Dangerous Stimuli Research Articles

Neural control of tumor immunity.

Communication between the nervous system and the immune system has evolved to optimally respond to potentially dangerous stimuli both from within and outside the body. Tumors pose a severe threat to an organism and current therapies are insufficient for tumor regression in the majority of cases. Studies show that tumors are innervated by peripheral nerves from the sensory, parasympathetic and sympathetic nervous systems. Interactions between cancer cells, nerves and immune cells regulate overall tumor progression. Clinical studies have indicated the potential of targeting the peripheral nervous system for promoting anti-tumor immune responses. This view point provides an opinion on the current evidence and therapeutic potential of manipulating neuro-immune communications in cancer.

Habituation to a predatory stimulus in a harvester (Arachnida, Opiliones)

Several studies have investigated habituation in a defensive context, but few have addressed responses to dangerous stimuli. In such cases, animals should not habituate since this could cost their lives. Here we have stimulated individuals of the harvester Mischonyx squalidus with a predatory stimulus (squeezing with tweezers) in repeated trials within and between days, and measured the occurrence and magnitude of nipping, a defensive behavior. Contrary to our expectations, they did habituate to this stimulus. The probability and magnitude of response declined over trials during each of three days of testing in a typical habituation pattern. During the trials we also observed other defensive behaviors. We discuss our results mainly considering alternative defensive responses. Our data show that we lack information on (1) the role played by the ambiguity of stimuli, (2) the role played by subsequent stimuli and (3) the importance of the array of defensive behaviors of a species in understanding habituation. Although ubiquitous across animals and therefore expected, habituation is described for the first time in the order Opiliones.

Alcohol use and the pain system.

The World Health Organization's epidemiological data from 2016 revealed that while 57% of the global population aged 15years or older had abstained from drinking alcohol in the previous year, more than half of the population in the Americas, Europe, and Western Pacific consumed alcohol. The spectrum of alcohol use behavior is broad: low-risk use (sensible and in moderation), at-risk use (e.g., binge drinking), harmful use (misuse) and dependence (alcoholism; addiction; alcohol use disorder). The at-risk use and misuse of alcohol is associated with the transition to dependence, as well as many damaging health outcomes and preventable causes of premature death. Recent conceptualizations of alcohol dependence posit that the subjective experience of pain may be a significant contributing factor in the transition across the spectrum of alcohol use behavior. This narrative review summarizes the effects of alcohol at all levels of the pain system. The pain system includes nociceptors as sensory indicators of potentially dangerous stimuli and tissue damage (nociception), spinal circuits mediating defensive reflexes, and most importantly, the supraspinal circuits mediating nocifensive behaviors and the perception of pain. Although the functional importance of pain is to protect from injury and further or future damage, chronic pain may emerge despite the recovery from, and absence of, biological damage (i.e., in the absence of nociception). Like other biological perceptual systems, pain is a construction contingent on sensory information and a history of individual experiences (i.e., learning and memory). Neuroadaptations and brain plasticity underlying learning and memory and other basic physiological functions can also result in pathological conditions such as chronic pain and addiction. Moreover, the negative affective/emotional aspect of pain perception provides embodied and motivational components that may play a substantial role in the transition from alcohol use to dependence.

Evaluation of the effects produced by triggering pyrotechnic articles for automotive use by exposure to various hazardous external stimuli

The object of the evaluation of the risk factors that may lead to the accidental initiation of the semi-finished products containing pyrotechnic articles in the process of handling / use / storage / transport is represented by the estimation and assessment of the risk of initiation / detonation of pyrotechnic devices, based on the quantification of the dangers specific to the operations with these types of products, carried out in various phases of the technological flow, used in the manufacture of electrical circuit breakage subassemblies in motor vehicles. Protection against detonation due to accidental initiation is of particular interest to safety because these detonations endanger the life and health of workers as a result of the uncontrollable effects of deflagration and pressure, the presence of toxic reaction products and the consumption of oxygen from ambient air, which workers must inspire. Accidental initiation / detonation of the pyrotechnic actuator can occur by exposing it to the following dangerous external stimuli: electrostatic charge/electrical discharge – with a potential greater than 25 kV; stray currents when passing a current of 0.4 A through the two actuator initiation pins; temperature – higher than 165 ⁰ C; mechanical shock.

Human Transient Receptor Potential Ankyrin 1 Channel: Structure, Function, and Physiology.

