Amygdala Reactivity and Mood-Congruent Memory in Individuals at Risk for Depressive Relapse

Department of Psychology, Stanford University, Stanford, CA 94305-2130, USA.
Biological Psychiatry (Impact Factor: 10.26). 02/2007; 61(2):231-9. DOI: 10.1016/j.biopsych.2006.05.004
Source: PubMed


According to cognitive diathesis-stress theories, a latent cognitive vulnerability to depression is activated by negative affect in individuals at risk for depressive relapse. This vulnerability can manifest as mood-congruent memory during sad mood and may involve amygdala response, which is implicated in memory for emotionally arousing stimuli. This study examined whether amygdala modulates memory for negatively valenced words before and after a sad mood induction in healthy individuals with and without a history of recurrent major depression.
Fourteen unmedicated remitted depressed (RD) and 14 matched never depressed (ND) individuals were scanned using functional magnetic resonance imaging (fMRI) while performing a self-referent encoding/evaluation task (SRET) preceding and following a sad mood challenge. After each SRET, participants' free recall was assessed.
Following sad mood induction, bilateral amygdala response during encoding of valenced words predicted increased recall of negative self-referent words for a subset of RD participants. This association was not present before the sad mood induction and was not evident in individuals without a history of depression, regardless of mood state.
These results are consistent with cognitive diathesis-stress theories and suggest a role for the amygdala in modulating mood-congruent memory during transient sad mood in individuals who are vulnerable to depression relapse.

