The transfer of social threat learning to decision making is robust to extinction.

Through traditional mass media and online social media, we are almost constantly exposed to second-hand experiences of trauma and violence, providing ample opportunities for us to learn about threats through social means. This social threat learning can influence instrumental decision making through a social learning to decision-making transfer process, resembling the so-called Pavlovian to instrumental transfer effect, resulting in consequences that can be maladaptive. Here, we assessed if this influence could be diminished by extinction learning, a procedure where a previously threatening stimulus is learned to be safe, and thereby mitigate possible maladaptive consequences. To this end, we recruited 251 participants to undergo a social threat learning procedure (where they observed someone else receive electric shocks to one out of two images), followed by either a social or direct extinction procedure (in which no shocks were given), before conducting an instrumental decision-making task to measure the strength of the transfer effect. Based on theoretical considerations and previous literature, we proposed two competing hypotheses: (a) extinction learning would diminish the transfer effect or (b) the transfer effect would be robust to extinction. Our results clearly demonstrate that the social to instrumental transfer effect is remarkedly robust to extinction, supporting the second hypotheses. Irrespective of whether extinction was carried out through direct experience or social means, learning about threats through second-hand aversive experiences strongly influence instrumental behavior, suggesting that potentially maladaptive effects of social threat learning are challenging to diminish. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Model-based representational similarity analysis of blood-oxygen-level-dependent fMRI captures threat learning in social interactions.

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.

Oxazepam and cognitive reappraisal: A randomised experiment.

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.

Social safety learning: Shared safety abolishes the recovery of learned threat.

Humans, like other social animals, learn about threats and safety in the environment through social cues. Yet, the processes that contribute to the efficacy of social safety learning during threat transmission remain unknown. Here, we developed a novel dyadic model of associative threat and extinction learning. In three separate social groups, we manipulated whether safety information during extinction was acquired via direct exposure to the conditioned stimulus (CS) in the presence of another individual (Direct exposure), via observation of other's safety behavior (Vicarious exposure), or via the combination of both (Shared exposure).These groups were contrasted against a fourth group receiving direct CS exposure alone (Asocial exposure). Based on skin conductance responses, we observed that all social groups outperformed asocial learning in inhibiting the recovery of threat, but only Shared exposure abolished threat recovery. These results suggest that social safety learning is optimized by a combination of direct exposure and vicariously transmitted safety signals. This work might help develop exposure therapies used to treat symptoms of threat and anxiety-related disorders to counteract maladaptive fears in humans.

Sleep restriction caused impaired emotional regulation without detectable brain activation changes-a functional magnetic resonance imaging study.

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 (p FWE < 0.05) and lateral orbital cortex (p FWE < 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.

Social threat learning transfers to decision making in humans.

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.

Author Correction: The interplay of social group biases in social threat learning.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.

The interplay of social group biases in social threat learning.

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.

Assessment of social transmission of threats in humans using observational fear conditioning.

Across the human life span, fear is often acquired indirectly by observation of the emotional expressions of others. The observational fear conditioning protocol was previously developed as a laboratory model for investigating socially acquired threat responses. This protocol serves as a suitable alternative to the widely used Pavlovian fear conditioning, in which threat responses are acquired through direct experiences. In the observational fear conditioning protocol, the participant (observer) watches a demonstrator being presented with a conditioned stimulus (CS) paired with an aversive unconditioned stimulus (US). The expression of threat learning is measured as the conditioned response (CR) expressed by the observer in the absence of the demonstrator. CRs are commonly measured as skin conductance responses, but behavioral and neural measures have also been implemented. The experimental procedure is suitable for divergent populations, can be administered by a graduate student and takes ∼40 min. Similar protocols are used in animals, emphasizing its value as a translational tool for studying socioemotional learning.

Effects of 25 mg oxazepam on emotional mimicry and empathy for pain: a randomized controlled experiment.

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.

Don't fear 'fear conditioning': Methodological considerations for the design and analysis of studies on human fear acquisition, extinction, and return of fear.

