Auto-biological beliefs—beliefs about one’s own biology—are an understudied component of personal identity. Research participants who are led to believe they are biologically vulnerable to affective disorders report more symptoms and less ability to control their mood; however, little is known about the impact of self-originating beliefs about risk for psychopathology, and whether such beliefs correspond to empirically derived estimates of actual vulnerability. Participants in a neuroimaging study (n = 1256) completed self-report measures of affective symptoms, perceived stress, and neuroticism, and an emotional face processing task in the scanner designed to elicit threat responses from the amygdala. A subsample (n = 63) additionally rated their own perceived neural response to threat (i.e., amygdala activity) compared to peers. Self-ratings of neural threat response were uncorrelated with actual threat-related amygdala activity measured via BOLD fMRI. However, self-ratings predicted subjective distress across a variety of self-report measures. In contrast, in the full sample, threat-related amygdala activity was uncorrelated with self-report measures of affective distress. These findings suggest that beliefs about one’s own biological threat response—while unrelated to measured neural activation—may be informative indicators of psychological functioning.

It was investigated whether concealing learned stimulus attributes (i.e., trustworthiness vs. untrustworthiness) has similar effects on the P3 amplitude than concealing stimulus familiarity. According to salience hypothesis, known, deceptive stimuli (probe) are (perceived) more relevant than truthful, unknown stimuli (irrelevant) evoking a more positive probe P3 amplitude. When all stimuli are known, concealing information is more cognitively demanding than non-concealing information evoking a less positive P3 amplitude according to the mental effort account. Ninety-seven participants concealed knowledge of previously learned faces in the familiarity condition (probe vs. irrelevant stimuli). In the trustworthiness condition, participants concealed untrustworthiness to previously learned faces and responded truthfully to previously learned trustworthy and untrustworthy faces (known, concealed vs. known, truthful stimuli). The parietal mean P3 amplitude was more positive for probe stimuli than for irrelevant stimuli in the familiarity condition providing evidence for the salience hypothesis. In the trustworthiness condition, concealing untrustworthiness showed the smallest parietal mean P3 amplitude suggesting evidence for the mental effort hypothesis. Individual differences of perpetrator’s sensitivity to injustice modulated the P3 amplitude in the trustworthiness condition.

Individual differences in trait levels of openness to experience and creativity have been theoretically linked to dopamine function. However, empirical evidence for this assumption is scarce, especially for causal connections. The present study aims to directly assess the influence of dopamine activity on the established association between openness to experience and divergent thinking (i.e., an index of creativity). We hypothesized that manipulating dopamine activity alters the relationship between self-reported openness to experience and ideational fluency and flexibility. In a placebo-controlled between-subjects design, 193 healthy male volunteers completed four divergent thinking tasks after they received either the dopamine-receptor blocker sulpiride (200 mg) or a placebo. The data revealed an interaction such that openness to experience was more positively associated with divergent thinking in the dopamine blocker group (r = 0.304) than in the placebo group (r = −0.002). Specifically, highly open individuals in the dopamine blocker group reached the highest divergent thinking scores. Thus, sulpiride administration selectively affected divergent thinking as a function of trait levels of openness to experience. Although somewhat limited by the unexpected absence of the association between openness to experience and divergent thinking in the placebo group, the present study provides novel evidence for an association between dopamine activity and both openness to experience and divergent thinking.

As demonstrated by neuroimaging data, the human brain contains systems that control responses to threat. The revised Reinforcement Sensitivity Theory of personality predicts that individual differences in the reactivity of these brain systems produce anxiety and fear-related personality traits. Here we discuss some of the challenges in testing this theory and, as an example, present a pilot study that aimed to dissociate brain activity during pursuit by threat and goal conflict. We did this by translating the Mouse Defense Test Battery for human fMRI use. In this version, dubbed the Joystick Operated Runway Task (JORT), we repeatedly exposed 24 participants to pursuit and goal conflict, with and without threat of electric shock. The runway design of JORT allowed the effect of threat distance on brain activation to be evaluated independently of context. Goal conflict plus threat of electric shock caused deactivation in a network of brain areas that included the fusiform and middle temporal gyri, as well as the default mode network core, including medial frontal regions, precuneus and posterior cingulate gyrus, and laterally the inferior parietal and angular gyri. Consistent with earlier research, we also found that imminent threat activated the midbrain and that this effect was significantly stronger during the simple pursuit condition than during goal conflict. Also consistent with earlier research, we found significantly greater hippocampal activation during goal conflict than pursuit by imminent threat. In conclusion, our results contribute knowledge to theories linking anxiety disorders to altered functioning in defensive brain systems and also highlight challenges in this research domain.

