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dc.contributor.advisorSpencer, Karen Anne
dc.contributor.advisorStevenson, Tyler
dc.contributor.authorHarvey-Carroll, Jessica-Lily
dc.coverage.spatial210en_US
dc.date.accessioned2023-03-02T09:52:00Z
dc.date.available2023-03-02T09:52:00Z
dc.date.issued2022-11-29
dc.identifier.urihttps://hdl.handle.net/10023/27085
dc.description.abstractThe developing embryo, and consequent post-natal phenotypes, are altered greatly by maternal signals. Following maternal stress, an increase in glucocorticoids within the embryonic environment occurs. Glucocorticoids are one such signal which can lead to profound post-natal phenotypic alterations. There is preliminary evidence suggesting pre-natal stress has the ability to alter post-natal diurnal behaviour. Accumulating evidence is present that glucocorticoid receptors can directly interact with and modify circadian clock genes. Studies are limited however, and the potential changes to the expression profile of circadian clock genes in daily behaviour have not yet been fully explored. This thesis tested the hypothesis that a major glucocorticoid hormone, corticosterone, can modify the development of the circadian clock system, alongside altering post-natal diurnal rhythms. In chapter 2, Japanese quail embryos were subjected to physiologically relevant doses of corticosterone. Pre-natal corticosterone exposure was found to alter core circadian gene expression immediately before hatching and in early post-natal life. Juvenile quail exposed to pre-natal corticosterone were found to spend more time eating and inactive. Both behaviours also featured an earlier onset in peak time compared to controls. In chapter 3, the cycling of core circadian clock genes was found to be altered in peripheral organs following pre-natal exposure to corticosterone. Finally, in chapter 4, maternal transmission of circadian clock genes was studied. Maternal circadian RNA deposition was found to be significantly altered if a maternal early life post-natal stress was experienced. This did not alter the embryonic transcription of circadian clock genes. Pre-natal maternal stress was found to alter offspring embryonic transcription of circadian clock genes. In this thesis, pre-natal exposure to glucocorticoids was found to elicit changes to the developing circadian system within the perinatal period. Alterations in peripheral circadian clocks, alongside key diurnal behaviours, were identified. Maternal life history was found to significantly affect the first-generation offspring circadian gene expression. Overall, this thesis presents amongst the first evidence that exposure to pre-natal glucocorticoids alone may have the potential to elicit alterations to both the development of the circadian system, and post-natal circadian behaviour in Japanese quail. This information contributes to the understanding of transgenerational alterations to the circadian system following maternal stress. This has significant implications for further understanding behavioural alterations following stress in organisms, in an increasingly stressful world.
dc.language.isoenen_US
dc.relationThe effects of developmental stress on circadian rhythm development and the expression of diurnal behaviours (Thesis data) Harvey-Carroll, J., University of St Andrews, 22 Aug 2024 DOI: https://doi.org/10.17630/fecf79b5-d0ec-41d0-bf79-b61945902887en
dc.relation.urihttps://doi.org/10.17630/fecf79b5-d0ec-41d0-bf79-b61945902887
dc.subjectAnimal behaviour
dc.subjectNeurobiology
dc.subjectCircadian rhythms
dc.subjectDevelopment
dc.subjectStress
dc.subject.lccQP84.6H28
dc.titleThe effects of developmental stress on circadian rhythm ontogeny and the expression of diurnal behavioursen_US
dc.typeThesisen_US
dc.contributor.sponsorBiotechnology and Biological Sciences Research Council (BBSRC)en_US
dc.type.qualificationlevelDoctoralen_US
dc.type.qualificationnamePhD Doctor of Philosophyen_US
dc.publisher.institutionThe University of St Andrewsen_US
dc.rights.embargoreasonEmbargo period has ended, thesis made available in accordance with University regulationsen
dc.identifier.doihttps://doi.org/10.17630/sta/317
dc.identifier.grantnumberBB/M010996/1en_US


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