Date of Award

5-2020

Document Type

Campus Access Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Developmental and Brain Sciences

First Advisor

Jin Ho Park

Second Advisor

Vivian Ciaramitaro

Third Advisor

Susan Zup

Abstract

Mechanisms underlying the regulation of either male or female reproductive behavior in the absence of gonadal hormones are not well understood. Further investigation will lead to better understanding of the prevalent individual differences observed in reproductive behavior and may lead to novel therapies for sexual dysfunction in growing clinical populations. To further our understanding of steroid-independent male sex behavior (MSB), our lab utilizes a rodent model in which ~30% of castrated male B6D2F1 hybrid mice display MSB many months after castration. To our knowledge, no studies have investigated whether females of this hybrid strain demonstrate steroid-independent female sex behavior (FSB), and the first two main studies of this dissertation explored this possibility. The first set of experiments found that a significant proportion (~30%) of ovariectomized B6D2F1 hybrid female mice demonstrated ovarian steroid-independent receptivity after a deprivation of circulating ovarian hormones for over 25 weeks. There were no differences in circulating estradiol or testosterone levels between those that were receptive and those that were not, and ovariectomized B6D2F1 receptive females had increased dendritic spine density in brain areas that regulate FSB relative to those of non-receptive females. The second set of experiments sought to further our understanding of potential steroid-independent FSB mediated by spinogenesis including a possible causal role, using intracranial Reelin to attempt induction of spinogenesis. However, Reelin had no effect on FSB. Ovarian steroid-independent receptivity was not demonstrated in ovariectomized B6D2F1 female mice. Potential variables which may have led to these contradicting results are discussed. The third set of experiments were designed to further our understanding of the underlying mechanisms by which gonadal hormones organize the normal maturation of neural circuitry that regulates steroid-independent MSB during the peripubertal periods of development. Our results indicate that exposure to gonadal steroids, specifically testosterone, during puberty was necessary for the expression of steroid-independent MSB in adulthood. However, gonadal steroids during puberty were not necessary for either testosterone or estradiol to activate MSB in adulthood. Furthermore, activation of MSB was initiated sooner in hybrid male mice castrated prior to puberty that were administered estradiol in adulthood compared to those that were provided testosterone.

Comments

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