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.
"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 ) ."
[Show abstract][Hide abstract] 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
"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). "
[Show abstract][Hide abstract] 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
"Thus, the amygdalo-hippocampal complex, orbitofrontal cortex , anterior cingulum and insula have been shown to be activated by both mental and physical tests, which are useful to evoke an autonomic stress response (Critchley et al., 2003; Williamson et al., 1997; Soufer et al., 1998; Harper et al., 1998). Stressors which require the completion of demanding and uncontrollable cognitive challenges in a context of negative social evaluation, such as the Trier Social Stress Test (TSST) induce increased activity of the medial prefrontal cortex (Kern et al., 2008; Urry et al., 2006), anterior cingulum (which may be of particular importance for generating autonomic cardiovascular responses; Critchley et al., 2000a,b, 2005; Critchley, 2005), insula (which probably works together with anterior cingulum, as both are components of a system underlying self awareness; Medford and Critchley, 2010), and deactivation of the hippocampalamygdala complex (Kern et al., 2008), probably to disinhibit the hypothalamus which commands the HPA and ANS (McEwen and Gianaros, 2010) responses. Dedovic et al. (2005) have used a variety of tests to induce stress by generating a social evaluative threat combining an arithmetic task and a social evaluative component, such as the Montreal Imaging Stress Task (MIST). "
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.