The transient receptor potential ion channel TRPA1 is a Ca2+-permeable nonselective cation channel widely expressed in sensory neurons, but also in many nonneuronal tissues typically possessing barrier functions, such as the skin, joint synoviocytes, cornea, and the respiratory and intestinal tracts. Here, the primary role of TRPA1 is to detect potential danger stimuli that may threaten the tissue homeostasis and the health of the organism. The ability to directly recognize signals of different modalities, including chemical irritants, extreme temperatures, or osmotic changes resides in the characteristic properties of the ion channel protein complex. Recent advances in cryo-electron microscopy have provided an important framework for understanding the molecular basis of TRPA1 function and have suggested novel directions in the search for its pharmacological regulation. This chapter summarizes the current knowledge of human TRPA1 from a structural and functional perspective and discusses the complex allosteric mechanisms of activation and modulation that play important roles under physiological or pathophysiological conditions. In this context, major challenges for future research on TRPA1 are outlined.

Neuromuscular basis of Drosophila larval rolling escape behavior.

When threatened by dangerous or harmful stimuli, animals engage in diverse forms of rapid escape behaviors. In Drosophila larvae, one type of escape response involves C-shaped bending and lateral rolling followed by rapid forward crawling. The sensory circuitry that promotes larval escape has been extensively characterized; however, the motor programs underlying rolling are unknown. Here, we characterize the neuromuscular basis of rolling escape behavior. We used high-speed, volumetric, Swept Confocally Aligned Planar Excitation (SCAPE) microscopy to image muscle activity during larval rolling. Unlike sequential peristaltic muscle contractions that progress from segment to segment during forward and backward crawling, muscle activity progresses circumferentially during bending and rolling escape behavior. We propose that progression of muscular contraction around the larva's circumference results in a transient misalignment between weight and the ground support forces, which generates a torque that induces stabilizing body rotation. Therefore, successive cycles of slight misalignment followed by reactive aligning rotation lead to continuous rolling motion. Supporting our biomechanical model, we found that disrupting the activity of muscle groups undergoing circumferential contraction progression leads to rolling defects. We use EM connectome data to identify premotor to motor connectivity patterns that could drive rolling behavior and perform neural silencing approaches to demonstrate the crucial role of a group of glutamatergic premotor neurons in rolling. Our data reveal body-wide muscle activity patterns and putative premotor circuit organization for execution of the rolling escape response.

Rapid withdrawal from a threatening animal is movement-specific and mediated by reflex-like neural processing

Responses to potentially dangerous stimuli are among the most basic animal behaviors. While research has shown that threats automatically capture the attention of human participants, research has failed to demonstrate automatic behavioral responses to threats in humans. Using a novel naturalistic paradigm, we show that two species of animals humans often report fearing trigger rapid withdrawal responses: participants withdrew their arm from photos of snakes and spiders faster, and with higher acceleration when compared to bird and butterfly stimuli. The behavior was specific to withdrawal as approach movements or button-press/release tasks failed to detect a similar difference. Moreover, between-participant differences in how aversive they found the stimuli predicted the participant's withdrawal speed, indicating that the paradigm was also sensitive to trait-level differences between individuals. Using electroencephalography (EEG), we show that the fast withdrawal was mediated by two attentional processes. First, fast withdrawal responses were associated with early amplification of sensory signals (40–110 ms after stimulus). Second, a later correlate of feature-based attention (early posterior negativity, EPN, 200–240 ms after stimulus) revealed the opposite pattern: Stronger EPN was associated with slower behavioral responses, suggesting that the deployment of attention towards the threatening stimulus features, or failure to “disengage” attention from the stimulus, was detrimental for withdrawal speed. Altogether, the results suggest that rapid behavioral withdrawal from a threatening animal is mediated by reflex-like attentional processing, and later, conscious attention to stimulus features may hinder escaping the treat.

Advances in neural circuits of innate fear defense behavior.

Fear, a negative emotion triggered by dangerous stimuli, can lead to psychiatric disorders such as phobias, anxiety disorders, and depression. Investigating the neural circuitry underlying congenital fear can offer insights into the pathophysiological mechanisms of related psychiatric conditions. Research on innate fear primarily centers on the response mechanisms to various sensory signals, including olfactory, visual, and auditory stimuli. Different types of fear signal inputs are regulated by distinct neural circuits. The neural circuits of the main and accessory olfactory systems receive and process olfactory stimuli, mediating defensive responses like freezing. Escape behaviors elicited by visual stimuli are primarily regulated through the superior colliculus and hypothalamic projection circuits. And auditory stimuli-induced responses, including escape, are mainly mediated through auditory cortex projection circuits. As for auditory stimuli, they are mainly triggered by the auditory cortical projection circuits, leading to escape and other responses. In this article, we review the research progress on the neural circuits of innate fear defensive behaviors in animals from different sensory systems, especially the projection circuits of olfactory, visual, and auditory systems, to provide references for the mechanistic study of related mental disorders.

