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Deletion of the Bax Gene Severley Impairs Sexual Behavior and Modestly Impairs Motor Function In Mice

During neural development, nearly 50% of all newly generated neurons undergo cell death after making provisional contact with their target cells. The functional consequences of eliminating this neuronal cell death are not known. Bax, a pro-apoptotic protein, is required for cell death in many neural regions. A null mutation of the Bax gene in mice has been shown to increase overall cell number and eliminate the sex differences in neuron number in the anteroventral periventricular nucleus (AVPV) and the principal nucleus of the bed nucleus of the stria terminalis (BNSTp). The aim of my Master’s thesis was to study male and female sexual behaviors and motor behavior in Bax -/- mice and their wild-type siblings. Animals were gonadectomized in adulthood and provided with ovarian hormones or with testosterone for tests of female and male sexual behaviors, respectively. Wild-type mice exhibited a sex difference in feminine sexual behavior, with high lordosis scores in females and low scores in males. This sex difference was eliminated by Bax deletion, with very low receptivity exhibited by both male and female Bax -/- mice. Male sexual behavior was not sexually dimorphic among wild-type mice, but mounts and pelvic thrusts were nearly absent in Bax -/- mice of both sexes. The knockouts did not display deficient motor strength or performance at low speeds on a RotaRod apparatus compared to wild type mice. At high speeds, however, Bax -/- animals exhibited impairments on the RotaRod. Therefore, developmental cell death may be required for exhibition of male and female sexual behaviors, and for coordination of relatively difficult motor tasks.