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http://hdl.handle.net/11375/13418
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DC Field | Value | Language |
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dc.contributor.advisor | deCatanzaro, Denys | en_US |
dc.contributor.author | Thorpe, Joelle B. | en_US |
dc.date.accessioned | 2014-06-18T17:03:51Z | - |
dc.date.available | 2014-06-18T17:03:51Z | - |
dc.date.created | 2013-09-19 | en_US |
dc.date.issued | 2013-10 | en_US |
dc.identifier.other | opendissertations/8239 | en_US |
dc.identifier.other | 9307 | en_US |
dc.identifier.other | 4601037 | en_US |
dc.identifier.uri | http://hdl.handle.net/11375/13418 | - |
dc.description.abstract | <p>Females experience reproductive plasticity in several situations. Under stress, females can experience implantation failure. In the presence of unfamiliar males, females can also experience implantation failure (Bruce effect), or hastened sexual maturation (Vandenbergh effect). Sexual maturation and implantation failure are also induced by 17β-estradiol (E<sub>2</sub>). Male mice excrete E<sub>2</sub> in their urine; furthermore, stress can increase endogenous E<sub>2</sub> in females. Accordingly, I explored the role of male urinary E<sub>2</sub> in the Bruce and Vandenbergh effects, and examined E<sub>2</sub> and progesterone (P<sub>4</sub>) during stress-induced implantation failure in mice. I showed that a male mouse’s ability to induce the Bruce and Vandenbergh effects depends on his urinary E<sub>2</sub>, as castration removed this ability,and injections of E<sub>2</sub> restored it and urinary E<sub>2</sub> levels. I also developed urinary measurements of the stress hormone, corticosterone, for use in subsequent stress studies. I showed that serum and urinary corticosterone follow a similar circadian rhythm, and that urinary corticosterone responds appropriately to acute stress in male mice. Also, urinary and serum corticosterone, P<sub>4</sub>, and E<sub>2</sub> in female mice show similar responses to stress, with slightly different time courses. Lastly, I showed that rat-exposure is stressful and causes implantation failure in female mice. Furthermore, P<sub>4</sub> suppressed and E<sub>2</sub> is elevated in stressed females losing their pregnancies. Exogenous P<sub>4</sub> did not mitigate stress-induced pregnancy failure, unless it was combined with a low dose of E<sub>2</sub>. Taken together, I suggest that exogenous and endogenous E<sub>2</sub> contribute to reproductive plasticity in female mice, particularly their ability to abandon early pregnancy.</p> | en_US |
dc.subject | endocrinology | en_US |
dc.subject | stress | en_US |
dc.subject | reproduction | en_US |
dc.subject | implantation | en_US |
dc.subject | estradiol | en_US |
dc.subject | progesterone | en_US |
dc.subject | corticosterone | en_US |
dc.subject | Biological Psychology | en_US |
dc.subject | Biology | en_US |
dc.subject | Endocrinology | en_US |
dc.subject | Physiology | en_US |
dc.subject | Biological Psychology | en_US |
dc.title | An Exploration of Female Reproductive Plasticity in the Context of Strange Male Exposure and Stress in Mice (Mus musculus) | en_US |
dc.type | thesis | en_US |
dc.contributor.department | Psychology | en_US |
dc.description.degree | Doctor of Philosophy (PhD) | en_US |
Appears in Collections: | Open Access Dissertations and Theses |
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fulltext.pdf | 1.94 MB | Adobe PDF | View/Open |
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