CORONAPHOBIA AS PSYCHODYNAMICS AND COPING MECHANISMS DURING THE COVID-19 PANDEMIC

Introduction – Since first appearing in Wuhan at the end of 2019, the corona virus has caused many losses in various aspects of human life. Starting from the physical-psychological aspect of health and socio-economic. Even now, the new policies adopted by the government also have a huge impact on people's daily habits. One of them is affecting a person's psychology, where the news about COVID-19 has been very developed, causing anxiety and fear among the community. With the many stressors that have emerged in this pandemic era, a person is required to have good coping skills to be able to cope with dangerous stimuli. For someone who has a bad coping skills, he will experience excessive fear and anxiety about the corona virus which is called coronaphobia. Methods – The author makes a review of 20 journals and 2 books discussing definitions, risk factors, psychodynamics, coping mechanisms and management of new phobias in this pandemic era. Results – From several literature reviews, the factors identified in this pandemic era were unforeseen reality, unending uncertainties, need of acquiring new practices and avoidance behavior, loss of faith in health infrastructure, contraction of COVID-19 by head of states, cautionary statements from international bodies, and infodemia. Discuss – Several identified factors factors are assumed to cause interference with routine life, catastrophizing interpretation of benign symptoms, and social amplification of risk which lead to coronaphobia. This requires a person to have a good coping mechanism to adapt to new habits of coexistence with this virus. If the coping mechanism of a person is bad, then the stressor will experience a psychosocial process causing a phobia against COVID-19 which is called coronaphobia. Conclusion – Coronaphobia is excessive fear and anxiety due to the various effects of the corona virus, be it related to thoughts, information or the illness it causes. This new phobia is caused by the emergence of several risk factors in this pandemic era, which undergo some psychosocial process. Individuals who use maladaptive coping mechanisms are more likely to engage in risky behavior and experience health problems than those with adaptive mechanisms. Therefore, a good coping strategy is needed to avoid the occurrence of psychological problems such as coronaphobia that often arise during this pandemics. Keywords: coronaphobia, COVID-19, psychodynamic, coping mechanism, fear.

Making good of a tricky start: How IgE and mast cells manage a protective sway in food allergy

The immune and nervous systems respond to dangerous stimuli to maintain homeostasis. In a recent issue of Nature, Florsheim etal. and Plum etal. uncover the crosstalk between immunoglobulin E (IgE)-mast-cell-mediated immune activation and neural responses driving behavioral avoidance of allergenic food.

Association between NLRP3 rs10754558 and CARD8 rs2043211 Variants and Susceptibility to Chronic Kidney Disease.

Nod-like receptor protein 3 (NLRP3) is a multi-protein complex belonging to the innate immune system, whose activation by danger stimuli promotes inflammatory cell death. Evidence supports the crucial role of NLRP3 inflammasome activation in the transition of acute kidney injury to Chronic Kidney Disease (CKD), by promoting both inflammation and fibrotic processes. Variants of NLRP3 pathway-related genes, such as NLRP3 itself and CARD8, have been associated with susceptibility to different autoimmune and inflammatory diseases. In this study, we investigated for the first time the association of functional variants of NLRP3 pathway-related genes (NLRP3-rs10754558, CARD8-rs2043211), with a susceptibility to CKD. A cohort of kidney transplant recipients, dialysis and CKD stage 3-5 patients (303 cases) and a cohort of elderly controls (85 subjects) were genotyped for the variants of interest and compared by using logistic regression analyses. Our analysis showed a significantly higher G allele frequency of the NLRP3 variant (67.3%) and T allele of the CARD8 variant (70.8%) among cases, compared with the control sample (35.9 and 31.2%, respectively). Logistic regressions showed significant associations (p < 0.001) between NLRP3 and CARD8 variants and cases. Our results suggest that the NLRP3 rs10754558 and CARD8 rs2043211 variants could be associated with a susceptibility to CKD.

Anti-inflammatory potential of platinum nanozymes: mechanisms and perspectives.

