S. Shaun Ho

Effects of childhood poverty and chronic stress on emotion regulatory brain function in adulthood

Significance Childhood poverty has been linked to emotion dysregulation, which is further associated with negative physical and psychological health in adulthood. The current study provides evidence of prospective associations between childhood poverty and adult neural activity during effortful attempts to regulate negative emotion. Adults with lower family income at age 9 exhibited reduced ventrolateral and dorsolateral prefrontal cortex activity and failure to suppress amygdala activation at age 24. Chronic stressor exposure across childhood mediated the relations between family income at age 9 and prefrontal cortex activity. The concurrent adult income, on the other hand, was not associated with neural activity. The information on the developmental timing of poverty effects and neural mechanisms may inform early interventions aimed at reducing health disparities. Childhood poverty has pervasive negative physical and psychological health sequelae in adulthood. Exposure to chronic stressors may be one underlying mechanism for childhood poverty−health relations by influencing emotion regulatory systems. Animal work and human cross-sectional studies both suggest that chronic stressor exposure is associated with amygdala and prefrontal cortex regions important for emotion regulation. In this longitudinal functional magnetic resonance imaging study of 49 participants, we examined associations between childhood poverty at age 9 and adult neural circuitry activation during emotion regulation at age 24. To test developmental timing, concurrent, adult income was included as a covariate. Adults with lower family income at age 9 exhibited reduced ventrolateral and dorsolateral prefrontal cortex activity and failure to suppress amygdala activation during effortful regulation of negative emotion at age 24. In contrast to childhood income, concurrent adult income was not associated with neural activity during emotion regulation. Furthermore, chronic stressor exposure across childhood (at age 9, 13, and 17) mediated the relations between family income at age 9 and ventrolateral and dorsolateral prefrontal cortex activity at age 24. The findings demonstrate the significance of childhood chronic stress exposures in predicting neural outcomes during emotion regulation in adults who grew up in poverty.

Trait anxiety modulates anterior cingulate activation to threat interference

Background: Individuals vary in the degree to which salient threatening stimuli disrupt or distract from goal‐directed cognitive processes. Excessive attention to threat or difficulty resolving the interference created by threat cues could contribute to anxious psychopathology; disruptions in frontal brain regions implicated in attentional control or resolution of emotional interference (e.g. anterior cingulate cortex, “ACC”) might play a role. In this study, we explored the hypothesis that trait anxiety would be associated with ACC activity in an attentional control task with varying levels of threat interference. Methods: During functional magnetic resonance imaging, 20 healthy individuals who varied in trait anxiety levels viewed angry, fearful, and neutral faces superimposed on an indoor or outdoor scene. In a high‐threat interference condition, subjects identified the gender of the face (Attend Face). In a low‐threat interference condition, they identified the scene type (Attend Scene). Whole‐brain analysis was used to compare Attend Face with Attend Scene for angry and fearful (versus neutral) faces. Contrasts were correlated with trait anxiety level. Results: Behavioral data confirmed that Attend Face produced greater threat interference than Attend Scene. Brain imaging results showed that trait anxiety was inversely associated with bilateral rostral ACC activity for Attend Face relative to Attend Scene for angry faces. A similar relationship was not seen for fearful faces. Conclusions: The rostral ACC is implicated in assessing the salience of emotional information and controlling attention to resolve emotional interference. The link between higher trait anxiety and decreased ACC activation for angry faces suggests reduced attentional control for signals of interpersonal threat in healthy anxiety‐prone individuals. Depression and Anxiety 28:194–201, 2011.

Childhood poverty and recruitment of adult emotion regulatory neurocircuitry

One in five American children grows up in poverty. Childhood poverty has far-reaching adverse impacts on cognitive, social and emotional development. Altered development of neurocircuits, subserving emotion regulation, is one possible pathway for childhood povertys ill effects. Children exposed to poverty were followed into young adulthood and then studied using functional brain imaging with an implicit emotion regulation task focused. Implicit emotion regulation involved attention shifting and appraisal components. Early poverty reduced left dorsolateral prefrontal cortex recruitment in the context of emotional regulation. Furthermore, this emotion regulation associated brain activation mediated the effects of poverty on adult task performance. Moreover, childhood poverty also predicted enhanced insula and reduced hippocampal activation, following exposure to acute stress. These results demonstrate that childhood poverty can alter adult emotion regulation neurocircuitry, revealing specific brain mechanisms that may underlie long-term effects of social inequalities on health. The role of poverty-related emotion regulatory neurocircuitry appears to be particularly salient during stressful conditions.

