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      Attachment-security priming attenuates amygdala activation to social and linguistic threat.

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          Abstract

          A predominant expectation that social relationships with others are safe (a secure attachment style), has been linked with reduced threat-related amygdala activation. Experimental priming of mental representations of attachment security can modulate neural responding, but the effects of attachment-security priming on threat-related amygdala activation remains untested. Using functional magnetic resonance imaging, the present study examined the effects of trait and primed attachment security on amygdala reactivity to threatening stimuli in an emotional faces and a linguistic dot-probe task in 42 healthy participants. Trait attachment anxiety and attachment avoidance were positively correlated with amygdala activation to threatening faces in the control group, but not in the attachment primed group. Furthermore, participants who received attachment-security priming showed attenuated amygdala activation in both the emotional faces and dot-probe tasks. The current findings demonstrate that variation in state and trait attachment security modulates amygdala reactivity to threat. These findings support the potential use of attachment security-boosting methods as interventions and suggest a neural mechanism for the protective effect of social bonds in anxiety disorders.

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          Most cited references43

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          Attentional bias in emotional disorders.

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            Central role of the brain in stress and adaptation: links to socioeconomic status, health, and disease.

            The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation (allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions (allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load.
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              Functional neuroimaging of major depressive disorder: a meta-analysis and new integration of base line activation and neural response data.

              Functional neuroimaging investigations of major depressive disorder can advance both the neural theory and treatment of this debilitating illness. Inconsistency of neuroimaging findings and the use of region-of-interest approaches have hindered the development of a comprehensive, empirically informed neural model of major depression. In this context, the authors sought to identify reliable anomalies in baseline neural activity and neural response to affective stimuli in major depressive disorder. The authors applied voxel-wise, whole-brain meta-analysis to neuroimaging investigations comparing depressed to healthy comparison groups with respect to baseline neural activity or neural response to positively and/or negatively valenced stimuli. Relative to healthy subjects, those with major depression had reliably higher baseline activity, bilaterally, in the pulvinar nucleus. The analysis of neural response studies using negative stimuli showed greater response in the amygdala, insula, and dorsal anterior cingulate cortex and lower response in the dorsal striatum and dorsolateral prefrontal cortex in individuals with major depressive disorder than in healthy subjects. The meta-analytic results support an elegant and neuroanatomically viable model of the salience of negative information in major depressive disorder. In this proposed model, high baseline pulvinar activity in depression first potentiates responding of the brain's salience network to negative information; next, and owing potentially to low striatal dopamine levels in depression, this viscerally charged information fails to propagate up the cortical-striatal-pallidalthalamic circuit to the dorsolateral prefrontal cortex for contextual processing and reappraisal.
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                Author and article information

                Journal
                Soc Cogn Affect Neurosci
                Social cognitive and affective neuroscience
                Oxford University Press (OUP)
                1749-5024
                1749-5016
                Jun 2015
                : 10
                : 6
                Affiliations
                [1 ] Institute of Psychiatry, King's College London, UK, School of Psychology, University of Exeter, UK, and Exeter Medical School, University of Exeter, UK.
                [2 ] Institute of Psychiatry, King's College London, UK, School of Psychology, University of Exeter, UK, and Exeter Medical School, University of Exeter, UK A.Karl@exeter.ac.uk.
                Article
                nsu127
                10.1093/scan/nsu127
                4448028
                25326039
                fa14576e-0230-4365-a677-38dedab082b0
                History

                amygdala,attachment,emotion,fMRI,fear,priming
                amygdala, attachment, emotion, fMRI, fear, priming

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