Armita Golkar

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.

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: Participants (n = 33) 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 emotional reappraisal.

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Learning from other individuals (e.g. social learning) is subjected to biases affecting whom to learn from. Consistent with research in animals, showing similarity-based learning biases and a general tendency to display pro-social responses to in-group individuals, we recently demonstrated that social learning of both fear and safety was enhanced when information was transmitted between same-race individuals. Here, we addressed how two different social group categories jointly affect the transmission of fears by investigating the interplay between racial and supporter group membership. We demonstrate that supporter group membership differentially influenced learning from a racial in-group vs. racial out-group individual. Thus, conditioned skin conductance responses in the same-race condition were significantly higher when fear was transmitted by an in-group (same team) vs. an out-group (rival team) individual, and were related to supporter team identification. However, supporter group membership did not influence learning from a racial out-group demonstrator, suggesting that the presence of an alternative alliance does not necessary reduce the influence of racial biases on social fear learning.

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 25 mg 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 25 mg oxazepam on emotional mimicry or empathy.

Social transmission of both threat and safety is ubiquitous, but little is known about the neural circuitry underlying vicarious safety learning. This is surprising given that these processes are critical to flexibly adapt to a changeable environment. To address how the expression of previously learned fears can be modified by the transmission of social information, two conditioned stimuli (CS+s) were paired with shock and the third was not. During extinction, we held constant the amount of direct, non-reinforced, exposure to the CSs (i.e. direct extinction), and critically varied whether another individual - acting as a demonstrator - experienced safety (CS+_{vic safety}) or aversive reinforcement (CS+_{vic reinf}). During extinction, vmPFC responses to the CS+_{vic reinf} increased but decreased to the CS+_{vic safety}. This pattern of vmPFC activity was reversed during a subsequent fear reinstatement test, suggesting a temporal shift in the involvement of the vmPFC. Moreover, only the CS+_{vic reinf} association recovered. Our data suggest that vicarious extinction prevents the return of conditioned fear responses and that this efficacy is reflected by diminished vmPFC involvement during extinction learning. The present findings may have important implications for understanding how social information influence the persistence of fear memories in individuals suffering from emotional disorders.

Social fear learning offers an efficient way to transmit information about potential threats; little is known, however, about the learning processes that counteract the social transmission of fear. In three separate experiments, we found that safety information transmitted from another individual (i.e., demonstrator) during preexposure prevented subsequent observational fear learning (Experiments 1-3), and this effect was maintained in a new context involving direct threat confrontation (Experiment 3). This protection from observational fear learning was specific to conditions in which information about both safety and danger was transmitted from the same demonstrator (Experiments 2-3) and was unaffected by increasing the number of the safety demonstrators (Experiment 3). Collectively, these findings demonstrate that observational preexposure can limit social transmission of fear. Future research is needed to better understand the conditions under which such effects generalize across individual demonstrators. (PsycINFO Database Record

Humans and nonhuman primates preferentially learn to fear and avoid archetypical fear-relevant stimuli. Yet how these learning biases influence adaptive behavior, the basic mechanistic underpinnings of these biases, and how they interact with learning experiences during the life span of an individual remain unknown. To study this, we investigated how 4 classes of fear-relevant stimuli (snakes, threatening in-group faces, racial out-group faces, and guns) influenced adaptive behavior. We showed that stimulus-driven biases have a dramatic influence that can either promote or corrupt adaptive behavior depending on how a bias relates to the environment. We quantified and compared the effects of different fear-relevant stimuli on instrumental behavior using a computational reinforcement learning model that formalized the idea that the bias reflects competition between an instrumental and a Pavlovian valuation system. These results were further clarified by 2 independent rating studies showing that perceived danger of the stimuli corresponded well with their influence on adaptive behavior.