The Reinforcement Sensitivity Theory of Personality has as its main foundation a Behavioural Inhibition System (BIS), defined by anxiolytic drugs, in which high trait sensitivity should lead to internalising, anxiety, disorders. Conversely, it has been suggested that low BIS sensitivity would be a characteristic of externalising disorders. BIS output should lead to increased arousal and attention as well as behavioural inhibition. Here, therefore, we tested whether an externalising disorder, Attention Deficit Hyperactivity Disorder (ADHD), involves low BIS sensitivity. Goal-Conflict-Specific Rhythmicity (GCSR) in an auditory Stop Signal Task is a right frontal EEG biomarker of BIS function. We assessed children diagnosed with ADHD-I (inattentive) or ADHD-C (combined) and healthy control groups for GCSR in: a) an initial smaller study in Dunedin, New Zealand (population ~120,000: 15 control, 10 ADHD-I, 10 ADHD-C); and b) a main larger one in Tehran, Iran (population ~9 [city]-16 [metropolis] million: 27 control, 18 ADHD-I, 21 ADHD-C). GCSR was clear in controls (particularly at 6–7 Hz) and in ADHD-C (particularly at 8–9 Hz) but was reduced in ADHD-I. Reduced attention and arousal in ADHD-I could be due, in part, to BIS dysfunction. However, hyperactivity and impulsivity in ADHD-C are unlikely to reflect reduced BIS activity. Increased GCSR frequency in ADHD-C may be due to increased input to the BIS. BIS dysfunction may contribute to some aspects of ADHD (and potentially other externalising disorders) and to some differences between the ADHD subtypes but other prefrontal systems (and, e.g. dopamine) are also important.

The trait of extraversion is one of the longest-standing domains that captures the social dimension of personality and can potentially explain the covariation of a wide variety of behaviors. To date, there is a growing recognition that human behavior should be specified not only through the psychological mechanisms underlying each trait but also through their underlying neurobehavioral systems. While imaging studies have revealed important initial insights into the structural and functional neural correlates of extraversion, current knowledge about the relationships between extraversion and brain structures is still rather limited, especially with regard to the relationship between extraversion and white matter (WM). In this study, we aimed to investigate WM microstructure in extraversion in greater depth. Thirty-five healthy volunteers (21 women; mean age 35) underwent magnetic resonance imaging, as a part of a larger project aimed at investigating the longitudinal effect of motor training. WM integrity was assessed using the diffusion tensor imaging technique combining multiple diffusion tensor measures. Extraversion was assessed by the Eysenck Personality Questionnaire-Revised. Voxelwise correlation analyses between fractional anisotropy, axial diffusivities, and radial diffusivities maps and extraversion score showed decreased connectivity in the right inferior fronto-occipital fasciculus and forceps major among individuals who had high extraversion ratings. In conclusion, individual differences in extraversion may reflect differential organization of the WM tracts connecting frontal cortex, temporal, and occipital areas, which are related to socioemotional and control functions.

Psychopathic traits predispose individuals toward antisocial behavior. Such antagonistic acts often result in “unsuccessful” outcomes such as incarceration. What mechanisms allow some people with relatively high levels of psychopathic traits to live “successful”, unincarcerated lives, in spite of their antisocial tendencies? Using neuroimaging, we investigated the possibility that “successful” psychopathic individuals exhibited greater development of neural structures that promote “successful” self-regulation, focusing on the ventrolateral prefrontal cortex (VLPFC). Across two structural magnetic resonance imaging studies of “successful” participants (Study 1: N = 80 individuals in long-term romantic relationships; Study 2: N = 64 undergraduates), we observed that gray matter density in the left and right VLPFC was positively associated with psychopathic traits. These preliminary results support a compensatory model of psychopathy, in which “successful” psychopathic individuals develop inhibitory mechanisms to compensate for their antisocial tendencies. Traditional models of psychopathy that emphasize deficits may be aided by such compensatory models that identify surfeits in neural and psychological processes.

Across a significant body of research, psychopathy has often been conceptualized as a biologically based malady. In this research, genetic and neurobiological differences have been conceptualized to underlie psychopathy, while affected individuals’ life experiences only influence expressed psychopathic features and their severity. Psychopathy research has largely ignored developmental evidence demonstrating significant influences of environment on both biological and behavioral processes, resulting in several prominent criticisms (Edens & Vincent, 2008; Loeber, Byrd, & Farrington, 2015). The current review was conducted with two main aims: (a) to collect and consider etiological evidence from the extant body of research on genetic and neurobiological factors in psychopathy; and (b) to evaluate findings from genetic, neurotransmitter, brain structure, and brain function studies in the context of relevant evidence from developmental research. Examples from research on adversity and traumatic stress, a common correlate of psychopathy, were used to highlight current research gaps and future directions to aid in the integration of developmental and neurobiological research agendas. While some promising evidence exists regarding possible underlying neurobiological processes of psychopathic traits, this evidence is insufficient to suggest a largely biological etiology for the disorder. Further, information from developmental and epigenetic research may suggest complex, multidimensional trajectories for individuals experiencing psychopathy. Based on these observations, the authors make several recommendations for future research, as well as for current clinical application and practice.

