2007
DOI: 10.1093/scan/nsm029
|View full text |Cite
|
Sign up to set email alerts
|

Amygdala–frontal connectivity during emotion regulation

Abstract: Successful control of affect partly depends on the capacity to modulate negative emotional responses through the use of cognitive strategies (i.e., reappraisal). Recent studies suggest the involvement of frontal cortical regions in the modulation of amygdala reactivity and the mediation of effective emotion regulation. However, within-subject inter-regional connectivity between amygdala and prefrontal cortex in the context of affect regulation is unknown. Here, using psychophysiological interaction analyses of… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

66
720
9
15

Year Published

2010
2010
2023
2023

Publication Types

Select...
7
2
1

Relationship

0
10

Authors

Journals

citations
Cited by 999 publications
(810 citation statements)
references
References 91 publications
66
720
9
15
Order By: Relevance
“…The findings for heart rate during anticipation and recovery and for skin conductance during recovery support the compensation hypothesis, which suggests that those with deficits will benefit more from an intervention that compensates that deficit, and are consistent with previous research showing that physiological activation (Davies et al, 2015;McClure et al, 2007) and emotional reactivity during a behavioral task (Niles et al, 2013) predict greater improvement following treatment. These findings are of particular interest because participants with more difficulty regulating emotion show decreased connectivity between areas of the PFC and the amygdala (Banks, Eddy, Angstadt, Nathan, & Phan, 2007). These findings suggest that targeting patients with the greatest neural deficits using interventions that directly address those deficits could improve treatment outcome for patients with anxiety.…”
Section: Discussionmentioning
confidence: 93%
“…The findings for heart rate during anticipation and recovery and for skin conductance during recovery support the compensation hypothesis, which suggests that those with deficits will benefit more from an intervention that compensates that deficit, and are consistent with previous research showing that physiological activation (Davies et al, 2015;McClure et al, 2007) and emotional reactivity during a behavioral task (Niles et al, 2013) predict greater improvement following treatment. These findings are of particular interest because participants with more difficulty regulating emotion show decreased connectivity between areas of the PFC and the amygdala (Banks, Eddy, Angstadt, Nathan, & Phan, 2007). These findings suggest that targeting patients with the greatest neural deficits using interventions that directly address those deficits could improve treatment outcome for patients with anxiety.…”
Section: Discussionmentioning
confidence: 93%
“…This functional connectivity is important for emotion regulation, which has previously been reported in that reduced connectivity between amygdala and DLPFC in individuals with internet gaming disorder is associated with higher levels of impulsivity [Ko et al, 2015]. Another study measuring the capacity to modulate negative emotional responses through the use of cognitive strategies showed that activity in specific areas of the frontal cortex, including DLPFC, covaried with amygdala activity, and that functional connectivity between these regions was dependent on applying cognitive strategies in the regulation of negative emotion [Banks et al, 2007]. Amygdala and DLPFC connectivity has similarly been associated with unipolar depression [Siegle et al, 2007].…”
Section: Discussionmentioning
confidence: 99%
“…In fact, one important role of DLPFC is in processing and regulating stressful, emotional responses -for instance, DLPFC shows activation when voluntarily suppressing sadness (Levesque et al, 2003) and co-activation with the amygdala during emotion reappraisal (Banks et al, 2007). Immediately following a stressful event, subcortical areas (such as the amygdala, hypothalamus and brainstem monoaminergic nuclei) trigger strong (albeit relatively unspecific) neuroendocrine responses, notably the activation of the sympatho-adreno-medullary system (SAM) and the hypothalamic-pituitary-adrenal (HPA) axis, thereby increasing noradrenaline and cortisol levels.…”
Section: Introductionmentioning
confidence: 99%