Functional differences in emotion processing during adolescence and early adulthood

Vink, Matthijs; Derks, Jolanda; Hoogendam, Janna Marie; Hillegers, Manon H. J.; Kahn, René S.

doi:10.1016/j.neuroimage.2014.01.035

Cited by 128 publications

(123 citation statements)

References 44 publications

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“…Taken together, the studies described so far collectively show that childhood is a developmentally unique period for parental buffering of CORT, emotional responding, amygdala reactivity, and amygdala-mPFC connectivity (see, eg, Decety et al, 2012;Egliston and Rapee, 2007;GabardDurnam et al, 2014;Gee et al, 2013bGee et al, , 2014Hibel et al, 2014b;Middlemiss et al, 2012;Sullivan, 2004, 2006;Papp et al, 2009;Seltzer et al, 2010Seltzer et al, , 2012Silvers et al, 2014;Sorce et al, 1985;Sullivan et al, 2000;Swartz et al, 2014;Vink et al, 2014). Importantly, we believe that the role of the parent in phasic modulation of the amygdala and mPFC is critical for circuit tone and for the long-term effectiveness of the circuit in emotion regulation.…”

Section: Phasic Parental Modulation Of Amygdala-prefrontal Circuitsmentioning

confidence: 88%

“…Research in typically developing populations has shown that amygdala-mPFC functional connectivity during a passive viewing emotional task changes dramatically across development, moving from a positive functional connection in childhood to a mature and negative connection in adolescence that more closely fits the top-down regulatory profile proposed for this circuit in adults (Gee et al, 2013b). Functional connectivity between amygdala and PFC has also been shown to increase across age during a moral or emotional judgment task (Decety et al, 2012;Vink et al, 2014). Similarly, functional connectivity between amygdala and mPFC during rest also exhibits profound developmental change.…”

Section: Pfc Developmentmentioning

confidence: 97%

“…Animal studies have demonstrated continued maturation of the intrinsic properties of amygdala principal neurons (eg, increases in maximal firing and peak resonance frequency; Ehrlich et al, 2012), and of inhibitory neurotransmitter systems within the amygdala (ie, γ-aminobutyric acid (GABA); Ehrlich et al, 2013) until early adolescence. In terms of functionality, the amygdala exhibits very robust responding to emotional events in childhood, with amygdala reactivity to emotional stimuli then decreasing across adolescence and into adulthood (Decety et al, 2012;Gee et al, 2013b;Tottenham, 2012;Vink et al, 2014); however, see Moore et al (2012) and Hare et al (2008) for a slightly different outcome. The strong early reactivity in the amygdala parallels the normatively high fear and emotionality that characterizes childhood; indeed, early childhood fears (ie, separation anxiety) are mediated by the excessively high amygdala activity observed during childhood (Gee et al, 2013a, b).…”

Section: Amygdala Developmentmentioning

confidence: 99%

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The Neuro-Environmental Loop of Plasticity: A Cross-Species Analysis of Parental Effects on Emotion Circuitry Development Following Typical and Adverse Caregiving

Callaghan

Tottenham

2015

Neuropsychopharmacol

233

210

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Early experiences critically shape the structure and function of the brain. Perturbations in typical/species-expected early experiences are known to have profound neural effects, especially in regions important for emotional responding. Parental care is one species-expected stimulus that plays a fundamental role in the development of emotion neurocircuitry. Emerging evidence across species suggests that phasic variation in parental presence during the sensitive period of childhood affects the recruitment of emotional networks on a moment-to-moment basis. In addition, it appears that increasing independence from caregivers cues the termination of the sensitive period for environmental input into emotion network development. In this review, we examine how early parental care, the central nervous system, and behavior come together to form a 'neuroenvironmental loop,' contributing to the formation of stable emotion regulation circuits. To achieve this end, we focus on the interaction of parental care and the developing amygdala-medial prefrontal cortex (mPFC) network-that is at the core of human emotional functioning. Using this model, we discuss how individual or group variations in parental independence, across chronic and brief timescales, might contribute to neural and emotional phenotypes that have implications for long-term mental health.

