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dc.contributor.advisorPeña, Catherine-
dc.contributor.authorJones, Parker-
dc.description.abstractDepression is one of the most prevalent mood disorders, but its causes are not fully understood. Both epidemiological and clinical data indicate that a history of early life stress (ELS) increases the risk of depression and other mood disorders. Additionally, thyroid function is crucial for proper brain development and there is evidence for an interaction between stress and thyroid function. While the literature suggests that there is a link between ELS and hypothyroidism in the development of depression later in life, how this interaction occurs is not fully understood. This thesis looks to address how early life stress may trigger an increased risk for depression later in life through altered thyroid function. This was approached in two parts. Part one was a search of previously published RNA sequencing data from the ventral tegmental area of mice with comparisons of gene expression for thyroid factors under different stress exposure conditions. These results showed that male and female mice experienced different gene expression of thyroid hormone factors in response to stress. This work informed part two that examined how thyroid-stimulating hormone levels are altered in response to ELS. This study revealed that ELS disrupts the naturally occurring difference in thyroid hormone levels in males and females. Taking these results into consideration with previously conducted behavioral assays suggests that thyroid function may facilitate the impact of ELS on depression-like behaviors.en_US
dc.titleEarly Life Stress Disrupts Thyroid Hormone Signaling in Miceen_US
dc.typePrinceton University Senior Theses
pu.certificateGlobal Health and Health Policy Programen_US
Appears in Collections:Neuroscience, 2017-2022
Global Health and Health Policy Program, 2017-2022

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