Explore the vast range of titles available.

Given the importance of emotion regulation in affective disorders, emotion regulation is at the focus of attempts to identify brain biomarkers of disease risk, treatment response, and brain development. However, to be useful as an indicator for individual characteristics of brain functions – particularly as a biomarker in a clinical context – ensuring reliability is a key challenge. Here, we systematically evaluated test-retest reliability of task-based functional magnetic resonance imaging (fMRI) activity within neural networks associated with emotion generation and regulation across three sessions. Acquiring fMRI data at ultra-high field (7T), we examined region- and voxel-wise test-retest reliability of brain activity in response to a well-established emotion regulation task for predefined region-of-interests (ROIs) implicated in four neural networks. Test-retest reliability varied considerably across the emotion regulation networks and respective ROIs. However, core emotion regulation regions, including the ventrolateral and dorsolateral prefrontal cortex (vlPFC and dlPFC) as well as the middle temporal gyrus (MTG) showed high reliability. Our findings thus support the role of these prefrontal and temporal regions as promising candidates for the study of individual differences in emotion regulation as well as for neurobiological biomarkers in clinical neuroscience research.

Abstract Childhood adversity is a major risk factor for emotional and cognitive disorders later in adulthood. Behavior monitoring, one of the most important components of cognitive control, plays a crucial role in flexible interaction with the environment. Here, we test a novel conceptual model discriminating between two distinct dimensions of childhood adversity (i.e. deprivation and threat) and examine their relations to dynamic stages of behavior monitoring. Sixty young healthy adults participated in this study using event-related potentials and the dynamic stages of behavior monitoring including response inhibition, error detection and post-error adjustments were investigated in a classical Go/NoGo task. Multiple regression analyses revealed that participants with higher severity of childhood adversity recruited more controlled attention, as indicated by larger (more negative) conflict detection–related NoGo-N2 amplitudes and larger (more negative) error detection–related error-related negativity amplitudes. Higher severity of childhood abuse (an indicator of threat) was related to smaller (less positive) error appraisal–related error positivity amplitudes on the neural level and subsequently lower post-error accuracy on the behavioral level. These results suggested that prefrontal-supported controlled attention is influenced by universal adversity in childhood while the error-related behavioral adjustment is mainly affected by childhood abuse, indicating the dimensions of deprivation and threat are at least partially distinct.

Emotion regulation and empathy represent highly intertwined psychological processes sharing common conceptual ground. Despite the wealth of research in these fields, the joint and distinct functional nature and topological features of these constructs have not yet been investigated using the same experimental approach. This study investigated the common and distinct neural correlates of emotion regulation and empathy using a meta-analytic approach. The regions that were jointly activated were then characterized using meta-analytic connectivity modeling and functional decoding of metadata terms. The results revealed convergent activity within the ventrolateral and dorsomedial prefrontal cortex as well as temporal regions. The functional decoding analysis demonstrated that emotion regulation and empathy were related to highly similar executive and internally oriented processes. This synthesis underlining strong functional and neuronal correspondence between emotion regulation and empathy could (i) facilitate greater integration of these two separate lines of literature, (ii) accelerate progress toward elucidating the neural mechanisms that support social cognition, and (iii) push forward the development of a common theoretical framework for these psychological processes essential to human social interactions.

