male characters, including the development of male internal reproductive structures from the wolffian system, male external genitalia (after reduction to dihydrotestosterone), and masculinization of the brain (after aromatization to estradiol in rodents, but not humans).
9.In the absence of the SRY gene, the indifferent gonad develops into an ovary, and in the absence of testosterone and AMH, the müllerian system develops into the female internal reproductive tract, the wolffian system regresses, and the external genitals develop in female form. In many ways, the female pattern may be considered to be the “default.”10. Disorders of sexual differentiation illustrate the processes involved. Individuals with Turner’s syndrome have only a single X chromosome; they develop into apparent females. Females with congenital adrenal hyperplasia produce excessive adrenal androstenedione and display partially masculinized external genitalia and behavioral changes. Individuals with an XY genotype but a defect in the androgen receptor gene are insensitive to androgens and develop into apparent females despite the presence of abdominal testes. Such individuals lack both müllerian-derived structures (due to the manufacture of AMH by the testes) and wolffian-derived structures (due to the insensitivity to androgen). These individuals, it is important to note, develop a normal female gender identity.11. Gonadal hormones influence the brain and behavior in two general ways: (1) organizationally, during a sensitive period in early life and (2) activationally, later in life. Organizational effects tend to be permanent, but activational effects tend to be reversible.12. In rodents, but not humans, the brains and behavior of males are organized and activated by testosterone only after local conversion of testosterone to estradiol by the enzyme aromatase. Females are protected from the potentially masculinizing effects of maternal estrogens by the presence of circulating -fetoprotein, which sequesters estrogens and prevents them from reaching the brain.13. Several vertebrate models have provided important details about the effects of gonadal secretions on the brain. The rat’s sexually dimorphic nucleus of the POA is much larger in males than in females, and this difference is attributable entirely to an organizational effect of testosterone (after aromatization to estradiol). The spinal nucleus of the bulbocavernosus, however, is organized differently—it is rescued in males indirectly by testosterone’s actions on the SNB’s target muscles. This sexual dimorphism depends on androgen receptor stimulation. Aromatization is apparently notinvolved, since early DHT treatments will also produce a male-like SNB.14. Social influences can have a marked effect on the process of sexual differentiation; for example, maternal behavior toward pups contributes to the development of the SNB sexual dimorphism.