Resolving Emotional Conflict: A Role for the Rostral Anterior Cingulate Cortex in Modulating Activity in the Amygdala

Center for Neurobiology and Behavior, Columbia University Medical Center, Neurological Institute Box 108, 710 West 168th Street, New York, New York 10032, USA.
Neuron (Impact Factor: 15.05). 10/2006; 51(6):871-82. DOI: 10.1016/j.neuron.2006.07.029
Source: PubMed


Effective mental functioning requires that cognition be protected from emotional conflict due to interference by task-irrelevant emotionally salient stimuli. The neural mechanisms by which the brain detects and resolves emotional conflict are still largely unknown, however. Drawing on the classic Stroop conflict task, we developed a protocol that allowed us to dissociate the generation and monitoring of emotional conflict from its resolution. Using functional magnetic resonance imaging (fMRI), we find that activity in the amygdala and dorsomedial and dorsolateral prefrontal cortices reflects the amount of emotional conflict. By contrast, the resolution of emotional conflict is associated with activation of the rostral anterior cingulate cortex. Activation of the rostral cingulate is predicted by the amount of previous-trial conflict-related neural activity and is accompanied by a simultaneous and correlated reduction of amygdalar activity. These data suggest that emotional conflict is resolved through top-down inhibition of amygdalar activity by the rostral cingulate cortex.

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    • "T-Tests were carried out to test the effects of exact or different incompatibility repetitions on reaction times and error rates. The term 'high-conflict resoltion' (HCR) refers to incompatible events that were preceded by another incompatible event; and was suggested by Etkin et al. (2006). It is thought that during these specific trials the conflict monitoring system is fully engaged due to the high-conflict detected on the trial before. "

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    • "The second spanned the rostral anterior cingulate cortex and medial orbital-frontal cortex, which have been implicated in numerous prior structural and functional MRI studies of PTSD (Kühn and Gallinat, 2013). These regions have neuroanatomical and functional connections with the amygdala and other subcortical components of emotional response systems (Bush et al., 2000; Etkin et al., 2006) and hypo-activation in these areas is thought to play a role in the emotion regulation and fear extinction deficits observed in PTSD (Patel et al., 2012). These findings should be considered in light of several limitations . "
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