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Section: Phasic Parental Modulation Of Amygdala-prefrontal Circuitsmentioning

confidence: 88%

Section: Pfc Developmentmentioning

confidence: 97%

Section: Amygdala Developmentmentioning

confidence: 99%

See 1 more Smart Citation

The Neuro-Environmental Loop of Plasticity: A Cross-Species Analysis of Parental Effects on Emotion Circuitry Development Following Typical and Adverse Caregiving

Callaghan

Tottenham

2015

Neuropsychopharmacol

233

210

View full text Add to dashboard Cite

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“…The PFC undergoes structural change into early adulthood (Giedd et al, 1999;Gogtay et al, 2004). These structural changes are paralleled by age-related decreases in amygdala activation and changes in medial prefrontal-amygdala connectivity (Gee et al, 2013b;Vink et al, 2014). Childhood stress may shift these trajectories by increasing amygdala activation, eg (McCrory et al, 2011;Swartz et al, 2015), spurring early development of prefrontal-amygdala connectivity following maternal deprivation (Gee et al, 2013a), or weakening prefrontal-amygdala connectivity following maltreatment experiences (Birn et al, 2014;Herringa et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Prefrontal–Amygdala Dysregulation to Threat in Pediatric Posttraumatic Stress Disorder

Wolf

Herringa

2015

Neuropsychopharmacol

121

117

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Functional abnormalities in fear circuitry are likely to underlie the pathophysiology of pediatric posttraumatic stress disorder (PTSD), but the few studies to date have yielded conflicting findings. Furthermore, network level functional connectivity and age-related disruptions in fear circuitry have not been thoroughly explored. In a cross-sectional design, 24 healthy and 24 medication-free youth with severe PTSD completed an event-related emotion-processing task during functional MRI. Youth viewed threat and neutral images, half of which were paired with a neutral male face. Group-and age-related differences in brain activation were examined in the medial prefrontal cortex (mPFC), amygdala, and hippocampus. Amygdala functional connectivity was examined using a seed-based approach. PTSD youth showed hyperactivation of the dorsal anterior cingulate cortex (dACC) to threat images. In the dorsomedial PFC (dmPFC), age positively predicted activation in healthy youth but negatively predicted activation in PTSD youth. In the amygdala functional connectivity analysis, PTSD youth showed decreased amygdala-mPFC connectivity to threat images. Furthermore, age positively predicted amygdala-vmPFC connectivity in healthy youth, but negatively predicted connectivity in PTSD youth. Finally, dmPFC activation and amygdala-mPFC connectivity were inversely related to PTSD severity. Pediatric PTSD involves abnormal functional activation and connectivity in fear circuitry. Specifically, dACC hyperactivation is consistent with abnormal promotion of fear responses, whereas reduced amygdala-mPFC connectivity suggests impaired regulation of amygdala responses to threat. Importantly, age-dependent decreases in dmPFC activation and amygdala-vmPFC connectivity may indicate abnormal developmental processes in key emotion pathways in pediatric PTSD.

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“…Emerging evidence in healthy samples demonstrates that LPFC activation during ER in childhood and adolescence is similar to activation observed in adults but increases linearly with age and is independent of emotional reactivity [134,135]. This age-related increase in LPFC is coupled with decreases in limbic activation and overall increased frontallimbic connectivity [136], indicating that over the course of normal adolescent development, improved ER abilities are facilitated by frontal-limbic neurodevelopment. However, these data are all collected from cross-sectional healthy samples across varying age ranges; no studies have conducted similar examinations in high-risk samples, and no longitudinal research has been published.…”

Section: Discussionmentioning

confidence: 83%

Beyond “Cold” Cognition: Exploring Cognitive Control of Emotion as a Risk Factor for Psychosis

Tully

Niendam

2014

Curr Behav Neurosci Rep

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The past 20 years of research examining psychosis risk factors has predominantly focused on "cold" cognitive (i.e., non-affective) processes. Despite identification of potential cognitive and associated brain-based vulnerability markers, our ability to identify those individuals at highest risk for future psychosis has not substantially improved. Consequently, researchers have begun to examine emotionprocessing deficits as potential psychosis vulnerability markers. Here we propose that a particular emotionprocessing domain, cognitive control of emotion, is a potential transdiagnostic mechanism underlying the heterogeneity of clinical presentation and psychosocial impairments observed in high-risk populations. Recent investigations indicate impaired cognitive control of emotion is observable across the psychosis spectrum and relates to important clinical and psychosocial outcomes relevant to the high-risk state. Moreover, preliminary evidence indicates treatment interventions aimed at improving cognitive control of emotion could reduce psychotic symptoms and improve functioning. We highlight gaps in current knowledge and propose five key avenues for future investigations.

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Functional differences in emotion processing during adolescence and early adulthood

Cited by 128 publications

References 44 publications

The Neuro-Environmental Loop of Plasticity: A Cross-Species Analysis of Parental Effects on Emotion Circuitry Development Following Typical and Adverse Caregiving

The Neuro-Environmental Loop of Plasticity: A Cross-Species Analysis of Parental Effects on Emotion Circuitry Development Following Typical and Adverse Caregiving

Prefrontal–Amygdala Dysregulation to Threat in Pediatric Posttraumatic Stress Disorder

Beyond “Cold” Cognition: Exploring Cognitive Control of Emotion as a Risk Factor for Psychosis

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