...

Social cognition allows humans to understand and predict other people's behavior by inferring or sharing their emotions, intentions and beliefs. Few studies have investigated the impact of one's own emotional state on understanding others. Here, we tested the effect of being in an angry state on empathy and theory of mind (ToM). In a between-groups design we manipulated anger status with different paradigms in three studies (autobiographical recall (N = 45), negative feedback (N = 49), frustration (N = 46)) and checked how this manipulation affected empathic accuracy and performance in the EmpaToM. All paradigms were successful in inducing mild anger. We did not find the expected effect of anger on empathy or ToM performance but observed small behavioral changes. Together, our results validate the use of three different anger induction paradigms and speak for rather weak behavioral effects of mild state anger on empathy and ToM.

Social interactions can be stressful, especially if they involve provocation or ambiguity. At the same time, such interactions necessitate social cognition. The question thus arises how stress affects social cognition and how personality attributes modulate this effect. The aim of the current study was to investigate the link between emotional reactivity, physical exercise, and social cognition under stress. As a measure of social cognition, we used spontaneous perspective taking, i.e., the degree to which participants represented the mental state of another agent. Studying young female participants, we investigated how physiological regulation, measured through resting heart-rate variability, is related to spontaneous social perspective taking under stress, and to predicted anger in an ambiguous social scenario. When controlling for resting heart rate, vagally mediated heart-rate variability was negatively correlated with the effect of stress on perspective taking, indicating that good physiological regulation supports social cognition under stress. Further, participants who reported to exercise at least once a week showed higher perspective taking under stress than less active participants. Finally, we found tentative evidence for participants who exercised regularly to show reduced predicted anger in response to an ambiguous provocation. Our findings suggest that good physiological regulation and regular physical exercise support social cognition under stress.

Winners are commonly assumed to compete more aggressively than losers. Here, we find overwhelming evidence for the opposite. We first demonstrate that low-ranking teams commit more fouls than they receive in top-tier soccer, ice hockey, and basketball men’s leagues. We replicate this effect in the laboratory, showing that male participants deliver louder sound blasts to a rival when placed in a low-status position. Using neuroimaging, we characterize brain activity patterns that encode competitive status as well as those that facilitate status-dependent aggression in healthy young men. These analyses reveal three key findings. First, anterior hippocampus and striatum contain multivariate representations of competitive status. Second, interindividual differences in status-dependent aggression are linked with a sharper status differentiation in the striatum and with greater reactivity to status-enhancing victories in the dorsal anterior cingulate cortex. Third, activity in ventromedial, ventrolateral, and dorsolateral prefrontal cortex is associated with trial-wise increases in status-dependent aggressive behavior. Taken together, our results run counter to narratives glorifying aggression in competitive situations. Rather, we show that those in the lower ranks of skill-based hierarchies are more likely to behave aggressively and identify the potential neural basis of this phenomenon.

Damage to the ventromedial prefrontal cortex (VMPFC) can cause maladaptive social behavior, but the cognitive processes underlying these behavioral changes are still uncertain. Here, we tested whether patients with acquired VMPFC lesions show altered approach-avoidance tendencies to emotional facial expressions. Thirteen patients with focal VMPFC lesions and 31 age- and gender-matched healthy controls performed an implicit approach-avoidance task in which they either pushed or pulled a joystick depending on stimulus color. While controls avoided angry faces, VMPFC patients displayed an incongruent response pattern characterized by both increased approach and reduced avoidance of angry facial expressions. The approach bias was stronger in patients with higher self-reported impulsivity and disinhibition, and in those with larger lesions. We further used linear ballistic accumulator modelling to investigate latent parameters underlying approach-avoidance decisions. Controls displayed negative drift rates when approaching angry faces, whereas VMPFC lesions abolished this pattern. In addition, VMPFC patients had weaker response drifts than controls during avoidance. Finally, patients showed reduced drift rate variability and shorter non-decision times, indicating impulsive and rigid decision-making. Our findings thus suggest that VMPFC damage alters the pace of evidence accumulation in response to social signals, eliminating a default, protective avoidant bias and facilitating dysfunctional approach behavior.