Childhood Cumulative Risk Exposure and Adult Amygdala Volume and Function

Considerable work indicates that early cumulative risk exposure is aversive to human development, but very little research has examined the neurological underpinnings of these robust findings. This study investigates amygdala volume and reactivity to facial stimuli among adults (mean 23.7 years of age, n = 54) as a function of cumulative risk exposure during childhood (9 and 13 years of age). In addition, we test to determine whether expected cumulative risk elevations in amygdala volume would mediate functional reactivity of the amygdala during socioemotional processing. Risks included substandard housing quality, noise, crowding, family turmoil, child separation from family, and violence. Total and left hemisphere adult amygdala volumes were positively related to cumulative risk exposure during childhood. The links between childhood cumulative risk exposure and elevated amygdala responses to emotionally neutral facial stimuli in adulthood were mediated by the corresponding amygdala volumes. Cumulative risk exposure in later adolescence (17 years of age), however, was unrelated to subsequent adult amygdala volume or function. Physical and socioemotional risk exposures early in life appear to alter amygdala development, rendering adults more reactive to ambiguous stimuli such as neutral faces. These stress‐related differences in childhood amygdala development might contribute to the well‐documented psychological distress as a function of early risk exposure.

Preliminary study of acute changes in emotion processing in trauma survivors with PTSD symptoms

Accumulating evidence suggests traumatic experience can rapidly alter brain activation associated with emotion processing. However, little is known about acute changes in emotion neurocircuits that underlie PTSD symptom development. To examine acute alterations in emotion circuit activation and structure that may be linked to PTSD symptoms, thirty-eight subjects performed a task of appraisal of emotional faces as their brains were functionally and structurally studied with MRI at both two weeks and three months after motor vehicle collision (MVC). As determined by symptoms reported in the PTSD Checklist at three months, sixteen survivors developed probable PTSD, whereas the remaining 22 did not meet criteria for PTSD diagnosis (non-PTSD). The probable PTSD group had greater activation than the non-PTSD group in dorsal and ventral medial prefrontal cortex (dmPFC and vmPFC) while appraising fearful faces within two weeks after MVC and in left insular cortex (IC) three months after MVC. dmPFC activation at two weeks significantly positively correlated with PTSD symptom severity at two weeks (R = 0.462, P = 0.006) and three months (R = 0.418, p = 0.012). Changes over time in dmPFC activation and in PTSD symptom severity were also significantly positively correlated in the probable PTSD group (R = 0.641, P = 0.018). A significant time by group interaction was found for volume changes in left superior frontal gyrus (SFG, F = 6.048, p = 0.019) that partially overlapped dmPFC active region. Between two weeks and three months, left SFG volume decreased in probable PTSD survivors. These findings identify alterations in frontal cortical activity and structure during the early post-trauma period that appear to be associated with development of PTSD symptoms.

Baby smile response circuits of the parental brain

The parent-infant dyad, characterized by contingent social interactions that develop over the first three months postpartum, may depend heavily on parental brain responses to the infant, including the capacity to smile. A range of brain regions may subserve this social key function in parents and contribute to similar capacities in normal infants, capacities that may go awry in circumstances of reduced care.

What’s in a baby-cry? Locationist and constructionist frameworks in parental brain responses

Parental brain responses to baby stimuli constitute a unique model to study brain-basis frameworks of emotion. Results for baby-cry and picture stimuli may fit with both locationist and psychological constructionist hypotheses. Furthermore, the utility of either model may depend on postpartum timing and relationship. Endocrine effects may also be critical for accurate models to assess mental health risk and treatment.

Automatic goals and conscious regulation in social cognitive affective neuroscience.

The Selfish Goal model challenges traditional agentic models that place conscious systems at the helm of motivation. We highlight the need for ongoing supervision and intervention of automatic goals by higher-order conscious systems with examples from social cognitive affective neuroscience. We contend that interplay between automatic and supervisory systems is required for adaptive human behavior.