The so-called 'replicability crisis' has sparked methodological discussions in many areas of science in general, and in psychology in particular. This has led to recent endeavours to promote the transparency, rigour, and ultimately, replicability of research. Originating from this zeitgeist, the challenge to discuss critical issues on terminology, design, methods, and analysis considerations in fear conditioning research is taken up by this work, which involved representatives from fourteen of the major human fear conditioning laboratories in Europe. This compendium is intended to provide a basis for the development of a common procedural and terminology framework for the field of human fear conditioning. Whenever possible, we give general recommendations. When this is not feasible, we provide evidence-based guidance for methodological decisions on study design, outcome measures, and analyses. Importantly, this work is also intended to raise awareness and initiate discussions on crucial questions with respect to data collection, processing, statistical analyses, the impact of subtle procedural changes, and data reporting specifically tailored to the research on fear conditioning.

Vicarious extinction learning during reconsolidation neutralizes fear memory.

BACKGROUND: Previous studies have suggested that fear memories can be updated when recalled, a process referred to as reconsolidation. Given the beneficial effects of model-based safety learning (i.e. vicarious extinction) in preventing the recovery of short-term fear memory, we examined whether consolidated long-term fear memories could be updated with safety learning accomplished through vicarious extinction learning initiated within the reconsolidation time-window. We assessed this in a final sample of 19 participants that underwent a three-day within-subject fear-conditioning design, using fear-potentiated startle as our primary index of fear learning. METHODS: On day 1, two fear-relevant stimuli (reinforced CSs) were paired with shock (US) and a third stimulus served as a control (CS). On day 2, one of the two previously reinforced stimuli (the reminded CS) was presented once in order to reactivate the fear memory 10 min before vicarious extinction training was initiated for all CSs. The recovery of the fear memory was tested 24 h later. RESULTS AND CONCLUSION: Vicarious extinction training conducted within the reconsolidation time window specifically prevented the recovery of the reactivated fear memory (p = 0.03), while leaving fear-potentiated startle responses to the non-reactivated cue intact (p = 0.62). These findings are relevant to both basic and clinical research, suggesting that a safe, non-invasive model-based exposure technique has the potential to enhance the efficiency and durability of anxiolytic therapies.

Neural signals of vicarious extinction learning.

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, ventromedial prefrontal cortex (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 influences the persistence of fear memories in individuals suffering from emotional disorders.

Immunization against social fear learning.

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

Significant grey matter changes in a region of the orbitofrontal cortex in healthy participants predicts emotional dysregulation.

The traditional concept of 'categorical' psychiatric disorders has been challenged as many of the symptoms display a continuous distribution in the general population. We suggest that this is the case for emotional dysregulation, a key component in several categorical psychiatric disorder constructs. We used voxel-based magnetic resonance imaging morphometry in healthy human subjects (n = 87) to study how self-reported subclinical symptoms associated with emotional dysregulation relate to brain regions assumed to be critical for emotion regulation. To measure a pure emotional dysregulation, we also corrected for subclinical symptoms of non-emotional attentional dysregulation. We show that such subclinical emotional symptoms correlate negatively with the grey matter volume of lateral orbitofrontal cortex bilaterally-a region assumed to be critical for emotion regulation and dysfunctional in psychiatric disorders involving emotional dysregulation. Importantly, this effect is mediated both by a decrease in volume associated with emotional dysregulation and an increase in volume due to non-emotional attentional dysregulation. Exploratory analysis suggests that other regions involved in emotional processing such as insula and ventral striatum also show a similar reduction in grey matter volume mirroring clinical disorders associated with emotional dysregulation. Our findings support the concept of continuous properties in psychiatric symptomatology.

Neural correlates of biased social fear learning and interaction in an intergroup context.