Social neuroscience studies have shown that the ventral striatum (VS), a highly reward-sensitive brain area, is activated when participants win competitive tasks. However, in these settings winning often entails both avoiding punishment and punishing the opponent. It is thus unclear whether the rewarding properties of winning are mainly associated to punishment avoidance, or if punishing the opponent can be additionally gratifying. In the present paper we explored the neurophysiological correlates of each outcome, aiming to better understand the development of aggression episodes. We previously introduced a competitive reaction time task that separates both effects: in half of the won trials, participants can physically punish their opponent (active trials), whereas in the other half they can only avoid a punishment (passive trials). We performed functional connectivity analysis seeded in the VS to test for differential network interactions in active compared to passive trials. The ...

In this chapter, we summarize and evaluate experimental approaches to situational research with an emphasis on virtual reality (VR). First, we outline different methods to partition variance in person and situation perception and highlight the advantages of experimental studies as a fixed-effect design. Next, we weigh the merits of some commonly employed methods to standardize situations in experimental settings. The core of the chapter is devoted to VR. After a brief historical and conceptual introduction, we discuss the value of VR as a research tool in terms of internal and external validity. Subsequently, we show how VR can aid the study of person-situation interactions using virtual replications of classical social psychology studies. Finally, we review recent studies that have pushed the boundaries of VR and enumerate the challenges yet to be overcome in the field. In sum, we aim to provide a succinct and encouraging primer on the use of VR for situation research.

Cultural differences in aggression are still poorly understood. The purpose of this article is to assess whether a tool for measuring aggression has the same meaning across cultures. Analyzing samples from Spain (n = 262), the United States (n = 344), and Hong Kong (n = 645), we used confirmatory factor analysis to investigate measurement invariance of the refined version of the Aggression Questionnaire (Bryant & Smith, 2001). The measurement of aggression was more equivalent between the Chinese and Spanish versions than between these two and the U.S. version. Aggression does not show invariance at the cultural level. Cultural variables such as affective autonomy or individualism could influence the meaning of aggression. Aggressive behavior models can be improved by incorporating cultural variables.

Despite remarkable progress in the past three decades, the aetiology of antisocial behaviour remains elusive. Using the developmental taxonomy theory of antisocial behaviour as a starting point, Christina Carlisi and colleagues 1 have made an important contribution by identifying structural brain correlates of antisocial behaviour that could be used to differentiate among individuals with life-course-persistent antisocial behaviour, those with adolescence-limited antisocial behaviour, and non-antisocial controls. Specifically, the authors report a brain-wide reduction of cortical surface area in individuals with life-course-persistent antisocial behaviour relative to participants with adolescence-limited antisocial behaviour (standardised β=-0·17 [95% CI-0·26 to-0·07], p=0·0008) and controls (standardised β=-0·18 [95% CI-0·24 to-0·11], p<0·0001). Additionally, both life-course-persistent and adolescence-limited antisocial behaviour were linked to different patterns of cortical thinning in a more restricted set of paralimbic regions relative to non-antisocial controls (life-course-persistent antisocial behaviour vs controls standardised β=-0·10 [95% CI-0·19 to-0·02], p=0·020; adolescence-limited antisocial behaviour vs controls standardised β=-0·08 [95% CI-0·16 to 0·00], p=0·039). These findings offer a considerable advance to the field and also provide an opportunity to reflect on unresolved issues concerning the use of neurobiological measures to capture and explain individual variability in antisocial behaviour. Although many challenges need to be overcome before the latter can be achieved, we restrict our focus to the issue of mapping brain structure onto function, and the application of the findings to the assessment of individuals with antisocial behaviour. Neuroimaging has become an important tool for studying the brain correlates of antisocial behaviour. There is great interest not only in understanding how alterations in brain structure can be used to characterise individuals with antisocial behaviour, but also in how disturbances in brain functioning relate to antisocial behaviour. 2 The majority of functional neuroimaging studies have used metrics that quantify the extent to which a particular set of brain regions is involved in carrying out task-relevant computations. Once identified, researchers typically generate inferences about which cognitive functions correspond to the observed pattern of activation, meaning that the interpretation could vary depending on the theoretical framework used. 3 Structural neuroimaging studies, by contrast, have the advantage of being less dependent on such inferences, but this strength can become a weakness when researchers rely too much on using cognitive frameworks to interpret results concerning brain structure. Such an approach leans heavily on the assumption that reduced brain matter in a particular region directly translates to a disturbance in the functioning of this region. Although this line of reasoning is quite prominent in the literature, it overlooks the issue that the field of cognitive neuroscience is still searching for a good strategy to determine selective associations between brain function and structure. In other words, there is still no agreement on what exactly each brain area computes and on how to best determine what a particular part of the brain does. 4,5 A study by Darby and colleagues 6 offers an example of one approach to bridging the function-structure gap in the context of antisocial behaviour. They found that lesions in various brain areas were linked to criminal behaviour and, importantly, that the lesions were embedded in a functional network involved in moral decision making. The rich Dunedin dataset, used by Carlisi and colleagues, allows a deeper study of antisocial behaviour-related structure-function relationships. One possibility in this regard would be to use the regions showing reduced cortical thickness in individuals with antisocial behaviour as seeds for follow-up functional connectivity analyses, which would permit probing of functional networks to investigate structure-dependent alterations, in a similar manner to Darby and colleagues. Note that such an approach has already proved to be viable in the study of psychopathic traits. 7 With regard to the practical relevance of the study, the findings might help to move the field closer to achieving the longstanding goal of incorporating neural data into assessment protocols for antisocial behaviour. 2 They point towards the possibility that metrics of brain structure can be useful tools for improving current taxonomies of individuals with antisocial behaviour.

