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Prefrontal-subcortical pathways mediating successful emotion regulation.

ABSTRACT: Although prefrontal cortex has been implicated in the cognitive regulation of emotion, the cortical-subcortical interactions that mediate this ability remain poorly understood. To address this issue, we identified a right ventrolateral prefrontal region (vlPFC) whose activity correlated with reduced negative emotional experience during cognitive reappraisal of aversive images. We then applied a pathway-mapping analysis on subcortical regions to locate mediators of the association between vlPFC activity and reappraisal success (i.e., reductions in reported emotion). Results identified two separable pathways that together explained approximately 50% of the reported variance in self-reported emotion: (1) a path through nucleus accumbens that predicted greater reappraisal success, and (2) a path through ventral amygdala that predicted reduced reappraisal success (i.e., more negative emotion). These results provide direct evidence that vlPFC is involved in both the generation and regulation of emotion through different subcortical pathways, suggesting a general role for this region in appraisal processes.

SUBMITTER: Wager TD

PROVIDER: S-EPMC2742320 | biostudies-literature | 2008 Sep

REPOSITORIES: biostudies-literature

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Prefrontal-subcortical pathways mediating successful emotion regulation.

Wager Tor D TD Davidson Matthew L ML Hughes Brent L BL Lindquist Martin A MA Ochsner Kevin N KN

Neuron 20080901 6

Although prefrontal cortex has been implicated in the cognitive regulation of emotion, the cortical-subcortical interactions that mediate this ability remain poorly understood. To address this issue, we identified a right ventrolateral prefrontal region (vlPFC) whose activity correlated with reduced negative emotional experience during cognitive reappraisal of aversive images. We then applied a pathway-mapping analysis on subcortical regions to locate mediators of the association between vlPFC a ...[more]

PMID: 18817740

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Project description:ObjectiveSuicidal ideation is a clinical exigency heightening the risk of suicide at different levels of suicidal behavior. This study sought to explore crucial correlates of this phenomenon with a structural equation modeling approach. Accordingly, the mediating role of depressive symptoms and difficulties in emotion regulation between childhood trauma and suicidal ideation were explored.MethodThe sample consisted of 372 university students (57.3% females, M = 20.75, SD = 2.25) who completed self-report measures examining experiences of childhood trauma, depressive symptoms, difficulties in emotion regulation, and suicidal ideation. Structural equation modeling was employed, and mediation analysis was conducted. Confirmatory factor analysis was used to test the measurement model of each construct before evaluating the conceptual mediated model.ResultsFindings indicate that depressive symptoms with difficulties in emotion regulation had the strongest association (r = 0.60, P = 0.001), then depressive symptoms and suicidal ideation (r = 0.58, P = 0.001), suicidal ideation with difficulties in emotion regulation (r = 0.45, P = 0.001) then suicidal ideation with childhood trauma (r = 0.39, P = 0.001), difficulties in emotion regulation with childhood trauma (r = 0.36 P = 0.001) and finally depressive symptoms and childhood trauma (r = 0.35, P = 0.001). Regarding indirect paths, difficulties in emotion regulation and depression function together (in a sequential path) to mediate the association between childhood trauma and suicidal ideation ( χ2(68) = 216.86, P < 0.01, CFI = 0.95, TLI = 0.93, RMSE = 0.077, CI [0.066 to 0.089], SRMR = 0.049).ConclusionResults demonstrate that childhood trauma, depressive symptoms, and difficulties in emotion regulation are linked to suicidal ideation, highlighting the necessity of recognizing and addressing suicidal ideation as well as the factors that contribute to suicidal ideation. Emotion regulation interventions can be effective in reducing the negative effects of childhood trauma and lowering the risk of suicide. These interventions can help in reducing depressive symptoms and improve overall mental well-being, leading to a lower risk of suicide.

Project description:Depression is among the most common comorbidities in multiple sclerosis and has severe psychosocial consequences. Alterations in neural emotion regulation in amygdala and prefrontal cortex have been recognized as key mechanism of depression but never been investigated in multiple sclerosis depression. In this cross-sectional observational study, we employed a functional MRI task investigating neural emotion regulation by contrasting regulated versus unregulated negative stimulus perception in 16 persons with multiple sclerosis and depression (47.9 ± 11.8 years; 14 female) and 26 persons with multiple sclerosis but without depression (47.3 ± 11.7 years; 14 female). We tested the impact of depression and its interaction with lesions in amygdala-prefrontal fibre tracts on brain activity reflecting emotion regulation. A potential impact of sex, age, information processing speed, disease duration, overall lesion load, grey matter fraction, and treatment was taken into account in these analyses. Patients with depression were less able (i) to downregulate negative emotions than those without (t = -2.25, P = 0.012, β = -0.33) on a behavioural level according to self-report data and (ii) to downregulate activity in a left amygdala coordinate (t = 3.03, P Family-wise error [FWE]-corrected = 0.017, β = 0.39). Moreover, (iii) an interdependent effect of depression and lesions in amygdala-prefrontal tracts on activity was found in two left amygdala coordinates (t = 3.53, pFWE = 0.007, β = 0.48; t = 3.21, pFWE = 0.0158, β = 0.49) and one right amygdala coordinate (t = 3.41, pFWE = 0.009, β = 0.51). Compatible with key elements of the cognitive depression theory formulated for idiopathic depression, our study demonstrates that depression in multiple sclerosis is characterized by impaired neurobehavioural emotion regulation. Complementing these findings, it shows that the relation between neural emotion regulation and depression is affected by lesion load, a key pathological feature of multiple sclerosis, located in amygdala-prefrontal tracts.

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Prefrontal-subcortical pathways mediating successful emotion regulation.

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Prefrontal-subcortical pathways mediating successful emotion regulation.

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