Inflammation is a complex process of the body in response to pathogen infections or dysregulated metabolism, involving the recruitment and activation of immune system components. Repeated dangerous stimuli or uncontrolled immune effector mechanisms can result in tissue injury. Reactive Oxygen Species (ROS) play key roles in physiological cell signaling as well as in the destruction of internalized pathogens. However, aberrant ROS production and release have deleterious effects on the surrounding environment, making ROS regulation a priority to reduce inflammation. Most of the current anti-inflammatory therapies rely on drugs that impair the release of pro-inflammatory mediators. Nevertheless, increasing the enzymatic activity to reduce ROS levels could be an alternative or complementary therapeutic approach to decrease inflammation. Nanozymes are nanomaterials with high catalytic activity that mimic natural enzymes, allowing biochemical reactions to take place. Such functional particles typically show different and regenerable oxidation states or catalytically reactive surfaces offering long-term activity and stability. In this scenario, platinum-based nanozymes (PtNZs) exhibit broad and efficient catalytic functionalities and can reduce inflammation mainly through ROS scavenging, e.g. by catalase and superoxide dismutase reactions. Dose-dependent biocompatibility and immune compatibility of PtNZs have been shown in different cells and tissues, both in vitro and in vivo. Size/shape/surface engineering of the nanozymes could also potentiate their efficacy to act at different sites and/or steps of the inflammation process, such as cytokine removal or specific targeting of activated leukocytes. In the present review, we analyze key inflammation triggering processes and the effects of platinum nanozymes under exemplificative inflammatory conditions. We further discuss potential platinum nanozyme design and improvements to modulate and expand their anti-inflammatory action.

The roles of HDAC with IMPDH and mTOR with JAK as future targets in the treatment of rheumatoid arthritis with combination therapy.

Various studies have shown that cytokines are important regulators in rheumatoid arthritis (RA). In synovial inflammation alteration of the enzyme HDAC, IMPDH enzyme, mTOR pathway, and JAK pathway increase cytokine level. These increased cytokine levels are responsible for the inflammation in RA. Inflammation is a physiological and normal reaction of the immune system against dangerous stimuli such as injury and infection. The cytokine-based approach improves the treatment of RA. To reach this goal, various researchers and scientists are working more aggressively by using a combination approach. The present review of combination therapy provides essential evidence about the possible synergistic effect of combinatorial agents. We have focused on the effects of HDAC inhibitor with IMPDH inhibitor and mTOR inhibitor with JAK inhibitor in combination for the treatment of RA. Combining various targeted strategies can be helpful for the treatment of RA.

Far from disgusted: The relationships between disgust sensitivity, dark personality traits, and biological sex

Disgust is an avoidant emotion which repulses from potentially dangerous stimuli and situations. Operating in a social context, disgust may prevent from engaging in an unrestricted sociosexuality and from violating moral norms. Meanwhile, people high in dark personality traits prefer short-term mating strategy and exhibit a tendency to transgress moral standards. Thus, it might be assumed that they should have decreased both moral and sexual disgust. In a preregistered study (N = 450; 52 % female) we tested our assumptions by examining the relationships between Dark Triad, vulnerable narcissism, and disgust sensitivity in moral and sexual domains. We also asked whether higher psychopathy and Machiavellianism in men would explain sex discrepancy in sexual disgust sensitivity. The results confirmed most of our hypotheses and showed that a) sexual and moral disgust are consistently, negatively correlated with all Dark Triad traits; b) there are considerable sex differences in sexual disgust and psychopathy; and c) increased psychopathy in men partially explains their lower sexual disgust sensitivity comparing to women. This study has taken a novel perspective in this research area, and may indicate the role of decreased disgust sensitivity in transgressing social norms by individuals high in dark personality traits.

Recent Advances in Multifunctional Antimicrobial Peptides as Immunomodulatory and Anticancer Therapy: Chromogranin A-Derived Peptides and Dermaseptins as Endogenous versus Exogenous Actors.

Antimicrobial peptides (AMPs) are produced by all living organisms exhibiting antimicrobial activities and representing the first line of innate defense against pathogens. In this context, AMPs are suggested as an alternative to classical antibiotics. However, several researchers reported their involvement in different processes defining them as Multifunctional AMPs (MF-AMPs). Interestingly, these agents act as the endogenous responses of the human organism against several dangerous stimuli. Still, they are identified in other organisms and evaluated for their anticancer therapy. Chromogranin A (CgA) is a glyco-phosphoprotein discovered for the first time in the adrenal medulla but also produced in several cells. CgA can generate different derived AMPs influencing numerous physiological processes. Dermaseptins (DRSs) are a family of α-helical-shaped polycationic peptides isolated from the skin secretions of several leaf frogs from the Phyllomedusidae family. Several DRSs were identified as AMPs and, until now, more than 65 DRSs have been classified. Recently, these exogenous molecules were characterized for their anticancer activity. In this review, we summarize the role of these two classes of MF-AMPs as an example of endogenous molecules for CgA-derived peptides, able to modulate inflammation but also as exogenous molecules for DRSs, exerting anticancer activities.