Short- and long-term treatment with glucocorticoids is widely used in clinical practice and frequently induces
features of iatrogenic Cushing syndrome, such as abdominally centered weight gain. Despite decades of glucocorticoids
usage, the mechanisms underlying these side effects are still only partly understood. One possibility
is that glucocorticoids impact subcortical (hypothalamus, amygdala, insula) and cortical (orbitofrontal and
cingulate cortex) brain regions involved in appetite regulation and reward processing. In the present study, we
used functional magnetic resonance imaging (fMRI) to study the acute effects of a prednisolone infusion on
reactivity of brain reward systems to food stimuli. Twenty healthy normal-weight men were tested in a randomized,
double-blind, cross-over study. After an overnight fast and infusion of either 250 mg prednisolone or
placebo (always administered between 8 and 9 A M), fMRI scans were taken while presenting food and object
pictures in a Go/NoGo (GNG) task. At home, participants were asked to register what they had eaten. On the
following morning they came back to the lab and had a supervised ad libitum breakfast at a standardized buffet.
Food-Go in contrast to Object-Go pictures yielded increased blood oxygen level dependent (BOLD) activity in
hippocampus, amygdala, orbitofrontal cortex, insula and anterior cingulate cortex. Prednisolone increased activation
in the bilateral amygdala and right insula for approach-associated food pictures. The buffet test did not
reveal significant differences in calorie consumption or preferences of different macronutrients. However, prednisolone-
induced insula reactivity to Food-Go images was associated with greater caloric intake, both at home
and in the standardized buffet. In sum, we observed a specific effect of prednisolone on the BOLD response of the
amygdala and insula to approach-associated food stimuli. As these brain areas have previously been implicated
in hedonic eating, the present pattern of results may reflect an increased anticipated reward value of food
modulated by glucocorticoids. These effects might potentially drive increased food intake and weight gain under
prolonged glucocorticoid treatment.

Implicit measures of aggressiveness are able to circumvent response biases that plague self‐reports, but it is unclear how they link to neural activation during aggressive interactions and to aggression‐related endocrine function. Here, we tested whether an implicit attentional bias toward antisocial semantic information was associated with endogenous testosterone (T) and cortisol (C) levels, as well as with aggressive behavior and amygdala reactivity to angry faces in a separate competitive paradigm. On Day one, participants (39 healthy young women) completed an emotional word Stroop task in which they had to indicate the font color of antisocial, prosocial, or neutral words. On Day two, we measured subjects’ brain activity during a competitive reaction time task in which the female opponent displayed angry or neutral facial expressions at the start of each trial and provoked participants with increasingly strong sound blasts. T and C were measured in saliva during a regular weekday as well as before and after scanning. We previously showed that aggression was associated with enhanced amygdala reactivity to angry faces in this sample. The present analyses revealed that subjects were slower to identify the font color of antisocial relative to neutral words, and that this attentional bias predicted higher aggression. T and C were uncorrelated with Stroop scores. Crucially, the relationship between implicit attention to antisocial words and aggression was mediated by amygdala reactivity to angry faces. Our data indicate that a tendency to dwell on implicit hostile cues reflects enhanced responsivity to overt anger displays.

