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Adverse environments are linked to elevated youth antisocial behavior. However, this relation is thought to depend, in part, on genetic susceptibility. The present study investigated whether polygenic risk for antisociality moderates relations between hostile environments and stable as well as dynamic antisocial behaviors across adolescence. We derived two antisocial-linked polygenic risk scores (PRS) ( N = 721) based on previous genome-wide association studies. Forms of antisocial behavior (nonaggressive conduct problems, physical aggression, social aggression) and environmental hostility (harsh parenting and school violence) were assessed at age 13, 15, and 17 years. Relations to individual differences stable across adolescence (latent stability) vs. time-specific states (timepoint residual variance) of antisocial behavior were assessed via structural equation models. Higher antisocial PRS, harsh parenting, and school violence were linked to stable elevations in antisocial behaviors across adolescence. We identified a consistent polygenic-environment interaction suggestive of differential susceptibility in late adolescence. At age 17, harsher parenting was linked to higher social aggression in those with higher antisocial PRS, and lower social aggression in those with lower antisocial PRS. This suggests that genetics and environmental hostility relate to stable youth antisocial behaviors, and that genetic susceptibility moderates home environment-antisocial associations specifically in late adolescence.

Difficulty recognizing negative emotions is linked to aggression in children. However, it remains unclear how certain types of emotion recognition (insensitivities vs. biases) are associated with functions of aggression and whether these relations change across childhood. We addressed these gaps in two diverse community samples (study 1: aged 4 and 8; N = 300; study 2: aged 5 to 13, N = 374). Across studies, children performed a behavioral task to assess emotion recognition (sad, fear, angry, and happy facial expressions) while caregivers reported children's overt proactive and reactive aggression. Difficulty recognizing fear (especially in early childhood) and sadness was associated with greater proactive aggression. Insensitivity to anger - perceiving angry faces as showing no emotion - was associated with increased proactive aggression, especially in middle-to-late childhood. Additionally, greater happiness bias - mistaking negative emotions as being happy - was consistently related to higher reactive aggression only in early childhood. Together, difficulty recognizing negative emotions was related to proactive aggression, however, the strength of these relations varied based on the type of emotion and developmental period assessed. Alternately, difficulty determining emotion valence was related to reactive aggression in early childhood. These findings demonstrate that distinct forms of emotion recognition are important for understanding functions of aggression across development.

Difficulty recognizing negative emotions (NEs) in children is linked to increased antisocial traits and externalizing problems. However, crucial aspects of this relation remain unclear, such as: whether NE recognition is associated with externalizing problems in general or only a particular subcomponent (i.e., aggression); whether subcomponents of NE recognition (i.e., insensitivity and misspecifications) are relatively more important; and how these relations change over the course of development. We assessed emotion recognition, overt aggression, attention deficit hyperactivity disorder (ADHD) symptoms, and oppositional defiant disorder (ODD) symptoms in an ethnically diverse sample of Canadian children (N = 150; 4-year-olds, N = 148; 8-year-olds) and followed up with them 1 year later (86.9% retention). Emotion recognition was assessed using a behavioral task and caregivers reported on children's externalizing symptoms. Children with lower NE recognition had higher initial, but not subsequent, overt aggression, even when controlling for nonaggressive externalizing symptoms (i.e., ADHD and ODD symptoms). NE recognition was not concurrently or longitudinally associated with nonaggressive externalizing symptoms. Age and gender did not moderate these findings. Both higher NE insensitivity (e.g., reporting a sad face appears neutral) and misspecifications (e.g., reporting a sad face appears angry) were significantly associated with higher concurrent overt aggression. In conclusion, both NE insensitivity and misspecifications were found to be uniquely important for children's overt aggression. These findings highlight the importance of different forms of NE recognition and differentiating between aggressive and nonaggressive externalizing problems in children., (© 2021 Wiley Periodicals LLC.)

Research investigating the link between the parasympathetic nervous system (PNS) and prosociality in childhood has yielded inconsistent findings. This relation has mainly been conceptualized as linear, however, the broader physiological literature suggests that children's physiological arousal and task performance may be related in an inverted U-shaped fashion-with peak performance at moderate levels of arousal. Therefore, we tested whether resting respiratory sinus arrhythmia (RSA)-a dispositional indicator of PNS activity-was quadratically related to child- and caregiver-reported sympathy and prosocial behaviors in an ethnically diverse sample of 4- and 8-year-olds (N = 300). We found a quadratic inverted U-shaped association between resting RSA and child-reported sympathy and prosocial behavior in 8-year-olds, whereas no consistent findings emerged for 4-year-olds. Therefore, moderate resting RSA in middle childhood may facilitate sympathy and prosocial behaviors. Dispositional over- or under-arousal of the PNS may impair children's ability to attend and respond to the distress of others by middle childhood., (© 2019 Wiley Periodicals, Inc.)

