Chapter 6 Summary

  1. A fertilized ovum immediately begins a series of cell divisions, becoming a conceptus. At the blastocyst stage, when the conceptus has developed a central cavity, it implants in the wall of the uterus and secretes human chorionic gonadotropin, which prevents regression of the maternal corpus luteum. Pregnancy is established at this point. After forming the extraembryonic membranes, the remaining tissue of the conceptus gives rise to the embryo.
  2. By about 6 weeks after conception the embryo has developed its body plan and most of its major organs and is known as a fetus. Further fetal development involves growth and the gradual onset of function in the various organ systems.
  3. Sex is usually determined by the sex chromosomes: The XX pattern causes female development, and the XY pattern causes male development. The key player in male development is the gene SRY, on the Y chromosome, which induces the embryo’s genital ridges to become testes. In female embryos, which lack SRY, other genes direct the genital ridges to become ovaries. Anomalous sex chromosome patterns include XXY, which causes Klinefelter syndrome, and XO, which causes Turner syndrome.
  4. The male and female internal reproductive tracts develop from different precursors—the Wolffian and Müllerian ducts. In XY embryos (normal males), the testes secrete anti-Müllerian hormone (AMH), which causes the Müllerian ducts to regress, and androgens, which cause the Wolffian ducts to develop further and produce the male internal anatomy. In XY embryos lacking functional androgen receptors (androgen insensitivity syndrome [AIS]), neither the male nor the female reproductive tract develops. In XX embryos (normal females), the lack of AMH allows the Müllerian ducts to develop further, and the lack of androgens allows the Wolffian ducts to regress, producing the female internal anatomy.
  5. The external genitalia of the two sexes develop from common precursors. The urethral folds give rise to the labia minora in females and to the shaft of the penis in males. The genital swellings give rise to the labia majora in females and the scrotum in males. The genital tubercle forms the external portion of the clitoris in females and the glans of the penis in males. Male-typical development of the external genitalia requires the presence of testosterone and its conversion to 5α-dihydrotestosterone (DHT). In genetically female fetuses that are exposed to high levels of androgens (as in congenital adrenal hyperplasia [CAH]), and in genetically male fetuses that lack androgen receptors (androgen insensitivity syndrome) or that cannot convert testosterone to DHT (5α-reductase deficiency), the external genitalia will be sex-atypical to a variable degree.
  6. Both ovaries and testes descend from their original lumbar position during fetal life. The ovaries descend into the pelvis, on either side of the uterus. The testes descend into the pelvis and then through the developing inguinal canal into the scrotum. If the testes fail to descend by 3 months after birth, spermatogenesis may be impaired.
  7. Exposure to sex hormones during fetal life is directly or indirectly responsible for the sexual differentiation of the central nervous system. These hormones cause the development of sexually dimorphic structures and circuits and, by doing so (at least in experimental animals), influence the kinds of sexual behaviors that are exhibited in adulthood. The effects of hormones on behavior are thought to occur in two main phases: organizational effects during prenatal brain development and activational (triggering) effects in adulthood.
  8. External factors also influence prenatal sexual development. These factors may include drugs such as synthetic sex hormones. After birth, social factors further influence the development of the brain and adult sexual behavior, to judge from experimental studies in nonhuman primates.
  9. Puberty is the biological transition from childhood to sexual maturity. It is marked by further development of the reproductive tracts and external genitalia, the appearance of secondary sexual characteristics (e.g., breasts or facial hair), signs of functional sexual maturity (i.e., onset of menstruation or ejaculation), and a growth spurt followed by cessation of growth. In the United States, puberty begins earlier in girls than in boys, and earlier in African-American girls than in white American girls. Precocious puberty (defined as puberty beginning before age 7 in girls or age 9 in boys) and delayed puberty can usually be treated medically, if necessary.
  10. Puberty is caused by a rise in the circulating levels of adrenal and gonadal sex steroids and growth hormone. Gonadal secretion is triggered by a rise in pituitary gonadotropins, which, in turn, is triggered by the onset of secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus. It is thought that the prime trigger for puberty is the attainment of a critical body weight, weight-to-height ratio, or body fat index. The body may communicate this information to the hypothalamus by means of the hormone leptin.
  11. In Western countries, puberty has been starting at progressively younger ages over the last 150 years. The most likely reason is a progressive change in nutritional practices, which have led to more rapid weight gain during childhood.
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