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Available from: Ian H Gotlib, Oct 10, 2015
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    • "Conversely, one proposed mechanism of ADMs is that they promote a positive bias in attention to counter dysphoric attention (Harmer & Cowen, 2013). Whereas amygdala reactivity to negative stimuli often normalizes following successful ADM (Arnone et al., 2012; Sheline et al., 2001) or CT (Fu et al., 2008), elevated amygdala reactivity is still observed in remitted patients following negative mood challenge, and is associated with dysphoric attention and memory biases (Ramel et al., 2007). The amygdala does not operate in isolation. "
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    ABSTRACT: The substantial health burden associated with major depressive disorder (MDD) is a product of both its high prevalence and the significant risk of relapse, recurrence, and chronicity. Establishing recurrence vulnerability factors (VFs) could improve the long-term management of MDD by identifying the need for further intervention in seemingly recovered patients. We present a model of sensitization in depression vulnerability, with an emphasis on the integration of behavioral and neural systems accounts. Evidence suggests that VFs fall into 2 categories: dysphoric attention and dysphoric elaboration. Dysphoric attention is driven by fixation on negative life events, and is characterized behaviorally by reduced executive control, and neurally by elevated activity in the brain's salience network. Dysphoric elaboration is driven by rumination that promotes overgeneral self- and contextual appraisals, and is characterized behaviorally by dysfunctional attitudes, and neurally by elevated connectivity within normally distinct prefrontal brain networks. Although few prospective VF studies exist from which to catalogue a definitive neurobehavioral account, extant data support the value of the proposed 2-factor model. Measuring the continued presence of these 2 VFs during recovery may more accurately identify remitted patients who would benefit from targeted prophylactic intervention. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
    Journal of Abnormal Psychology 02/2015; 124(1):38-53. DOI:10.1037/abn0000031 · 4.86 Impact Factor
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    • "After the elaboration , children began the Facial Emotion Processing task. Given that the original goals of the PDS included exploring the effects of a history of preschool-onset major depression on the brain, the mood induction was of interest because previous work has shown that negative mood induction can reactivate affective processing biases (Scher et al., 2005) and amygdala responses to emotional stimuli (Ramel et al., 2007) specifically in patients with a history of depression. Of note however, there were no correlations between induction-related activity during the elaboration period and fearful–neutral face activity in the Facial Emotion Processing task in our regions of interest (all ps N 0.18). "
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    ABSTRACT: Accumulating evidence suggests a role for stress exposure, particularly during early life, and for variation in genes involved in stress response pathways in neural responsivity to emotional stimuli. Understanding how individual differences in these factors predict differences in emotional responsivity may be important for understanding both normative emotional development and for understanding the mechanisms underlying internalizing disorders, like anxiety and depression, that have often been related to increased amygdala and hippocampus responses to negatively valenced emotional stimuli. The present study examined whether stress exposure and genetic profile scores (10 single nucleotide polymorphisms within four hypothalamic-pituitary-adrenal axis genes: CRHR1, NR3C2, NR3C1, and FKBP5) predict individual differences in amygdala and hippocampus responses to fearful vs. neutral faces in school-age children (7-12 year olds; N=107). Experience of more stressful and traumatic life events predicted greater left amygdala responses to negative emotional stimuli. Genetic profile scores interacted with sex and pubertal status to predict amygdala and hippocampus responses. Specifically, genetic profile scores were a stronger predictor of amygdala and hippocampus responses among pubertal vs. prepubertal children where they positively predicted responses to fearful faces among pubertal girls and positively predicted responses to neutral faces among pubertal boys. The current results suggest that genetic and environmental stress-related factors may be important in normative individual differences in responsivity to negative emotional stimuli, a potential mechanism underlying internalizing disorders. Further, sex and pubertal development may be key moderators of the effects of stress-system genetic variation on amygdala and hippocampus responsivity, potentially relating to sex differences in stress-related psychopathology. Copyright © 2015. Published by Elsevier Inc.
    01/2015; 109. DOI:10.1016/j.neuroimage.2015.01.017
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    • "This study used a validated Mood Induction Procedure (MIP) combined with brief temperature stimulation. The MIP, which combined 7 minutes of autobiographical recall and music (see File S1), has been previously shown to effectively induce both acute sad [28] and happy [29] moods. Brief temperature stimuli were administered using a procedure similar to the methods used previously by our lab in young adults with current MDD and HC subjects [19] (see below). "
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    ABSTRACT: Recent evidence suggests that sensitivity to the emotional sequela of experimental thermal pain(measured by emotional unpleasantness) is heightened in individuals with major depressive disorder(MDD), a phenomenon we termed "emotional allodynia". The aim of this study was to examine whether acute happy and sad mood induction alters emotional allodynia in MDD. We hypothesized that emotional allodynia will be a robust characteristic of individuals with MDD compared to healthy controls. Thus, it would remain following acute mood induction, independent of valence. Twenty-one subjects with current MDD and 21 well-matched healthy subjects(HC) received graded brief temperature stimuli following happy and sad mood inductions procedures(MIP). All subjects rated the intensity and affect(pleasantness/unpleasantness) of each stimulus. Sensory(pain intensity) and affective(pain unpleasantness) thresholds were determined by methods of constant stimuli. The MIPs reliably induced happy and sad mood and the resulting induced mood and subjective arousal were not different between the groups at the time of temperature stimulation. Compared to HC, MDD individuals demonstrated emotional allodynia. We found significantly decreased affective pain thresholds whereby significantly lower temperatures became unpleasant in the MDD compared to the HC group. This was not observed for the sensory pain thresholds. Within the MDD, the affective pain thresholds were significantly lower than the corresponding pain intensity thresholds, whereby non-painful temperatures were already unpleasant for the MDD irrespective of the induced mood. This was not observed for the HC groups where the affective and pain intensity thresholds were comparable. These findings suggest that emotional allodynia may be a chronic characteristic of current MDD. Future studies should determine if emotional allodynia persists after psychological or pharmacological interventions. Finally, longitudinal work should examine whether emotional allodynia is a result of or vulnerability for depression and the role it plays in the increased susceptibility for pain complaints in this disorder.
    PLoS ONE 11/2013; 8(11):e80507. DOI:10.1371/journal.pone.0080507 · 3.23 Impact Factor
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