Background-Emotion regulation strategies are thought to differ in when and how they influence the emotion-generative process. However, no study to date has directly probed the neural bases of two contrasting (e.g., cognitive versus behavioral) emotion regulation strategies. This study used functional magnetic resonance imaging (fMRI) to examine cognitive reappraisal (a cognitive strategy thought to have its impact early in the emotion-generative process) and expressive-suppression (a behavioral strategy thought to have its impact later in the emotion-generative process).

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A confirmatory factor analysis was performed to evaluate the factorial validity of the Beck Depression Inventory–Second Edition (BDI‐II) in a large sample of undergraduates (N = 576). Results suggest that the revised measure is internally consistent and consists of two underlying factors assessing cognitive‐affective and somatic symptoms of depression. Results support the use of the BDI‐II as a severity measure of symptoms of depression. © 2000 John Wiley & Sons, Inc. J Clin Psychol 56: 545–551, 2000.

This study examined the effects of mindfulness-based stress reduction (MBSR) on the brain-behavior mechanisms of self-referential processing in patients with social anxiety disorder (SAD). Sixteen patients underwent functional magnetic resonance imaging while encoding self-referential, valence, and orthographic features of social trait adjectives. Post-MBSR, 14 patients completed neuroimaging. Compared to baseline, MBSR completers showed (a) increased self-esteem and decreased anxiety, (b) increased positive and decreased negative self-endorsement, (c) increased activity in a brain network related to attention regulation, and (d) reduced activity in brain systems implicated in conceptual-linguistic self-view. MBSR-related changes in maladaptive or distorted social self-view in adults diagnosed with SAD may be related to modulation of conceptual self-processing and attention regulation. Self-referential processing may serve as a functional biobehavioral target to measure the effects of mindfulness training.

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Anticipatory emotional responses play a crucial role in preparing individuals for impending challenges. They do this by triggering a coordinated set of changes in behavioral, autonomic, and neural response systems. In the present study, we examined the biobehavioral impact of varying levels of anticipatory anxiety, using a shock anticipation task in which unpredictable electric shocks were threatened and delivered to the wrist at variable intervals and intensities (safe, medium, strong). This permitted investigation of a dynamic range of anticipatory anxiety responses. In two studies, 95 and 51 healthy female participants, respectively, underwent this shock anticipation task while providing continuous ratings of anxiety experience and electrodermal responding (Study 1) and during fMRI BOLD neuroimaging (Study 2). Results indicated a step-wise pattern of responding in anxiety experience and electrodermal responses. Several brain regions showed robust responses to shock anticipation relative to safe trials, including the hypothalamus, periaqueductal gray, caudate, precentral gyrus, thalamus, insula, ventrolateral PFC, dorsomedial PFC, and ACC. A subset of these regions demonstrated a linear pattern of increased responding from safe to medium to strong trials, including the bilateral insula, ACC, and inferior frontal gyrus. These responses were modulated by individual differences in neuroticism, such that those high in neuroticism showed exaggerated anxiety experience across the entire task, and reduced brain activation from medium to strong trials in a subset of brain regions. These findings suggest that individual differences in neuroticism may influence sensitivity to anticipatory threat and provide new insights into the mechanism through which neuroticism may confer risk for developing anxiety disorders via dysregulated anticipatory responses.

Objective Many studies have shown that 5-HTTLPR genotype interacts with exposure to stress in conferring risk for psychopathology. However, the specific neural mechanisms through which this gene-by-environment interaction confers risk remain largely unknown, and no study to date has directly examined the modulatory effects of the 5-HTTLPR on corticolimbic circuit responses during exposure to acute stress. Methods An acute laboratory stressor was administered to 51 healthy women during BOLD fMRI scanning. In this task, electric shocks of uncertain intensity were threatened and unpredictably delivered to the wrist after a long anticipatory cue period of unpredictable duration. Results Relative to those carrying the L allele, SS homozygotes showed enhanced activation during threat anticipation in a network of regions including amygdala, hippocampus, anterior insula, thalamus, pulvinar, caudate, precuneus, anterior cingulate cortex, and medial prefrontal cortex. SS homozygotes also displayed enhanced positive coupling between medial prefrontal cortex activation and anxiety experience, whereas individuals carrying the L allele displayed enhanced negative coupling between insula activation and perceived success at regulating anxiety. Conclusions The present findings suggest that, when exposed to stress, SS homozygotes may preferentially engage neural systems which enhance fear and arousal, modulate attention toward threat, and perseverate on emotional salience of the threat. This may be one mechanism underlying risk for psychopathology conferred by the S allele upon exposure to life stressors.

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