Interpersonal provocation presents an approach-avoidance conflict to the provoked person: responding aggressively might yield the joy of retribution, whereas withdrawal can provide safety. Experimental aggression studies typically measure only retaliation intensity, neglecting whether individuals want to confront the provocateur at all. To overcome this shortcoming of previous measures, we developed and validated the Fight-or-Escape paradigm (FOE). The FOE is a competitive reaction time (RT) task in which the winner can choose the volume of a sound blast to be directed at his/her opponent. Participants face two ostensible opponents who consistently select either high or low punishments. At the beginning of each trial, subjects are given the chance to avoid the encounter for a limited number of times. In a first experiment (n = 27, all women), we found that fear potentiation (FP) of the startle response was related to lower scores in a composite measure of aggression and avoidance against the provoking opponent. In a second experiment (n = 34, 13 men), we altered the paradigm such that participants faced the opponents in alternating rather than in random order. Participants completed the FOE as well as the Dot-Probe Task (DPT) and the Approach-Avoidance Task (AAT). Subjects with higher approach bias scores in the AAT avoided the provoking opponent less frequently. Hence, individuals with high threat reactivity and low approach motivation displayed more avoidant responses to provocation, whereas participants high in approach motivation were more likely to engage in aggressive interactions when provoked. The FOE is thus a promising laboratory measure of avoidance and aggression.

Much research has focused on why individuals react aggressively to provocation, but it is also crucial to understand why they avoid confrontation. Here, we investigated the neural basis of aggressive and avoidant responses to interpersonal provocation. Brain regions typically recruited when thinking about others' intentions were activated when avoiding an encounter, but less so against a highly provoking rival. The basolateral amygdala, a structure involved in rapid threat detection, was more active when participants avoided a highly provoking opponent. This indicates that provocation increases threat anticipation, thereby leading to cognitive and behavioral disengagement. Our study thus identifies plausible neuropsychological processes underlying avoidant and aggressive reactions to provocation and helps to resolve inconsistencies in the neuroscientific literature on aggression.

Exogenous glucocorticoids are known to trigger affective changes, but these are highly variable across individuals. A better understanding of how synthetic glucocorticoids impact the processing of negative emotions in the human brain might help to predict such changes. In the present functional magnetic resonance imaging (fMRI) study, we sought to uncover the slow effects of a synthetic glucocorticoid infusion on the neural response to socio-emotional scenes using a within-participant, double-blind, placebo-controlled design. In two separate sessions, 20 young males were given either an intravenous prednisolone dose (250 mg) or placebo in a cross-over, randomized order. Four hours later, they were scanned while viewing drawings of persons in a neutral or negative emotional situation. On the next morning participants provided a blood sample for serum cortisol measurement, which served as a manipulation check. Prednisolone strongly suppressed morning cortisol, and heightened brain reactivity to emotional stimuli in left amygdala, left caudate head, right inferior frontal gyrus, bilateral supplementary motor area, and right somatosensory cortex. Amygdala reactivity was related to lower self-reported fatigue and higher irritability in the prednisolone condition. Moreover, prednisolone blunted inferior frontal and amygdala connectivity with other regions of the emotion-processing neural circuitry. Our results suggest specific brain pathways through which exogenous glucocorticoids may labilize affect.

Social neuroscience studies have shown that the ventral striatum (VS), a highly reward-sensitive brain area, is activated when participants win competitive tasks. However, in these settings winning often entails both avoiding punishment and punishing the opponent. It is thus unclear whether the rewarding properties of winning are mainly associated to punishment avoidance, or if punishing the opponent can be additionally gratifying. In the present paper we explored the neurophysiological correlates of each outcome, aiming to better understand the development of aggression episodes. We previously introduced a competitive reaction time task that separates both effects: in half of the won trials, participants can physically punish their opponent (active trials), whereas in the other half they can only avoid a punishment (passive trials). We performed functional connectivity analysis seeded in the VS to test for differential network interactions in active compared to passive trials. The VS showed greater connectivity with areas involved in reward valuation (orbitofrontal cortex), arousal (dorsal thalamus and posterior insula), attention (inferior occipital gyrus), and motor control (supplementary motor area) in active compared to passive trials, whereas connectivity between the VS and the inferior frontal gyrus decreased. Interindividual variability in connectivity strength between VS and posterior insula was related to aggressive behavior, whereas connectivity between VS and supplementary motor area was related to faster reaction times in active trials. Our results suggest that punishing a provoking opponent when winning might adaptively favor a “competitive state” in the course of an aggressive interaction.