This study used functional MRI (fMRI) to examine a novel aspect of emotion regulation in adolescent development: whether age predicts differences in both the concurrent and lasting effects of emotion regulation on amygdala response. In the first active regulation phase of the testing session, fMRI data was collected while 56 healthy individuals (age range: 10.50–22.92 years) reappraised aversive stimuli so as to diminish negative responses to them. After a short delay, the second re-presentation phase involved passively viewing the aversive images from the reappraisal task. During active regulation, older individuals showed greater drops in negative affect and inverse rostrolateral prefrontal-amygdala connectivity. During re-presentation, older individuals continued to show lasting reductions in the amygdala response to aversive stimuli they had previously reappraised, an effect mediated by rostrolateral PFC. These data suggest that one source of heightened emotionality in adolescence is a diminished ability to cognitively down-regulate aversive reactions.
Neuroimaging research has identified systems that facilitate minimizing negative emotion, but how the brain is able to transform the valence of an emotional response from negative to positive is unclear. Behavioral and psychophysiological studies suggest a distinction between minimizing reappraisal, which entails diminishing the arousal elicited by negative stimuli, and positive reappraisal, which instead changes the emotional valence of arousal from negative to positive. Here we show that successful minimizing reappraisal tracked with decreased activity in the amygdala, but successful positive reappraisal tracked with increased activity in regions involved in computing reward value, including the ventral striatum and ventromedial pFC (vmPFC). Moreover, positive reappraisal enhanced positive connectivity between vmPFC and amygdala, and individual differences in positive connectivity between vmPFC and amygdala, ventral striatum, dorsomedial pFC, and dorsolateral pFC predicted greater positive reappraisal success. These data broaden models of emotion regulation as quantitative dampening of negative emotion and identify activity in a network of brain valuation, arousal, and control regions as a neural basis for the ability to create positive meaning from negative experiences.
The present neuroimaging study investigated two aspects of difficulties with emotion associated with Borderline Personality Disorder (BPD1): affective lability and difficulty regulating emotion. While these two characteristics have been previously linked to BPD symptomology, it remains unknown whether individual differences in affective lability and emotion regulation difficulties are subserved by distinct neural substrates within a BPD sample. To address this issue, sixty women diagnosed with BPD were scanned while completing a task that assessed baseline emotional reactivity as well as top-down emotion regulation. More affective instability, as measured by the Affective Lability Scale (ALS2), positively correlated with greater amygdala responses on trials assessing emotional reactivity. Greater difficulties with regulating emotion, as measured by the Difficulties with Emotion Regulation Scale (DERS3), was negatively correlated with left inferior frontal gyrus (IFG4) recruitment on trials assessing regulatory ability. These findings suggest that, within a sample of individuals with BPD, greater bottom-up amygdala activity is associated with heightened affective lability. By contrast, difficulties with emotion regulation are related to reduced IFG recruitment during emotion regulation. These results point to distinct neural mechanisms for different aspects of BPD symptomology.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.