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      The Trier Social Stress Test: Principles and practice

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          Abstract

          Researchers interested in the neurobiology of the acute stress response in humans require a valid and reliable acute stressor that can be used under experimental conditions. The Trier Social Stress Test (TSST) provides such a testing platform. It induces stress by requiring participants to make an interview-style presentation, followed by a surprise mental arithmetic test, in front of an interview panel who do not provide feedback or encouragement. In this review, we outline the methodology of the TSST, and discuss key findings under conditions of health and stress-related disorder. The TSST has unveiled differences in males and females, as well as different age groups, in their neurobiological response to acute stress. The TSST has also deepened our understanding of how genotype may moderate the cognitive neurobiology of acute stress, and exciting new inroads have been made in understanding epigenetic contributions to the biological regulation of the acute stress response using the TSST. A number of innovative adaptations have been developed which allow for the TSST to be used in group settings, with children, in combination with brain imaging, and with virtual committees. Future applications may incorporate the emerging links between the gut microbiome and the stress response. Future research should also maximise use of behavioural data generated by the TSST. Alternative acute stress paradigms may have utility over the TSST in certain situations, such as those that require repeat testing. Nonetheless, we expect that the TSST remains the gold standard for examining the cognitive neurobiology of acute stress in humans.

          Highlights

          • The TSST is the human experimental gold standard for evaluating the neurobiology of acute stress.

          • The HPA axis response to the TSST is higher in males and lower in older adults.

          • Genotype and epigenetic factors moderate the neurobiological response to the TSST.

          • Multiple adaptations of the TSST are available for different testing contexts.

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          Most cited references144

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          The social psychology of creativity: A componential conceptualization.

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            Salivary cortisol as a biomarker in stress research.

            Salivary cortisol is frequently used as a biomarker of psychological stress. However, psychobiological mechanisms, which trigger the hypothalamus-pituitary-adrenal axis (HPAA) can only indirectly be assessed by salivary cortisol measures. The different instances that control HPAA reactivity (hippocampus, hypothalamus, pituitary, adrenals) and their respective modulators, receptors, or binding proteins, may all affect salivary cortisol measures. Thus, a linear relationship with measures of plasma ACTH and cortisol in blood or urine does not necessarily exist. This is particularly true under response conditions. The present paper addresses several psychological and biological variables, which may account for such dissociations, and aims to help researchers to rate the validity and psychobiological significance of salivary cortisol as an HPAA biomarker of stress in their experiments.
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              Transferring the blues: Depression-associated gut microbiota induces neurobehavioural changes in the rat.

              The gut microbiota interacts with the host via neuroimmune, neuroendocrine and neural pathways. These pathways are components of the brain-gut-microbiota axis and preclinical evidence suggests that the microbiota can recruit this bidirectional communication system to modulate brain development, function and behaviour. The pathophysiology of depression involves neuroimmune-neuroendocrine dysregulation. However, the extent to which changes in gut microbiota composition and function mediate the dysregulation of these pathways is unknown. Thirty four patients with major depression and 33 matched healthy controls were recruited. Cytokines, CRP, Salivary Cortisol and plasma Lipopolysaccharide binding protein were determined by ELISA. Plasma tryptophan and kynurenine were determined by HPLC. Fecal samples were collected for 16s rRNA sequencing. A Fecal Microbiota transplantation was prepared from a sub group of depressed patients and controls and transferred by oral gavage to a microbiota-deficient rat model. We demonstrate that depression is associated with decreased gut microbiota richness and diversity. Fecal microbiota transplantation from depressed patients to microbiota-depleted rats can induce behavioural and physiological features characteristic of depression in the recipient animals, including anhedonia and anxiety-like behaviours, as well as alterations in tryptophan metabolism. This suggests that the gut microbiota may play a causal role in the development of features of depression and may provide a tractable target in the treatment and prevention of this disorder.
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                Author and article information

                Contributors
                Journal
                Neurobiol Stress
                Neurobiol Stress
                Neurobiology of Stress
                Elsevier
                2352-2895
                12 November 2016
                February 2017
                12 November 2016
                : 6
                : 113-126
                Affiliations
                [a ]APC Microbiome Institute, Biosciences Building, University College Cork, Cork, Ireland
                [b ]Department of Psychiatry & Neurobehavioural Science, University College Cork, Cork, Ireland
                [c ]School of Applied Psychology, Enterprise Centre, University College Cork, North Mall, Cork, Ireland
                [d ]Department of Anatomy & Neuroscience, Western Gateway Building, University College Cork, Cork, Ireland
                Author notes
                []Corresponding author. Neurogastroenterology Lab, Biosciences Building, University College Cork, Cork, Ireland.Neurogastroenterology LabUniversity College CorkBiosciences BuildingCorkIreland andrewallen@ 123456ucc.ie
                [∗∗ ]Corresponding author. Room 1.15, Biosciences Building, University College Cork, Cork, Ireland.University College CorkRoom 1.15, Biosciences BuildingCorkIreland G.Clarke@ 123456ucc.ie
                [1]

                Equal contributions.

                Article
                S2352-2895(16)30022-4
                10.1016/j.ynstr.2016.11.001
                5314443
                28229114
                a574e7c8-284b-4b24-a78c-cbceb4cf4fad
                © 2016 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 30 June 2016
                : 3 November 2016
                : 7 November 2016
                Categories
                Article

                stress,cognition,hpa axis,epigenetics,genotype
                stress, cognition, hpa axis, epigenetics, genotype

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