Pain memories are hypothesized to be critically involved in the transition of pain from an acute to a chronic state. To help elucidate the underlying neurobiological mechanisms of pain memory, we developed novel paradigms to study context-dependent pain hypersensitivity in mouse and human subjects, respectively. We find that both mice and people become hypersensitive to acute, thermal nociception when tested in an environment previously associated with an aversive tonic pain experience. This sensitization persisted for at least 24 hr and was only present in males of both species. In mice, context-dependent pain hypersensitivity was abolished by castrating male mice, pharmacological blockade of the hypothalamic-pituitary-adrenal axis, or intracerebral or intrathecal injections of zeta inhibitory peptide (ZIP) known to block atypical protein kinase C (including the protein kinase Mζ isoform). In humans, men, but not women, self-reported higher levels of stress when tested in a room previously associated with tonic pain. These models provide a new, completely translatable means for studying the relationship between memory, pain, and stress., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Empathy is a psychological construct that allows individuals to understand and share the emotions of others. The ability to share emotional states relies on basic social mechanisms, such as mimicry and emotional contagion, which are considered building blocks for empathy. Mimicking another's emotional or physical state is essential for successful social interactions and is found in a number of animal species. For the current review we focus on emotional state sharing in rodents, a core feature of empathy that is often measured using pain and fear as proxies; we also discuss prosociality in rodents. The evidence for empathy in rodents shows that rats and mice consistently imitate arousal states and behaviors of conspecifics and will even sacrifice personal gain to relieve the distress of a conspecific. These behaviors support basic processes that are crucial for the survival of individual animals and give us insight into the neural mechanisms that govern empathy-related behaviors., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Unlabelled: Recent efforts have suggested that the β-adrenergic receptor (β-AR) system may be a novel and viable therapeutic target for pain reduction; however, most of the work to date has focused on the β(2)-adrenergic receptor (AR). Here, we compared the antinociceptive effects of enantiomeric configurations of propranolol and bupranolol, two structurally similar nonselective β-blocking drugs, against mouse models of inflammatory and chronic pain. In addition, we calculated in silico docking and measured the binding properties of propranolol and bupranolol for all 3 β-ARs. Of the agents examined, S-bupranolol is superior in terms of its antinociceptive effect and exhibited fewer side effects than propranolol or its associated enantiomers. In contrast to propranolol, S-bupranolol exhibited negligible β-AR intrinsic agonist activity and displayed a full competitive antagonist profile at β(1)/β(2)/β(3)-ARs, producing a unique blockade of β(3)-ARs. We have shown that S-bupranolol is an effective antinociceptive agent in mice without negative side effects. The distinctive profile of S-bupranolol is most likely mediated by its negligible β-AR intrinsic agonist activity and unique blockade of β(3)-AR. These findings suggest that S-bupranolol instead of propranolol may represent a new and effective treatment for a variety of painful conditions., Perspective: The S enantiomer of bupranolol, a β-receptor antagonist, shows greater antinociceptive efficacy and a superior preclinical safety profile and it should be considered as a unique β-adrenergic receptor compound to advance future clinical pain studies., (Copyright © 2015 American Pain Society. Published by Elsevier Inc. All rights reserved.)

Empathy for another's physical pain has been demonstrated in humans [1] and mice [2]; in both species, empathy is stronger between familiars. Stress levels in stranger dyads are higher than in cagemate dyads or isolated mice [2, 3], suggesting that stress might be responsible for the absence of empathy for the pain of strangers. We show here that blockade of glucocorticoid synthesis or receptors for adrenal stress hormones elicits the expression of emotional contagion (a form of empathy) in strangers of both species. Mice and undergraduates were tested for sensitivity to noxious stimulation alone and/or together (dyads). In familiar, but not stranger, pairs, dyadic testing was associated with increased pain behaviors or ratings compared to isolated testing. Pharmacological blockade of glucocorticoid synthesis or glucocorticoid and mineralocorticoid receptors enabled the expression of emotional contagion of pain in mouse and human stranger dyads, as did a shared gaming experience (the video game Rock Band) in human strangers. Our results demonstrate that emotional contagion is prevented, in an evolutionarily conserved manner, by the stress of a social interaction with an unfamiliar conspecific and can be evoked by blocking the endocrine stress response., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

We found that exposure of mice and rats to male but not female experimenters produces pain inhibition. Male-related stimuli induced a robust physiological stress response that results in stress-induced analgesia. This effect could be replicated with T-shirts worn by men, bedding material from gonadally intact and unfamiliar male mammals, and presentation of compounds secreted from the human axilla. Experimenter sex can thus affect apparent baseline responses in behavioral testing.