•Repeated retrieval strengthened consolidated memories, while repeated suppression had a modest negative effect.•Pattern reinstatements of individual memories were detected in the visual area, parietal lobe, and hippocampus after 24 h.•After repeated retrieval, reduced activity amplitude was associated with increased distinctiveness of activity patterns in the ventral visual cortex and right precuneus.•Repeated suppression was associated with the reduced lateral prefrontal activity, but unchanged mnemonic representations. Memories are not stored as static engrams, but as dynamic representations affected by processes occurring after initial encoding. Previous studies revealed changes in activity and mnemonic representations in visual processing areas, parietal lobe, and hippocampus underlying repeated retrieval and suppression. However, these neural changes are usually induced by memory modulation immediately after memory formation. Here, we investigated 27 healthy participants with a two-day functional Magnetic Resonance Imaging study design to probe how established memories are dynamically modulated by retrieval and suppression 24 h after learning. Behaviorally, we demonstrated that established memories can still be strengthened by repeated retrieval. By contrast, repeated suppression had a modest negative effect, and suppression-induced forgetting was associated with individual suppression efficacy. Neurally, we demonstrated item-specific pattern reinstatements in visual processing areas, parietal lobe, and hippocampus. Then, we showed that repeated retrieval reduced activity amplitude in the ventral visual cortex and hippocampus, but enhanced the distinctiveness of activity patterns in the ventral visual cortex and parietal lobe. Critically, reduced activity was associated with enhanced representation of idiosyncratic memory traces in the ventral visual cortex and precuneus. In contrast, repeated memory suppression was associated with reduced lateral prefrontal activity, but relative intact mnemonic representations. Our results replicated most of the neural changes induced by memory retrieval and suppression immediately after learning and extended those findings to established memories after initial consolidation. Active retrieval seems to promote episode-unique mnemonic representations in the neocortex after initial encoding but also consolidation.

Inhibitory control is crucial for regulating emotions and may also enable memory control. However, evidence for their shared neurobiological correlates is limited. Here, we report meta-analyses of neuroimaging studies on emotion regulation, or memory control and link neural commonalities to transcriptional commonalities using the Allen Human Brain Atlas (AHBA). Based on 95 functional magnetic resonance imaging studies, we reveal a role of the right inferior parietal lobule embedded in a frontal–parietal–insular network during emotion regulation and memory control, which is similarly recruited during response inhibition. These co-activation patterns also overlap with the networks associated with ‘inhibition’, ‘cognitive control’ and ‘working memory’ when consulting the Neurosynth. Using the AHBA, we demonstrate that emotion regulation- and memory control-related brain activity patterns are associated with transcriptional profiles of a specific set of ‘inhibition-related’ genes. Gene ontology enrichment analysis of these ‘inhibition-related’ genes reveal associations with the neuronal transmission and risk for major psychiatric disorders as well as seizures and alcoholic dependence. In summary, this study identified a neural network and a set of genes associated with inhibitory control across emotion regulation and memory control. These findings facilitate our understanding of the neurobiological correlates of inhibitory control and may contribute to the development of brain stimulation and pharmacological interventions.

Background In-vivo observations of neural processes during human aggressive behavior are difficult to obtain, limiting the number of studies in this area. To address this gap, the present study implemented a social reactive aggression paradigm in 29 healthy men, employing non-violent provocation in a two-player game to elicit aggressive behavior in fMRI settings. Results Participants responded more aggressively after high provocation reflected in taking more money from their opponents. Comparing aggression trials after high provocation to those after low provocation revealed activations in neural circuits involved in aggression: the medial prefrontal cortex (mPFC), the orbitofrontal cortex (OFC), the dorsolateral prefrontal cortex (dlPFC), the anterior cingulate cortex (ACC), and the insula. In general, our findings indicate that aggressive behavior activates a complex, widespread brain network, reflecting a cortico-limbic interaction and overlapping with circuits underlying negative emotions and conflicting decision-making. Brain activation during provocation in the OFC was associated with the degree of aggressive behavior in this task. Conclusion Therefore, data suggest there is greater susceptibility for provocation, rather than less inhibition of aggressive tendencies, in individuals with higher aggressive responses. This further supports the hypothesis that reactive aggression can be seen as a consequence of provocation of aggressive emotional responses and parallel evaluative regulatory processes mediated mainly by the insula and prefrontal areas (OFC, mPFC, dlPFC, and ACC) respectively.

