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dc.contributor.authorMarasco, Valeria
dc.contributor.authorHerzyk, Pawel
dc.contributor.authorRobinson, Jane
dc.contributor.authorSpencer, Karen Anne
dc.identifier.citationMarasco , V , Herzyk , P , Robinson , J & Spencer , K A 2016 , ' Pre- and post-natal stress programming : developmental exposure to glucocorticoids causes long-term brain-region specific changes to transcriptome in the precocial Japanese quail ' , Journal of Neuroendocrinology , vol. 28 , no. 5 . ,
dc.identifier.otherPURE: 241920337
dc.identifier.otherPURE UUID: 758dfecc-f3a0-4863-a170-4ffe41293c91
dc.identifier.otherBibtex: urn:b1047cbf3bb48b6fe0e6c509beb2765d
dc.identifier.otherScopus: 84990201268
dc.identifier.otherWOS: 000377513600007
dc.identifier.otherORCID: /0000-0002-2851-9379/work/78205003
dc.descriptionFunding was provided by a Kelvin Smith PhD Scholarship from the University of Glasgow (VM, PH, JR, and KAS), and Biotechnology and Biological Sciences Research Council David Phillips Research Fellowship (K.A.S.).en
dc.description.abstractExposure to stress during early development can permanently influence an individual's physiology and behavior, and affect its subsequent health. The extent to which elevated glucocorticoids cause such long-term “programming” remains largely untested. Here, using the Japanese quail as our study species, we independently manipulated exposure to corticosterone during pre- and/or post-natal development and investigated the subsequent effects on global gene expression profiles within the hippocampus and hypothalamus upon adulthood. Our results showed that the changes in transcriptome profiles in response to corticosterone exposure clearly differed between the hippocampus and the hypothalamus. We also showed that these effects depended on the developmental timing of exposure and identified brain-region specific gene expression patterns that were either (1) similarly altered by corticosterone regardless of the developmental stage in which hormonal exposure occurred, or (2) specifically and uniquely altered by either pre-natal or post-natal exposure to corticosterone. Corticosterone-treated birds showed alterations in networks of genes which included known markers of the programming actions of early life adversity (e.g. brain-derived neurotrophic factor, and mineralocorticoid receptor within the hippocampus; corticotropin-releasing hormone and serotonin receptors in the hypothalamus). Altogether, these findings provide for the first time experimental support to the hypothesis that exposure to elevated glucocorticoids during development may be a key hormonal signaling pathway through which the long-term phenotypic effects associated with early life adversity emerge and potentially persist throughout the lifespan. These data also highlight that stressors might have different long-lasting impacts on the brain transcriptome depending on the developmental stage in which they are experienced; more work is now required to relate these mechanisms to organismal phenotypic differences.
dc.relation.ispartofJournal of Neuroendocrinologyen
dc.rights© 2016 The Authors. Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.en
dc.subjectEarly life stressen
dc.subjectPre- and post-natal glucocorticoid exposureen
dc.subjectBrain transcriptomeen
dc.subjectQH301 Biologyen
dc.subjectBF Psychologyen
dc.subjectRC0321 Neuroscience. Biological psychiatry. Neuropsychiatryen
dc.subjectEndocrinology, Diabetes and Metabolismen
dc.subjectEndocrine and Autonomic Systemsen
dc.subjectCellular and Molecular Neuroscienceen
dc.subjectSDG 3 - Good Health and Well-beingen
dc.titlePre- and post-natal stress programming : developmental exposure to glucocorticoids causes long-term brain-region specific changes to transcriptome in the precocial Japanese quailen
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews. School of Psychology and Neuroscienceen
dc.description.statusPeer revieweden

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