The computational psychopathology of emotion.

Mood and anxiety disorders involve recurring, maladaptive patterns of distinct emotions and moods. Here, we argue that understanding these maladaptive patterns first requires understanding how emotions and moods guide adaptive behavior. We thus review recent progress in computational accounts of emotion that aims to explain the adaptive role of distinct emotions and mood. We then highlight how this emerging approach could be used to explain maladaptive emotions in various psychopathologies. In particular, we identify three computational factors that may be responsible for excessive emotions and moods of different types: self-intensifying affective biases, misestimations of predictability, and misestimations of controllability. Finally, we outline how the psychopathological roles of these factors can be tested, and how they may be used to improve psychotherapeutic and psychopharmacological interventions.

Serotonin modulates asymmetric learning from reward and punishment in healthy human volunteers.

Instrumental learning is driven by a history of outcome success and failure. Here, we examined the impact of serotonin on learning from positive and negative outcomes. Healthy human volunteers were assessed twice, once after acute (single-dose), and once after prolonged (week-long) daily administration of the SSRI citalopram or placebo. Using computational modelling, we show that prolonged boosting of serotonin enhances learning from punishment and reduces learning from reward. This valence-dependent learning asymmetry increases subjects' tendency to avoid actions as a function of cumulative failure without leading to detrimental, or advantageous, outcomes. By contrast, no significant modulation of learning was observed following acute SSRI administration. However, differences between the effects of acute and prolonged administration were not significant. Overall, these findings may help explain how serotonergic agents impact on mood disorders.

Ruminative Tendency Relates to Ventral Striatum Functionality: Evidence From Task and Resting-State fMRI.

BACKGROUND: Ruminative responding involves repetitive and passive thinking about one's negative affect. This tendency interferes with initiation of goal-directed rewarding strategies, which could alleviate depressive states. Such reward-directed response selection has been shown to be mediated by ventral striatum/nucleus accumbens (VS/NAcc) function. However, to date, no study has examined whether trait rumination relates to VS/NAcc functionality. Here, we tested whether rumination moderates VS/NAcc function both in response to reward and during a ruminative state. METHODS: Trait rumination was considered dimensionally using Rumination Response Scale (RRS) scores. Our sample (N = 80) consisted of individuals from a community sample and from patients diagnosed with major depressive disorder, providing a broad range of RRS scores. Participants underwent fMRI to assess two modes of VS/NAcc functionality: 1) in response to reward, and 2) during resting-state, as a proxy for ruminative state. We then tested for associations between RRS scores and VS/NAcc functional profiles, statistically controlling for overall depressive symptom severity. RESULTS: RRS scores correlated positively with VS/NAcc response to reward. Furthermore, we noted that higher RRS scores were associated with increased ruminative-dependent resting-state functional connectivity of the VS/NAcc with the left orbitofrontal cortex. CONCLUSIONS: These findings suggest that ruminative tendencies manifest in VS/NAcc reward- and rumination-related functions, providing support for a theoretical-clinical perspective of rumination as a habitual impairment in selection of rewarding, adaptive coping strategies.

Attenuating anger and aggression with neuromodulation of the vmPFC: A simultaneous tDCS-fMRI study.

Angry outbursts during interpersonal provocations may lead to violence and prevails in numerous pathological conditions. In the anger-infused Ultimatum Game (aiUG), unfair monetary offers accompanied by written provocations induce anger. Rejection of such offers relates to aggression, whereas acceptance to anger regulation. We previously demonstrated the involvement of the ventro-medial prefrontal cortex (vmPFC) in accepting unfair offers and attenuating anger during an aiUG, suggestive of its role in anger regulation. Here, we aimed to enhance anger regulation by facilitating vmPFC activity during anger induction, using anodal transcranial direct current stimulation (tDCS) and simultaneously with functional Magnetic Resonance Imaging to validate modulation of vmPFC activity. In a cross-over, sham-controlled, double-blind study, participants (N = 25) were each scanned twice, counterbalancing sham and active tDCS applied during administration of the aiUG. Outcome measures included the effect of active versus sham stimulation on vmPFC activity, unfair offers' acceptance rates, self-reported anger, and aggressive behavior in a subsequent reactive aggression paradigm. Results indicate that active stimulation led to increased vmPFC activity during the processing of unfair offers, increased acceptance rates of these offers, and mitigated the increase in self-reported anger following the aiUG. We also noted a decrease in subsequent aggressive behavior following active stimulation, but only when active stimulation was conducted in the first experimental session. Finally, an exploratory finding indicated that participants with a stronger habitual tendency to use suppression as an emotion regulation strategy, reported less anger following the aiUG in the active compared to sham stimulation conditions. Findings support a potential causal link between vmPFC functionality and the experience and expression of anger, supporting vmPFC's role in anger regulation, and providing a promising avenue for reducing angry and aggressive outbursts during interpersonal provocations in various psychiatric and medical conditions.