Psychoneuroendocrinology
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Psychoneuroendocrinology · Jun 2014
Randomized Controlled TrialThe impact of attentional training on the salivary cortisol and alpha amylase response to psychosocial stress: importance of attentional control.
This study examined the effects of three consecutive days of attentional training on the salivary alpha amylase (sAA), cortisol, and mood response to the Trier Social Stress Test (TSST). The training was designed to elicit faster disengagement of attention away from threatening facial expressions and faster shifts of attention toward positive ones. ⋯ This is among the first experimental manipulations to demonstrate that attentional training can elicit a paradoxical increase in three different markers of stress reactivity. These findings suggest that attentional training, in certain individuals, can have iatrogenic effects.
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Psychoneuroendocrinology · Jun 2014
Randomized Controlled TrialBrief mindfulness meditation training alters psychological and neuroendocrine responses to social evaluative stress.
To test whether a brief mindfulness meditation training intervention buffers self-reported psychological and neuroendocrine responses to the Trier Social Stress Test (TSST) in young adult volunteers. A second objective evaluates whether pre-existing levels of dispositional mindfulness moderate the effects of brief mindfulness meditation training on stress reactivity. ⋯ The present study provides an initial indication that brief mindfulness meditation training buffers self-reported psychological stress reactivity, but also increases cortisol reactivity to social evaluative stress. This pattern may indicate that initially brief mindfulness meditation training fosters greater active coping efforts, resulting in reduced psychological stress appraisals and greater cortisol reactivity during social evaluative stressors.
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Psychoneuroendocrinology · Jun 2014
Randomized Controlled TrialBrief cognitive intervention can modulate neuroendocrine stress responses to the Trier Social Stress Test: buffering effects of a compassionate goal orientation.
The hypothalamic-pituitary-adrenal (HPA) axis is a critical mediator linking stress to health. Understanding how to modulate its reactivity could potentially help reduce the detrimental health effects of HPA axis activation. Social evaluative threat is a potent activator of this system. Access to control and coping responses can reduce its reactivity to pharmacological activation. Compassionate or affiliative behaviors may also moderate stress reactivity. Impact of these moderators on social evaluative threat is unknown. Here, we tested the hypotheses that interventions to increase control, coping, or compassionate (versus competitive) goals could reduce HPA-axis response to social evaluative threat. ⋯ Brief intervention to shift focus from competitive self-promotion to a goal orientation of helping-others can reduce HPA-axis activation to a potent psychosocial stressor. This supports the potential for developing brief interventions as inoculation tools to reduce the impact of predictable stressors and lends support to growing evidence that compassion and altruistic goals can moderate the effects of stress.
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Psychoneuroendocrinology · Apr 2014
Absence of the gut microbiota enhances anxiety-like behavior and neuroendocrine response to acute stress in rats.
Establishment of the gut microbiota is one of the most important events in early life and emerging evidence indicates that the gut microbiota influences several aspects of brain functioning, including reactivity to stress. To better understand how the gut microbiota contributes to a vulnerability to the stress-related psychiatric disorders, we investigated the relationship between the gut microbiota, anxiety-like behavior and HPA axis activity in stress-sensitive rodents. We also analyzed the monoamine neurotransmitters in the brain upper structures involved in the regulation of stress and anxiety. ⋯ In stress-sensitive F344 rats, absence of the gut microbiota exacerbates the neuroendocrine and behavioral responses to acute stress and the results coexist with alterations of the dopaminergic turnover rate in brain upper structures that are known to regulate reactivity to stress and anxiety-like behavior.
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Psychoneuroendocrinology · Apr 2014
Glucocorticoid receptor activation impairs hippocampal plasticity by suppressing BDNF expression in obese mice.
Diabetes and obesity are associated with perturbation of adrenal steroid hormones and impairment of hippocampal plasticity, but the question of whether these conditions recruit glucocorticoid-mediated molecular cascades that are comparable to other stressors has yet to be fully addressed. We have used a genetic mouse model of obesity and diabetes with chronically elevated glucocorticoids to determine the mechanism for glucocorticoid-induced deficits in hippocampal synaptic function. ⋯ Synaptic deficits evoked by exposure to elevated corticosterone levels in db/db mice are attributable to glucocorticoid receptor-mediated transrepression of AP-1 actions at BDNF promoters I and IV. db/db mice exhibit corticosterone-mediated reductions in brain-derived neurotrophic factor (BDNF), and a change in the ratio of TrkB to P75NTR that silences the functional response to BDNF stimulation. Lentiviral suppression of glucocorticoid receptor expression rescues behavioral and synaptic function in db/db mice, and also reinstates BDNF expression, underscoring the relevance of molecular mechanisms previously demonstrated after psychological stress to the functional alterations observed in obesity and diabetes.