Associations linking a fearful experience to a member of a social group other than one's own (out-group) are more resistant to change than corresponding associations to a member of one's own (in-group) (Olsson et al., 2005; Kubota et al., 2012), providing a possible link to discriminative behavior. Using a fear conditioning paradigm, we investigated the neural activity underlying aversive learning biases towards in-group (White) and out-group (Black) members, and their predictive value for discriminatory interactive behavior towards novel virtual members of the racial out-group (n=20). Our results indicate that activity in brain regions previously linked to conditioned fear and perception of individuals belonging to the racial out-groups, or otherwise stigmatized groups, jointly contribute to the expression of race-based biases in learning and behavior. In particular, we found that the amygdala and anterior insula (AI) played key roles in differentiating between in-group and out-group faces both when the faces were paired with an aversive event (acquisition) and when no more shocks were administered (extinction). In addition, functional connectivity between the amygdala and the fusiform gyrus increased during perception of conditioned out-group faces. Moreover, we showed that brain activity in the fear-learning-bias network was related to participants' discriminatory interactions with novel out-group members on a later day. Our findings are the first to identify the neural mechanism of fear learning biases towards out-group members, and its relationship to interactive behavior. Our findings provide important clues towards understanding the mechanisms underlying biases between social groups.

A clash of values: Fear-relevant stimuli can enhance or corrupt adaptive behavior through competition between Pavlovian and instrumental valuation systems.

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.

Learned fear to social out-group members are determined by ethnicity and prior exposure.

Humans, like other animals, have a tendency to preferentially learn and retain some associations more readily than others. In humans, preferential learning was originally demonstrated for certain evolutionary prepared stimuli, such as snakes and angry faces and later extended to human social out-groups based on race (Olsson et al., 2005). To address the generality of this social learning bias, we examined if this learning bias extended to two separate classes of social out-groups represented by neutral Black and Middle-Eastern faces in 38 White (Swedish) participants. We found that other-ethnicity alone was not sufficient to induce an out-group learning bias; it was observed for Black, but not Middle-Eastern, out-group faces. Moreover, an exploratory analysis showed that growing up in an ethnically diverse environment was inversely related to the learning bias toward Middle-Eastern, but not Black, out-groups faces, suggesting that learned fears toward Middle-Eastern faces might be more permeable to environmental factors. Future research should address how both the quantity and quality of inter-group contact modulate out-group learning.

Social learning of fear and safety is determined by the demonstrator's racial group.

Social learning offers an efficient route through which humans and other animals learn about potential dangers in the environment. Such learning inherently relies on the transmission of social information and should imply selectivity in what to learn from whom. Here, we conducted two observational learning experiments to assess how humans learn about danger and safety from members ('demonstrators') of an other social group than their own. We show that both fear and safety learning from a racial in-group demonstrator was more potent than learning from a racial out-group demonstrator.

BDNFval66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall.

Brain-derived neurotrophic factor (BDNF), the most abundant neutrophin in the mammalian central nervous system, is critically involved in synaptic plasticity. In both rodents and humans, BDNF has been implicated in hippocampus- and amygdala-dependent learning and memory and has more recently been linked to fear extinction processes. Fifty-nine healthy participants, genotyped for the functional BDNFval66met polymorphism, underwent a fear conditioning and 24h-delayed extinction protocol while skin conductance and blood oxygenation level dependent (BOLD) responses (functional magnetic resonance imaging) were acquired. We present the first report of neural activation pattern during fear acquisition 'and' extinction for the BDNFval66met polymorphism using a differential conditioned stimulus (CS)+ > CS- comparison. During conditioning, we observed heightened allele dose-dependent responses in the amygdala and reduced responses in the subgenual anterior cingulate cortex in BDNFval66met met-carriers. During early extinction, 24h later, we again observed heightened responses in several regions ascribed to the fear network in met-carriers as opposed to val-carriers (insula, amygdala, hippocampus), which likely reflects fear memory recall. No differences were observed during late extinction, which likely reflects learned extinction. Our data thus support previous associations of the BDNFval66met polymorphism with neural activation in the fear and extinction network, but speak against a specific association with fear extinction processes.