Historically, studies of the role of endogenous hormones in developmental differentiation of the sexes have suggested that mammalian sexual differentiation is mediated primarily by testicular androgens, and that exposure to androgens in early life leads to a male brain as defined by neuroanatomy and behavior. The female brain has been assumed to develop via a hormonal default mechanism, in the absence of androgen or other hormones. Ovarian hormones have significant effects on the development of a sexually dimorphic cortical structure, the corpus callosum, which is larger in male than in female rats. In the females, removal of the ovaries as late as Day 16 increases the cross-sectional area of the adult corpus callosum. Treatment with low-dose estradiol starting on Day 25 inhibits this effect. Female callosa are also enlarged by a combination of daily postnatal handling and exogenous testosterone administered prior to Day 8. The effects of androgen treatment are expressed early in development, with males and testosterone-treated females having larger callosa than control females as early as Day 30. The effects of ovariectomy do not appear until after Day 55. These findings are more consistent with other evidence of a later sensitive period for ovarian feminization as compared to androgenic masculinization.

Heat shocks effective for the production of triploid brown trout (Salmo trutta) were optimized: 28 °C shocks lasting 10 to 15 minutes and applied 5 minutes after fertilization induce very high rates of triploidy (close to 100%) without causing much mortality; they can therefore be proposed for mass production of triploid brown trout. Female homogamety in that species is also demonstrated from analysis of gynogenetic progenies and progenies of sex-inverted females. Although the efficiency of masculinizing hormonal treatments requires further improvement, production of all-female sterile populations is now possible in this species promising for European sea-farming.