An Exploration of Female Reproductive Plasticity in the Context of Strange Male Exposure and Stress in Mice (Mus musculus)

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 (E₂). Male mice excrete E₂ in their urine; furthermore, stress can increase endogenous E₂ in females. Accordingly, I explored the role of male urinary E₂ in the Bruce and Vandenbergh effects, and examined E₂ and progesterone (P₄) 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 E₂, as castration removed this ability,and injections of E₂ restored it and urinary E₂ 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, P₄, and E₂ 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, P₄ suppressed and E₂ is elevated in stressed females losing their pregnancies. Exogenous P₄ did not mitigate stress-induced pregnancy failure, unless it was combined with a low dose of E₂. Taken together, I suggest that exogenous and endogenous E₂ contribute to reproductive plasticity in female mice, particularly their ability to abandon early pregnancy.</p>