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Past research has shown that attributions of intentions to other's actions determine how we experience these actions and their consequences. Yet, it is unknown how such attributions affect our learning and memory. Addressing this question, we combined neuroimaging with an interactive threat learning paradigm in which two interaction partners (confederates) made choices that had either threatening (shock) or safe (no shock) consequences for the participants. Importantly, participants were led to believe that one partner intentionally caused the delivery of shock, whereas the other did not (i.e. unintentional partner). Following intentional versus unintentional shocks, participants reported an inflated number of shocks and a greater increase in anger and vengeance. We applied a model-based representational similarity analysis to blood-oxygen-level-dependent (BOLD)-MRI patterns during learning. Surprisingly, we did not find any effects of intentionality. The threat value of actions, however, was represented as a trial-by-trial increase in representational similarity in the insula and the inferior frontal gyrus. Our findings illustrate how neural pattern formation can be used to study a complex interaction.

Background: Cognitive reappraisal is a strategy for emotional regulation, important in the context of anxiety disorders. It is not known whether anxiolytic effects of benzodiazepines affect cognitive reappraisal. Aims: We aimed to investigate the effect of 25 mg oxazepam on cognitive reappraisal. Methods: In a preliminary investigation, 33 healthy male volunteers were randomised to oxazepam or placebo, and then underwent an experiment where they were asked to use cognitive reappraisal to upregulate or downregulate their emotional response to images with negative or neutral emotional valence. We recorded unpleasantness ratings, skin conductance, superciliary corrugator muscle activity, and heart rate. Participants completed rating scales measuring empathy (Interpersonal Reactivity Index, IRI), anxiety (State-Trait Anxiety Inventory, STAI), alexithymia (Toronto Alexithymia Scale-20, TAS-20), and psychopathy (Psychopathy Personality Inventory-Revised, PPI-R). Results: Upregulation to negative-valence images in the cognitive reappraisal task caused increased unpleasantness ratings, corrugator activity, and heart rate compared to downregulation. Upregulation to both negative- and neutral-valence images caused increased skin conductance responses. Oxazepam caused lower unpleasantness ratings to negative-valence stimuli, but did not interact with reappraisal instruction on any outcome. Self-rated trait empathy was associated with stronger responses to negative-valence stimuli, whereas self-rated psychopathic traits were associated with weaker responses to negative-valence stimuli. Conclusions: While 25 mg oxazepam caused lower unpleasantness ratings in response to negative-valence images, we did not observe an effect of 25 mg oxazepam on cognitive reappraisal., This work was supported by the Swedish Society for Medicine and the Osher Center for Integrative Medicine.

Sleep restriction has been proposed to cause impaired emotional processing and emotional regulation by inhibiting top-down control from prefrontal cortex to amygdala. Intentional emotional regulation after sleep restriction has, however, never been studied using brain imaging. We aimed here to investigate the effect of partial sleep restriction on emotional regulation through cognitive reappraisal. Forty-seven young (age 20–30) and 33 older (age 65–75) participants (38/23 with complete data and successful sleep intervention) performed a cognitive reappraisal task during fMRI after a night of normal sleep and after restricted sleep (3 h). Emotional downregulation was associated with significantly increased activity in the dorsolateral prefrontal cortex (pFWE < 0.05) and lateral orbital cortex (pFWE < 0.05) in young, but not in older subjects. Sleep restriction was associated with a decrease in self-reported regulation success to negative stimuli (p< 0.01) and a trend towards perceiving all stimuli as less negative (p = 0.07) in young participants. No effects of sleep restriction on brain activity nor connectivity were found in either age group. In conclusion, our data do not support the idea of a prefrontal-amygdala disconnect after sleep restriction, and neural mechanisms underlying behavioural effects on emotional regulation after insufficient sleep require further investigation.

In today’s world, mass-media and online social networks present us with unprecedented exposure to second-hand, vicarious experiences and thereby the chance of forming associations between previously innocuous events (e.g., being in a subway station) and aversive outcomes (e.g., footage or verbal reports from a violent terrorist attack) without direct experience. Such social threat, or fear, learning can have dramatic consequences, as manifested in acute stress symptoms and maladaptive fears. However, most research has so far focused on socially acquired threat responses that are expressed as increased arousal rather than active behavior. In three experiments (n = 120), we examined the effect of indirect experiences on behaviors by establishing a link between social threat learning and instrumental decision making. We contrasted learning from direct experience (i.e., Pavlovian conditioning) (experiment 1) against two common forms of social threat learning - social observation (experiment 2) and verbal instruction (experiment 3) - and how this learning transferred to subsequent instrumental decision making using behavioral experiments and computational modeling. We found that both types of social threat learning transfer to decision making in a strong and surprisingly inflexible manner. Notably, computational modeling indicated that the transfer of observational and instructed threat learning involved different computational mechanisms. Our results demonstrate the strong influence of others’ expressions of fear on one’s own decisions and have important implications for understanding both healthy and pathological human behaviors resulting from the indirect exposure to threatening events.

