| Popis: |
While it is readily accepted that exposure to testicular secretions during a limited, sensitive stage of perinatal development permanently alters an organism’s behavioural responsivity to gonadal hormones in adulthood, it is unclear which hormone(s) mediates the events. Identity of the hormone or combination of hormones that bring about behavioural defeminization (suppression of female-typical responses) and behavioural masculinization (enhancement of male-typical responses) is critical for our eventual understanding of the neural mechanisms underlying sexual differentiation. Testosterone, the major secretory product of the developing testes (Resko et al. 1968; Corbier et al. 1978) is a likely candidate for the differentiating hormone. Indeed testosterone or testosterone propionate mimics the action of the testes when given to neonatally castrated males or females during perinatal development (Harris and Levine 1965; Whalen and Edwards 1967; Thomas et al. 1982 and others). However, this androgen is readily metabolized in peripheral and neural tissues (Mainwaring 1977) and one of its metabolites is oestrogen (Reddy et al. 1974). Moreover, oestrogens can also cause defeminization in rats (Wilson 1943; Feder and Whalen 1965). Since oestrogen is formed from circulating androgens within specific neural tissues, it has been postulated that oestrogens mediate sexual differentiation (Naftolin et al. 1975; Naftolin and MacLusky 1984). |