Neuronal Encoding of Emotional Valence and Intensity in the Monkey Amygdala.

Neuropsychological and neuroimaging studies have suggested that the primate amygdala plays an essential role in processing the emotional valence and intensity of visual stimuli, which is necessary for determining whether to approach or avoid a stimulus. However, the neuronal mechanisms underlying the evaluation of emotional value remain unknown. In the present study, we trained male macaque monkeys to perform an operant conditioning task in which fractal visual patterns were associated with three different amounts of air puff delivered to the cheek (negative) or liquid reward (positive). After confirming that the monkeys successfully differentiated the emotional valence and intensity of the visual stimuli, we analyzed neuronal responses to the stimuli in the amygdala. Most amygdala neurons conveyed information concerning the emotional valence and/or intensity of the visual stimuli, and the majority of those conveying information about emotional valence responded optimally to negative stimuli. Further, some amygdala neurons conveyed information related to both emotional valence and intensity, whereas a small portion conveyed information related to emotional intensity alone. These results indicate that the primate amygdala encodes both emotional valence and intensity, highlighting its important role in the avoidance of dangerous stimuli and animal survival.SIGNIFICANCE STATEMENT Evaluating the emotional value of visual stimuli is essential for animal survival, especially in primates. Emotional value is estimated from the emotional valence and intensity of stimuli, and evidence indicates that the amygdala is likely to play a major role in processing these types of information. To our knowledge, the current study is the first to examine the responses of neurons in the monkey amygdala to visual stimuli that differ in emotional valence and intensity simultaneously. Our data suggest that the amygdala plays an important role in the evaluation of emotional stimuli and in the decision to escape negative and harmful stimuli.

Trauma and Memory

A theory of traumatic memory was developed by Breuer and Freud in “Studies on Hysteria” based on Charcot’s theory on the traumatic origin of mental disorders. This was again developed in DSM-III in 1980 with the introduction of posttraumatic stress disorder (PTSD), where traumatic memory was conceptualized as a core of the syndrome and set in causal relationship with its manifestations. This implied that “trauma” tended to be seen as something static and reified, like a “thing” in the mind. It is shown that this conceptualisation diverts attention from the dynamic and reorganizing processes in the traumatized person’s mind, body and relations to others. The psychoanalytic conceptualization includes a wider spectre of the manifestations in posttraumatic conditions and it differs in the understanding of underlying processes. What is common for both childhood and adult trauma and their posttraumatic manifestations are deficiencies in symbolization processes related to the traumatic experiences. The signal anxiety function fails and the ego is overwhelmed by automatic or annihilation anxiety. The ability to distinguish between real danger and neutral stimuli which function as triggers fails. As anxiety related to trauma cannot be mentalized, fragments of the self are split off and evacuated. These experiences remain as fragmented bits and pieces that can express themselves in bodily pain, dissociated states of mind, nightmares and relational disturbances. Thus, the consequences of psychological trauma may be conceptualised as processes characterised by splitting off of not mentalized inner objects/introjects and parts of the mental apparatus. These processes are illustrated with a short clinical vignette.

Ferroptosis resistance cooperates with cellular senescence in the overt stage of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.

Cellular senescence and ferroptosis are the two main, fine-tuned processes in tissue damage restraint; however, they can be overactivated in pathologies such as nonalcoholic fatty liver disease/nonalcoholic steatohepatitis (NAFLD/NASH), becoming dangerous stimuli. Senescence is characterized by a decline in cell division and an abnormal release of reactive oxygen species (ROS), and ferroptosis is represented by iron deposition associated with an excessive accumulation of ROS. ROS and cellular stress pathways are also drivers of NAFLD/NASH development. The etiology of NAFLD/NASH lies in poor diets enriched in fat and sugar. This food regimen leads to liver steatosis, resulting in progressive degeneration of the organ, with a late onset of irreversible fibrosis and cirrhosis. Few studies have investigated the possible connection between senescence and ferroptosis in NAFLD/NASH progression, despite the two events sharing some molecular players. We hypothesized a possible link between senescence and ferroptosis in a NAFLD background. To thoroughly investigate this in the context of “Western-style” diet (WSD) abuse, we used an amylin-modified liver NASH mouse model. The main NASH hallmarks have been confirmed in this model, as well as an increase in apoptosis, and Ki-67 and p53 expression in the liver. Senescent beta-galactosidase-positive cells were elevated, as well as the expression of the related secretory molecules Il-6 and MMP-1. Features of DNA damage and iron-overload were found in the livers of NASH mice. Gpx4 (glutathione peroxidase 4) expression, counteracting ferroptotic cell death, was increased. Notably, an increased number of senescent cells showing overexpression of gpx4 was also found. Our data seem to suggest that senescent cells acquire a gpx4-mediated mechanism of ferroptosis resistance and thus remain in the liver, fostering the deterioration of liver fitness.