Associative and sensorimotor learning for parenting involves mirror neurons under the influence of oxytocin.

Mirror neuron-based associative learning may be understood according to associative learning theories, in addition to sensorimotor learning theories. This is important for a comprehensive understanding of the role of mirror neurons and related hormone modulators, such as oxytocin, in complex social interactions such as among parent-infant dyads and in examples of mirror neuron function that involve abnormal motor systems such as depression.

Speaker 4: Go Okada, Japan

Objectives: There is growing evidence that many emotionregulation processes operate at implicit levels, and the ability to regulate emotions without the need for conscious effort is important for mental health. The glucocorticoid hormones (cortisol in humans) are crucial for stress responses and adaptation, and posttraumatic stress disorder (PTSD) has been associated with both cortisol dysregulation and abnormalities in brain regions involved in emotion regulation. However, how cortisol affects implicit emotion regulation in PTSD, until now has not been studied. In the present study, we examined the effects of exogenous synthetic cortisol (hydrocortisone, HCT) administration on emotion regulation neurocircuits in individuals with and without PTSD. Methods: Here, we used administration of HCT, functional magnetic resonance imaging (fMRI) and the shifting emotion appraisal task (SEAT) which probes neurocircuits of two types of implicit emotion regulation i.e., attention shifting and cognitive appraisal to examine the effect of cortisol on emotion regulation neurocircuits. Using counter-balanced, placebo-controlled, double-blind, within-subject design, 11 individuals diagnosed with PTSD and 11 healthy controls were scanned with bloodoxygen-level-dependent sensitive whole-brain fMRI on 3.0 Tesla GE Signa System, while performing the SEAT on two separate occasions, once following 100mg HCT administration and once following Placebo administration. Preprocessing of fMRI data and analyses were conducted in Statistical Parametric Mapping 8 (SPM8; the Wellcome Trust Centre for Neuroimaging). Results: Experimental manipulation robustly activated neurocircuits involved in emotional regulation by attention shifting and cognitive appraisal respectively. Shifting attention to background context resulted in significant activation in the place processing areas such as parahippocampal place area and attention control areas such as dorsolateral PFC. Cognitive appraisal elicited significant activity in the broad area of medial and left lateral PFC. Differential cortisol modulations of task related activation were observed in the hippocampus and subgenual anterior cingulate cortex (sgACC) between in controls and in patients with PTSD. The left hippocampus activation during shifting attention to background context was decreased by HCT administration in patients with PTSD while increased in Controls. Differential activation during cognitive appraisal was significant in the sgACC, and this effect is mainly driven by enhanced activation of this area by HCT administration in patients with PTSD. Conclusions: We used a probe of the implicit emotion regulation processes to assess how cortisol affects the emotion regulation neurocircuits, and demonstrated that elevation of cortisol is associated with reduced activity in the hippocampus during shifting attention to background context and increased activity in the sgACC during cognitive appraisal only in patients with PTSD. These results suggest that the way hormonal activity affects the brain regions involved in emotion regulation is altered in patients with PTSD, possibly reflecting altered sensitivity of the glucocorticoid receptor in these regions in patients with PTSD. S27: CINP –ICGP Panel Molecular Mechanisms of Late Life Mood and Cognitive Disorders: Targets for Prevention and Intervention Chair: Gwenn Smith, USA Co-Chair: Jeong Lan Kim, Republic of Korea Speaker 1: John O’Brien, UK Title: Neuroinflammatory changes in late life depression: the NIMROD study John T O’Brien,1, Li Su1, Yetunde O Faluyi1, Young T Hong2,3, Tim D Fryer2,3, Guy B Williams2,3, Robert Arnold1, Luca Passamonti3, Patricia Vázquez Rodríguez3, Ajenthan Surendranathan1, W Richard Bevan-Jones1, Franklin Aigbirhio2,3, James B Rowe3,4,5 1 Department of Psychiatry, University of Cambridge, UK, 2 Wolfson Brain Imaging Centre, University of Cambridge, UK. 3 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK., 4 Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK., 5 Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.