Emotional mimicry and empathy are mechanisms underlying social interaction. Benzodiazepines have been proposed to inhibit empathy and promote antisocial behaviour. First, we aimed to investigate the effects of oxazepam on emotional mimicry and empathy for pain, and second, we aimed to investigate the association of personality traits to emotional mimicry and empathy. Participants (n= 76) were randomized to 25mg oxazepam or placebo. Emotional mimicry was examined using video clips with emotional expressions. Empathy was investigated by pain stimulating the participant and a confederate. We recorded self-rated experience, activity in major zygomatic and superciliary corrugator muscles, skin conductance, and heart rate. In the mimicry experiment, oxazepam inhibited corrugator activity. In the empathy experiment, oxazepam caused increased self-rated unpleasantness and skin conductance. However, oxazepam specifically inhibited neither emotional mimicry nor empathy for pain. Responses in both experiments were associated with self-rated empathic, psychopathic and alexithymic traits. The present results do not support a specific effect of 25mg oxazepam on emotional mimicry or empathy.

Despite mounting reports about the negative effects of chronic occupational stress on cognitive and emotional functions, the underlying mechanisms are unknown. Recent findings from structural MRI raise the question whether this condition could be associated with a functional uncoupling of the limbic networks and an impaired modulation of emotional stress. To address this, 40 subjects suffering from burnout symptoms attributed to chronic occupational stress and 70 controls were investigated using resting state functional MRI. The participants' ability to up-regulate, down-regulate, and maintain emotion was evaluated by recording their acoustic startle response while viewing neutral and negatively loaded images. Functional connectivity was calculated from amygdala seed regions, using explorative linear correlation analysis. Stressed subjects were less capable of down-regulating negative emotion, but had normal acoustic startle responses when asked to up-regulate or maintain emotion and when no regulation was required. The functional connectivity between the amygdala and the anterior cingulate cortex correlated with the ability to down-regulate negative emotion. This connectivity was significantly weaker in the burnout group, as was the amygdala connectivity with the dorsolateral prefrontal cortex and the motor cortex, whereas connectivity from the amygdala to the cerebellum and the insular cortex were stronger. In subjects suffering from chronic occupational stress, the functional couplings within the emotion-and stress-processing limbic networks seem to be altered, and associated with a reduced ability to down-regulate the response to emotional stress, providing a biological substrate for a further facilitation of the stress condition., AuthorCount:6

Much of the progress in understanding the mechanisms underlying the formation and persistence of fear memories comes from studies of Pavlovian conditioning and extinction. Recently, considerable interest has been turn to strategies that facilitate the development and persistence of extinction. This interest has been particularly fueled by the fact that the findings may have important clinical implications by identifying the conditions during which extinction may permanently prevent the recovery of learned fears. The overall aim of this thesis was to identify the temporal factors that drive fear extinction learning (Study I) and to investigate different approaches to preventing the return of fear that occurs after extinction (Study II-IV). More specifically, we assessed the effects of initiating extinction training within the consolidation (Study II) or reconsolidation (Study III) time window and the effects of optimizing safety learning during fear extinction through social observation (Study IV). In Study I, we evaluated two critical accounts of extinction by separately manipulating the number of non-reinforced trials and the cumulated non-reinforced exposure time during extinction training. Our data did not support that extinction is driven by the cumulative duration of non-reinforced exposure, but rather the number of trials appeared critical. In fact, many extinction trials with a duration shorter than the acquisition trial duration facilitated extinction learning, but this effect did not predict the recovery of fear. In Study II, we found that extinction training initiated within, but not outside, the consolidation time window yielded less extinction of both fear-potentiated startle and shock expectancy ratings, while selectively preventing the return of fear-potentiated startle during a subsequent reinstatement test. Contrary, in Study III, extinction training initiated within the reconsolidation time window did not prevent the recovery of fear, as measured by

Theories of emotion propose that responses to emotional pictures can occur independently of whether or not people are aware of the picture content. Because evidence from dissociation paradigms is inconclusive, we manipulated picture awareness gradually and studied whether emotional responses varied with degree of awareness. Spider fearful and non-fearful participants viewed pictures of spiders and flowers at four levels of backward masking while electrodermal activity and heart rate were measured continuously. Recognition ratings confirmed that participants’ picture awareness decreased with masking. Critically, effects of spider fear on emotion ratings and heart rate also decreased with masking. These findings suggest that effects of spider fear on emotion ratings and heart rate are closely related to picture awareness.