Nerve Growth Factor (NGF) as Partaker in the Modulation of UV-Response in Cultured Human Conjunctival Fibroblasts.

Corroborating data sustain the pleiotropic effect of nerve growth factor (NGF) in the protection of the visual system from dangerous stimuli, including ultraviolet (UV). Since UV exposure might promote ocular surface changes (conjunctival inflammation and matrix rearrangement), as previously reported from in vivo studies sustaining some protective NGF effects, in vitro cultures of human conjunctival fibroblasts (FBs) were developed and exposed to a single UV exposure over 15 min (0.277 W/m2), either alone or supplemented with NGF (1–10–100 ng/mL). Conditioned media and cell monolayers were collected and analyzed for protein release (ELISA, ELLA microfluidic) and transcript expression (real-time PCR). A specific “inflammatory to remodeling” pattern (IL8, VEGF, IL33, OPN, and CYR61) as well as a few epigenetic transcripts (known as modulator of cell differentiation and matrix-remodeling (DNMT3a, HDAC1, NRF2 and KEAP1)) were investigated in parallel. UV-exposed FBs (i), showed no proliferation or significant cytoskeleton rearrangement; (ii), displayed a trkANGFR/p75NTR phenotype; and (iii), synthesized/released IL8, VEGF-A, IL33, OPN, and CYR61, as compared to unexposed ones. NGF addition counteracted IL8, IL33, OPN, and CYR61 protein release merely at lower NGF concentrations but not VEGF. NGF supplementation did not affect DNMT3a or HDAC1 transcripts, while it significantly upregulated NRF2 at lowest NGF doses and did not change KEAP1 expression. Taken together, a single UV exposure activated conjunctival FBs to release pro-inflammatory/fibrogenic factors in association with epigenetic changes. The effects were selectively counteracted by NGF supplementation in a dose-dependent fashion, most probably accountable to the trkANGFR/p75NTR phenotype. Further in vitro studies are underway to better understand this additional NGF pleiotropic effect. Since UV-shield impairments represent a worldwide alert and UV radiation can slowly affect ocular surface homeostasis (photo-ageing, cataract) or might exacerbate ocular diseases with a preexisting fibrosis (pterygium, VKC), these findings on NGF modulation of UV-exposed FBs might provide additional information for protecting the ocular surface (homeostasis) from low-grade long-lasting UV insults.

No trait anxiety influences on early and late differential neuronal responses to aversively conditioned faces across three different tasks

The human brain's ability to quickly detect dangerous stimuli is crucial in selecting appropriate responses to possible threats. Trait anxiety has been suggested to moderate these processes on certain processing stages. To dissociate such different information-processing stages, research using classical conditioning has begun to examine event-related potentials (ERPs) in response to fear-conditioned (CS +) faces. However, the impact of trait anxiety on ERPs to fear-conditioned faces depending on specific task conditions is unknown. In this preregistered study, we measured ERPs to faces paired with aversive loud screams (CS +) or neutral sounds (CS −) in a large sample (N = 80) under three different task conditions. Participants had to discriminate face-irrelevant perceptual information, the gender of the faces, or the CS category. Results showed larger amplitudes in response to aversively conditioned faces for all examined ERPs, whereas interactions with the attended feature occurred for the P1 and the early posterior negativity (EPN). For the P1, larger CS + effects were observed during the perceptual distraction task, while the EPN was increased for CS + faces when deciding about the CS association. Remarkably, we found no significant correlations between ERPs and trait anxiety. Thus, fear-conditioning potentiates all ERP amplitudes, some processing stages being further modulated by the task. However, the finding that these ERP differences were not affected by individual differences in trait anxiety does not support theoretical accounts assuming increased threat processing or reduced threat discrimination depending on trait anxiety.