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Abstract The behavioral and neural responses to social exclusion were examined in women randomized to four conditions, varying in levels of attractiveness and friendliness. Informed by evolutionary theory, we predicted that being socially excluded by attractive unfriendly women would be more distressing than being excluded by unattractive women, irrespective of their friendliness level. Our results contradicted most of our predictions but provide important insights into women’s responses to interpersonal conflict. Accounting for rejection sensitivity, P300 event-related potential amplitudes were largest when women were excluded by unattractive unfriendly women. This may be due to an expectancy violation or an annoyance with being excluded by women low on social desirability. An examination of anger rumination rates by condition suggests the latter. Only attractive women’s attractiveness ratings were lowered in the unfriendly condition, indicating they were specifically punished for their exclusionary behavior. Women were more likely to select attractive women to compete against with one exception—they selected the Black attractive opponent less often than the White attractive opponent when presented as unfriendly. Finally, consistent with studies on retaliation in relation to social exclusion, women tended to rate competitors who rejected them as being more rude, more competitive, less attractive, less nice, and less happy than non-competitors. The ubiquity of social exclusion and its pointed emotional and physiological impact on women demands more research on this topic.

Abstract In this narrative review, we examine biological processes linking psychological stress and cognition, with a focus on how psychological stress can activate multiple neurobiological mechanisms that drive cognitive decline and behavioral change. First, we describe the general neurobiology of the stress response to define neurocognitive stress reactivity. Second, we review aspects of epigenetic regulation, synaptic transmission, sex hormones, photoperiodic plasticity, and psychoneuroimmunological processes that can contribute to cognitive decline and neuropsychiatric conditions. Third, we explain mechanistic processes linking the stress response and neuropathology. Fourth, we discuss molecular nuances such as an interplay between kinases and proteins, as well as differential role of sex hormones, that can increase vulnerability to cognitive and emotional dysregulation following stress. Finally, we explicate several testable hypotheses for stress, neurocognitive, and neuropsychiatric research. Together, this work highlights how stress processes alter neurophysiology on multiple levels to increase individuals’ risk for neurocognitive and psychiatric disorders, and points toward novel therapeutic targets for mitigating these effects. The resulting models can thus advance dementia and mental health research, and translational neuroscience, with an eye toward clinical application in cognitive and behavioral neurology, and psychiatry.

Bullying victimization is a form of psychological stress that is associated with poor outcomes in the areas of mental health and learning. Although the emotional maladjustment and memory impairment following interpersonal stress are well documented, the mechanisms of complex cerebral dysfunctions have neither been outlined nor studied in depth in the context of childhood bullying victimization. As a contribution to the cross-disciplinary field of developmental psychology and neuroscience, we review the neuropathophysiology of early life stress, as well as general psychological stress to synthesize the data and clarify the versatile dynamics within neuronal networks linked to bullying victimization. The stress-induced neuropsychological cascade and associated cerebral networks with a focus on cognitive and emotional convergence are described. The main findings are that stress-evoked neuroendocrine reactivity relates to neuromodulation and limbic dysregulation that hinder emotion processing and executive functioning such as semantic cognition, cognitive flexibility, and learning. Developmental aspects and interacting neural mechanisms linked to distressed cognitive and emotional processing are pinpointed and potential theory-of-mind nuances in targets of bullying are presented. The results show that childhood stress psychopathology is associated with a complex interplay where the major role belongs to, but is not limited to, the amygdala, fusiform gyrus, insula, striatum, and prefrontal cortex. This interplay contributes to the sensitivity toward facial expressions, poor cognitive reasoning, and distress that affect behavioral modulation and emotion regulation. We integrate the data on major brain dynamics in stress neuroactivity that can be associated with childhood psychopathology to help inform future studies that are focused on the treatment and prevention of psychiatric disorders and learning problems in bullied children and adolescents.

Aversive events can evoke strong emotions that trigger cerebral neuroactivity to facilitate behavioral and cognitive shifts to secure physiological stability. However, upon intense and/or chronic exposure to such events, the neural coping processes can be maladaptive and disrupt mental well-being. This maladaptation denotes a pivotal point when psychological stress occurs, which can trigger subconscious, “automatic” neuroreactivity as a defence mechanism to protect the individual from potential danger including overwhelming unpleasant feelings and disturbing or threatening thoughts.The outcomes of maladaptive neural activity are cognitive dysfunctions such as altered memory, decision making, and behavior that impose a risk for mental disorders. Although the neurocognitive phenomena associated with psychological stress are well documented, the complex neural activity and pathways related to stressor detection and stress coping have not been outlined in detail. Accordingly, we define acute and chronic stress-induced pathways, phases, and stages in relation to novel/unpredicted, uncontrollable, and ambiguous stressors. We offer a comprehensive model of the stress-induced alterations associated with multifaceted pathophysiology related to cognitive appraisal and executive functioning in stress.