Self-identification as a victim of violence may lead to increased negative emotions and stress and thus, may change both structure and function of the underlying neural network(s). In a trans-diagnostic sample of individuals who identified themselves as victims of violence and a matched control group with no prior exposure to violence, we employed a social exclusion paradigm, the Cyberball task, to stimulate the re-experience of stress. Participants were partially excluded in the ball-tossing game without prior knowledge. We analyzed group differences in brain activity and functional connectivity during exclusion versus inclusion in exclusion-related regions. The victim group showed increased anger and stress levels during all conditions. Activation patterns during the task did not differ between groups but an enhanced functional connectivity between the IFG and the right vmPFC distinguished victims from controls during exclusion. This effect was driven by aberrant connectivity in victims during inclusion rather than exclusion, indicating that victimization affects emotional responses and inclusion-related brain connectivity rather than exclusion-related brain activity or connectivity. Victims may respond differently to the social context itself. Enhanced negative emotions and connectivity deviations during social inclusion may depict altered social processing and may thus affect social interactions.

Although sex differences in aggression have been investigated for decades, little is known about the underlying neurobiology of this phenomenon. To address this gap, the present study implemented a social reactive aggression paradigm in 20 women and 22 men, employing a modified Taylor Aggression Task (mTAT) to provoke aggressive behavior in an fMRI setting. Subjects were provoked by money subtraction from a fake opponent and given the opportunity to retaliate likewise. In the absence of behavioral differences, male and female subjects showed differential brain activation patterns in response to provocation. Men had higher left amygdala activation during high provocation. This amygdala activation correlated with trait anger scores in men, but not in women. Also, men showed a positive association between orbitofrontal cortex, rectal gyrus and anterior cingulate cortex (ACC) activity in the provocation contrast and their tendency to respond aggressively, whereas women displayed a negative association. As the rectal gyrus and OFC have been attributed a crucial role in automatic emotion regulation, this finding points toward the assumption that highly aggressive men use automatic emotion regulation to a greater extent in response to provocation compared to highly aggressive women.

Moving from strictly localized “amygdala-centered” concepts and top-down prefrontal control systems to broader interactive network dynamics (Smith and Lane, 2015; Morawetz et al., 2020) has clearly increased our understanding of how emotions can be controlled using a variety of emotion regulation (ER) strategies and analytic approaches (Morawetz et al., 2017). An acute state of hunger or sleep deprivation may make a person less able or willing to engage in regulatory behavior, leading to a host of sub-optimal decision processes. Emotion control, regardless of whether implicit or explicit ER, necessarily requires the intactness of important cognitive features (Braunstein et al., 2017). [...]situational interference or facilitation of cognitive abilities will have downstream consequences for eventual attempts to regulate emotion. [...]Wiener et al. describe, for the case of essential hypertonia, how the thalamic pulvinar nucleus might be engaged in the dysregulation of interactions between emotion processing brain networks and attentional/cognitive brain networks, which gives rise to a vicious cycle of negative emotion-physiology interactions.

Anhedonia, reduced positive affect and enhanced negative affect are integral characteristics of major depressive disorder (MDD). Emotion dysregulation, e.g. in terms of different emotion processing deficits, has consistently been reported. The aim of the present study was to investigate mood changes in depressive patients using a multidimensional approach for the measurement of emotional reactivity to mood induction procedures. Experimentally, mood states can be altered using various mood induction procedures. The present study aimed at validating two different positive mood induction procedures in patients with MDD and investigating which procedure is more effective and applicable in detecting dysfunctions in MDD. The first procedure relied on the presentation of happy vs. neutral faces, while the second used funny vs. neutral cartoons. Emotional reactivity was assessed in 16 depressed and 16 healthy subjects using self-report measures, measurements of electrodermal activity and standardized analyses of facial responses. Positive mood induction was successful in both procedures according to subjective ratings in patients and controls. In the cartoon condition, however, a discrepancy between reduced facial activity and concurrently enhanced autonomous reactivity was found in patients. Relying on a multidimensional assessment technique, a more comprehensive estimate of dysfunctions in emotional reactivity in MDD was available than by self-report measures alone and this was unsheathed especially by the mood induction procedure relying on cartoons. The divergent facial and autonomic responses in the presence of unaffected subjective reactivity suggest an underlying deficit in the patients' ability to express the felt arousal to funny cartoons. Our results encourage the application of both procedures in functional imaging studies for investigating the neural substrates of emotion dysregulation in MDD patients. Mood induction via cartoons appears to be superior to mood induction via faces and autobiographical material in uncovering specific emotional dysfunctions in MDD.