Castration or treatment with an anti-androgen of male rats immediately after birth favours a female differentiation of the hypothalamic mating centre(s). Treatment of such animals with oestrogen when grown up causes female sexual behaviour (Feder & Whalen, 1965; Grady, Phoenix & Young, 1965; Neumann & Elger, 1966).
In genuine homosexuality of human males there is, however, a normal or at least nearly normal androgen level after puberty. Therefore, a satisfactory hormonal explanation of genuine male homosexuality is only possible if androgens were also able to induce predominantly receptive female activity in a geno- and phenotypically male organism. This 'homosexual model' was produced in animal experiments, in which it was shown that male rats castrated neonatally and treated with androgen when adult displayed predominantly female sexual behaviour (Dörner, 1967).
In the present experiments this 'homosexual model' was re-investigated. Furthermore, the possibility of preventing androgen-induced feminine sexual behaviour by androgen administration during
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