Amygdala and Ventromedial Prefrontal Cortex Are Inversely Coupled During Regulation of Negative Affect and Predict the Diurnal Pattern of Cortisol Secretion Among Older Adults
Department of Psychiatry, University of Wisconsin–Madison, Madison, Wisconsin, United StatesThe Journal of Neuroscience : The Official Journal of the Society for Neuroscience (Impact Factor: 6.34). 05/2006; 26(16):4415-25. DOI: 10.1523/JNEUROSCI.3215-05.2006
Among younger adults, the ability to willfully regulate negative affect, enabling effective responses to stressful experiences, engages regions of prefrontal cortex (PFC) and the amygdala. Because regions of PFC and the amygdala are known to influence the hypothalamic-pituitary-adrenal axis, here we test whether PFC and amygdala responses during emotion regulation predict the diurnal pattern of salivary cortisol secretion. We also test whether PFC and amygdala regions are engaged during emotion regulation in older (62- to 64-year-old) rather than younger individuals. We measured brain activity using functional magnetic resonance imaging as participants regulated (increased or decreased) their affective responses or attended to negative picture stimuli. We also collected saliva samples for 1 week at home for cortisol assay. Consistent with previous work in younger samples, increasing negative affect resulted in ventral lateral, dorsolateral, and dorsomedial regions of PFC and amygdala activation. In contrast to previous work, decreasing negative affect did not produce the predicted robust pattern of higher PFC and lower amygdala activation. Individuals demonstrating the predicted effect (decrease < attend in the amygdala), however, exhibited higher signal in ventromedial prefrontal cortex (VMPFC) for the same contrast. Furthermore, participants displaying higher VMPFC and lower amygdala signal when decreasing compared with the attention control condition evidenced steeper, more normative declines in cortisol over the course of the day. Individual differences yielded the predicted link between brain function while reducing negative affect in the laboratory and diurnal regulation of endocrine activity in the home environment.
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- "Research on emotion regulation has converged on a top– down model whereby neural responses to emotional stimuli in the amygdala and ventral striatum are downregulated by prefrontal regions [Johnstone et al., 2007; Kober et al., 2010; Phillips et al., 2008; Urry et al., 2006; Wager et al., 2008]. However, to date, it remains unclear which brain regions mediate the emotion regulation processes between the cortical control and the subcortical affective system, and which cognitive mechanisms underlie this mediation process. "
ABSTRACT: The use of top-down cognitive control mechanisms to regulate emotional responses as circumstances change is critical for mental and physical health. Several theoretical models of emotion regulation have been postulated; it remains unclear, however, in which brain regions emotion regulation goals (e.g., the downregulation of fear) are represented. Here, we examined the neural mechanisms of regulating emotion using fMRI and identified brain regions representing reappraisal goals. Using a multimethodological analysis approach, combining standard activation-based and pattern-information analyses, we identified a distributed network of lateral frontal, temporal, and parietal regions implicated in reappraisal and within it, a core system that represents reappraisal goals in an abstract, stimulus-independent fashion. Within this core system, the neural pattern-separability in a subset of regions including the left inferior frontal gyrus, middle temporal gyrus, and inferior parietal lobe was related to the success in emotion regulation. Those brain regions might link the prefrontal control regions with the subcortical affective regions. Given the strong association of this subsystem with inner speech functions and semantic memory, we conclude that those cognitive mechanisms may be used for orchestrating emotion regulation. Hum Brain Mapp, 2015. © 2015 Wiley Periodicals, Inc.Human Brain Mapping 11/2015; DOI:10.1002/hbm.23053 · 5.97 Impact Factor
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- "subjects showed hypoactivity in the dlPFC and lOFC ( Carlsson et al . , 2004 ) as well as mPFC ( Hermann et al . , 2007 , 2009 ) . However , in addition to activation of the vlPFC and down - regulation of the amygdala during some effortful regulation tasks with negative emotional stimuli , some studies have found possible mediation via the vmPFC ( Urry et al . , 2006 ; Johnstone et al . , 2007 ) . While this may be similar to pathway p4 , it does not explain lOFC activity in some studies ( Phillips et al . , 2003 ; Carlsson et al . , 2004 ; Wager et al . , 2008 ; Golkar et al . , 2012 ) ."
ABSTRACT: A hypothesis is proposed for five visual fear signaling pathways in humans, based on an analysis of anatomical connectivity from primate studies and human functional connectvity and tractography from brain imaging studies. Earlier work has identified possible subcortical and cortical fear pathways known as the “low road” and “high road,” which arrive at the amygdala independently. In addition to a subcortical pathway, we propose four cortical signaling pathways in humans along the visual ventral stream. All four of these traverse through the LGN to the visual cortex (VC) and branching off at the inferior temporal area, with one projection directly to the amygdala; another traversing the orbitofrontal cortex; and two others passing through the parietal and then prefrontal cortex, one excitatory pathway via the ventral-medial area and one regulatory pathway via the ventral-lateral area. These pathways have progressively longer propagation latencies and may have progressively evolved with brain development to take advantage of higher-level processing. Using the anatomical path lengths and latency estimates for each of these five pathways, predictions are made for the relative processing times at selective ROIs and arrival at the amygdala, based on the presentation of a fear-relevant visual stimulus. Partial verification of the temporal dynamics of this hypothesis might be accomplished using experimental MEG analysis. Possible experimental protocols are suggested.Frontiers in Systems Neuroscience 08/2015; 9(101). DOI:10.3389/fnsys.2015.00101
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- "Similarly, in humans, recall of extinguished fear memories increases vmPFC reactivity in response to the CS+ (Milad et al., 2007; Phelps et al., 2004), and is positively associated with vmPFC thickness (Milad et al., 2005). Also, on a different emotion regulation task involving cognitive reappraisal of a negative event, the amygdala showed stronger coupling with the dlPFC, OFC, Subgenual ACC, and dmPFC, with the extent of such coupling being positively associated with post-reappraisal attenuation of negative affect (Banks et al., 2007; Ochsner et al., 2002; Urry et al., 2006). Indeed, weak amygdala-mPFC connections result in pathological emotional over-arousal (Milad et al., 2008; Milad et al., 2009; Motzkin et al., 2015). "
ABSTRACT: 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. Also, 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 behaviour come together to form a 'neuro-environmental 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-which 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.Neuropsychopharmacology accepted article preview online, 21 July 2015. doi:10.1038/npp.2015.204.Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 07/2015; DOI:10.1038/npp.2015.204 · 7.05 Impact Factor
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