Mindfulness and anxiety are often linked as inversely related traits and there have been several theoretical and mediational models proposed suggesting such a relationship between these two traits. The current review report offers an account of self-report measures, behavioral, electrophysiological, hemodynamic, and biological studies, which provide converging evidence for an inverse relationship between mindfulness and anxiety. To our knowledge, there are no comprehensive accounts of empirical evidence that investigate this relationship. After reviewing several empirical studies, we propose a schematic model, where a stressor can trigger the activation of amygdala which activates the hypothalamic–pituitary–adrenal (HPA) pathway. This hyperactive HPA axis leads to a cascade of psychological, behavioral, electrophysiological, immunological, endocrine, and genetic reactions in the body, primarily mediated by a sympathetic pathway. Conversely, mindfulness protects from deleterious effects of these triggered reactions by downregulating the HPA axis activity via a parasympathetic pathway. Finally, we propose a model suggesting a comprehensive scheme through which mindfulness and anxiety may interact through emotion regulation. It is recommended that future mindfulness intervention studies should examine a broad spectrum of measurement indices where possible, keeping logistic feasibility in mind and look at mindfulness in conjunction with anxiety rather than independently.

Psychologists have identified multiple different forms of conflict, such as information processing conflict and goal conflict. As such, there is a need to examine the similarities and differences in neurology between each form of conflict. To address this, we conducted a comprehensive electroencephalogram (EEG) analysis of Shadli, Glue, McIntosh, and McNaughton’s calibrated stop-signal task (SST) goal-conflict task. Specifically, we examined changes in scalp-wide current source density (CSD) power and coherence across a wide range of frequency bands during the calibrated SST (n = 34). We assessed differences in EEG between the high and low goal-conflict conditions using hierarchical analyses of variance (ANOVAs). We also related goal-conflict EEG to trait anxiety, neuroticism, Behavioural Inhibition System (BIS)-anxiety and revised BIS (rBIS) using regression analyses. We found that changes in CSD power during goal conflict were limited to increased midfrontocentral theta. Conversely, coherence increased across 23 scalp-wide theta region pairs and one frontal delta region pair. Finally, scalp-wide theta significantly predicted trait neuroticism but not trait anxiety, BIS-anxiety or rBIS. We conclude that goal conflict involves increased midfrontocentral CSD theta power and scalp-wide theta-dominated coherence. Therefore, compared with information processing conflict, goal conflict displays a similar EEG power profile of midfrontocentral theta but a much wider coherence profile. Furthermore, the increases in theta during goal conflict are the characteristic of BIS-driven activity. Therefore, future research should confirm whether these goal-conflict effects are driven by the BIS by examining whether the effects are attenuated by anxiolytic drugs. Overall, we have identified a unique network of goal-conflict EEG during the calibrated SST.

A common and mostly effective emotion regulation strategy is reappraisal. During reappraisal, activity in cognitive control brain regions increases and activity in brain regions associated with emotion responding (e.g., the amygdala) diminishes. Immediately after reappraisal, it has been observed that activity in the amygdala increases again, which might reflect a paradoxical aftereffect. While there is extensive empirical evidence for these neural correlates of emotion regulation, only few studies targeted the association with individual differences in personality traits. The aim of this study is to investigate these associations more thoroughly. Seventy-six healthy participants completed measures of broad personality traits (Big Five, Positive and Negative Affect) as well as of more narrow traits (habitual use of emotion regulation) and performed an experimental fMRI reappraisal task. Participants were instructed to either permit their emotions or to detach themselves from the presented negative and neutral pictures. After each picture, a relaxation period was included. Reappraisal success was determined by arousal ratings and activity in the amygdala. During reappraisal, we found activation in the prefrontal cortex and deactivation in the left amygdala. During the relaxation period, an immediate aftereffect was found in occipital regions and marginally in the amygdala. Neither personality traits nor habitual use of emotion regulation predicted reappraisal success or the magnitude of the aftereffect. We replicated typical activation and deactivation patterns during intentional emotion regulation and partially replicated the immediate aftereffect in the amygdala. However, there was no association between personality traits and emotion regulation success.

Using electroencephalography (EEG) power measures within conventional delta, theta, alpha, beta, and gamma bands, the aims of the current study were to highlight cortical correlates of subjective perception of cold pain (CP) and the associations of these measures with behavioral inhibition system (BIS), fight-flight-freeze system (FFFS), and behavioral approach system personality traits. EEG was recorded in 55 healthy right-handed women under (i) a white noise interruption detection condition (Baseline); (ii) enduring CP induced by the cold cup test. CP and Baseline EEG band power scores within conventional frequency bands served for covariance analyses. We found that: (1) higher Pain scorers had higher EEG beta power changes at left frontal, midline central, posterior temporal leads; (2) higher BIS was associated with greater EEG delta activity changes at parietal scalp regions; (3) higher FFFS was associated with higher EEG delta activity changes at temporal and left-parietal regions, and with lower EEG gamma activity changes at right parietal regions. High FFFS, compared to Low FFFS scorers, also showed a lower gamma power across the midline, posterior temporal, and parietal regions. Results suggest a functional role of higher EEG beta activity in the subjective perception of tonic pain. EEG delta activity underpins conflict resolution system responsible for passive avoidance control of pain, while higher EEG delta and lower EEG gamma activity changes, taken together, underpin active avoidance system responsible for pain escape behavior.