Background: A clinical characteristic of posttraumatic stress disorder (PTSD) is persistently elevated fear responses to stimuli associated with the traumatic event. The objective herein is to determine whether extinction of fear responses is impaired in PTSD and whether such impairment is related to dysfunctional activation of brain regions known to be involved in fear extinction, viz., amygdala, hippocampus, ventromedial prefrontal cortex (vmPFC), and dorsal anterior cingulate cortex (dACC). Methods: Sixteen individuals diagnosed with PTSD and 15 trauma-exposed non-PTSD controls (TENCs) underwent a two-day fear conditioning and extinction protocol in a 3T fMRI scanner. Conditioning and extinction training were conducted on day 1. Extinction recall (or extinction memory) test was conducted on day 2 (extinguished conditioned stimuli presented in the absence of shock). Skin conductance response (SCR) was scored throughout the experiment as an index of the conditioned response. Results: SCR data revealed no significant differences between groups during acquisition and extinction of conditioned fear on day 1. On day 2, however, PTSD subjects showed impaired recall of extinction memory. Analysis of fMRI data showed greater amygdala activation in the PTSD group during day 1 extinction learning. During extinction recall, lesser activation in hippocampus and vmPFC, and greater activation in dACC, was observed in the PTSD group. The magnitude of extinction memory across all subjects was correlated with activation of hippocampus and vmPFC during extinction recall testing. Conclusions: These findings support the hypothesis that fear extinction is impaired in PTSD. They further suggest that dysfunctional activation in brain structures that mediate fear extinction learning, and especially its recall, underlie this impairment.

Little is known about normative variation in stress response over the adolescent transition. This study examined neuroendocrine and cardiovascular responses to performance and peer rejection stressors over the adolescent transition in a normative sample. Participants were 82 healthy children (ages 7-12 years, n=39, 22 females) and adolescents (ages 13-17, n=43, 20 females) recruited through community postings. Following a habituation session, participants completed a performance (public speaking, mental arithmetic, mirror tracing) or peer rejection (exclusion challenges) stress session. Salivary cortisol, alpha amylase (sAA), systolic and diastolic blood pressure (SBP, DBP), and heart rate (HR) were measured throughout. Adolescents showed significantly greater cortisol, sAA, SBP and DBP stress response relative to children. Developmental differences were most pronounced in the performance stress session for cortisol and DBP, and in the peer rejection session for sAA and SBP. Heightened physiological stress responses in typical adolescents may facilitate adaptation to new challenges of adolescence and adulthood. In high-risk adolescents, this normative shift may tip the balance toward stress response dysregulation associated with depression and other psychopathology. Specificity of physiological response by stressor type highlights the importance of a multi-system approach to the psychobiology of stress and may also have implications for understanding trajectories to psychopathology.

To advance our understanding of how biological and behavioral processes interact to determine risk or resilience, theorists suggest that social developmental models will need to include multiple measurements of stress-related biological processes. Identified in the early 1990s as a surrogate marker Journal of Social and Personal Relationships Downloaded from of the sympathetic nervous system component of the stress response, salivary ␣-amylase has not been employed to test biosocial models of stress vulnerability in the context of child development until now. In this report, we describe a standard assay that behavioral scientists can use to improve the next generation of studies and specific recommendations about sample collection, preparation, and storage are presented. More importantly, four studies are presented with motherinfant dyads (N = 86), preschoolers (N = 54), children (N = 54), and adolescents (N = 29) to illustrate individual differences in stress-related change in ␣-amylase levels, that patterns of ␣-amylase stress reactivity distinctly differ from those measured by salivary cortisol, and associations between individual differences in ␣-amylase and social relationships, health, negative affectivity, cognitive/academic/behavior problems, and cardiovascular reactivity. We conclude that the integration of measurements of the adrenergic component of the locus ceruleus/autonomic (sympathetic) nervous system, as indexed by salivary ␣-amylase, into the study of biosocial relationships may extend our understanding of child health and development to new limits.

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Neuroimaging studies of posttraumatic stress disorder (PTSD) have reported functional abnormalities in brain regions involved in fear conditioning, extinction, and emotion regulation. These findings have prompted researchers to consider whether PTSD can be characterized as a stress-induced fear circuitry disorder. In this review, the authors summarize the results of functional neuroimaging studies and conclude that there is a strong argument for characterizing PTSD as a stress-induced fear circuitry disorder. They also acknowledge that (a) fear is not the only emotion associated with PTSD, (b) a state of fear is not required to observe fear-circuitry abnormalities in this disorder, and (c) not all functional abnormalities in PTSD are related to fear circuitry. Implications for future diagnostic classifications are discussed.