title: Deletion of the Bax gene disrupts sexual behavior and modestly impairs motor function in mice.
abstract: Cell death is a nearly ubiquitous feature of the developing nervous system, and differential death in males and females contributes to several well studied sex differences in neuron number. Nonetheless, the functional importance of neuronal cell death has been subjected to few direct tests. Bax, a pro-apoptotic protein, is required for cell death in many neural regions. Deletion of the Bax gene in mice increases neuron number in several areas and eliminates sex differences in cell number in the brain and spinal cord. Here, sexual and motor behaviors were examined in Bax-/- mice and their wild-type siblings to test the functional consequences of preventing Bax-dependent cell death. Animals were gonadectomized in adulthood and provided with ovarian hormones or with testosterone for tests of feminine and masculine 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. Masculine sexual behavior was not sexually dimorphic among wild-type mice, but mounts and pelvic thrusts were nearly eliminated in Bax-/- mice of both sexes. Motor strength and performance at low speeds on a RotaRod apparatus did not differ by sex or Bax gene status. However, Bax-/- animals exhibited impairments on the RotaRod at higher speeds. Thus, developmental cell death may be required for masculine and feminine sexual behaviors and the fine tuning of motor coordination.
authors.affiliation: Department of Psychology and Neuroscience and Behavior Program, University of Massachusetts, Amherst, Massachusetts 01003, USA.
authors.forename: Jigyasa
authors.initials: J
authors.lastname: Jyotika
authors.forename: Jill
authors.initials: J
authors.lastname: McCutcheon
authors.forename: Julie
authors.initials: J
authors.lastname: Laroche
authors.forename: Jeffrey D
authors.initials: JD
authors.lastname: Blaustein
authors.forename: Nancy G
authors.initials: NG
authors.lastname: Forger
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D001921:Brain / Q000196:embryology / Q000254:growth & development / Q000378:metabolism; D002470:Cell Survival / Q000235:genetics; D002490:Central Nervous System / Q000196:embryology* / Q000254:growth & development / Q000378:metabolism; D003307:Copulation / Q000502:physiology; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000235:genetics*; D012739:Gonadal Steroid Hormones / Q000378:metabolism / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009043:Motor Activity / Q000502:physiology; D019957:Motor Skills Disorders / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism; D012727:Sex Characteristics; D012726:Sexual Behavior, Animal / Q000502:physiology; D012735:Sexual Dysfunction, Physiological / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D013116:Spinal Cord / Q000196:embryology / Q000254:growth & development / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000235:genetics*
chemical_list: C494827:Bax protein, mouse; D012739:Gonadal Steroid Hormones; D051028:bcl-2-Associated X Protein