sexology

EMBRYOLOGY: DEVELOPMENT OF SEXUAL AND GENERATIVE ORGANS

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Gates 1 and 2: Chromosomal (or Genetic and Gonadal) Sex
Gate 3: Hormonal Sex
Gate 4: Internal Sexual Anatomy
Gate 5: External Sexual Anatomy
Gate Six: Sexual Dimorphism in Neural Tendencies
Development of the Mammary Glands
Puberty
Anomalous Developments of the Sexual and Generative Organs

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Embryology is the science that describes and explains the development of an organism before its birth. In humans, the main development of the sexual and reproductive organs occurs between the 4th and 18th weeks of pregnancy. This development is closely associated with development of a pair of temporary kidneys, which are replaced in the third month by the permanent kidneys.

Psychosexual development, of which the anatomical development of the sexual and generative organs is an integral and interactive part, has been compared with an analogy to a road map with six prenatal and six postnatal gates (See Table 1) The sex prenatal gates are the following:

1. Chromosomal (or genetic) sex (established at fertilization);2. Gonadal sex (established between weeks 6 and 12 of gestation);
3. Hormonal sex (with a critical period extending from the third month to death);
4. and 5 Internal and external sexual anatomy (in the second and third month);
6. Neural template encoding (from the second month to death).

The postnatal gates begin at birth with

7. Gender assignment.

This is followed by

8. Gender scripting;9. Gender role;
10. Gender identity (which is finalized age three);
11. Gender orientation (which appears to be finalized somewhere between age five and the onset of puberty); and
12. Adult gender identity-role;

This entry covers only the six prenatal gates of psychosexual development.

The timing and limits on the outcome of development at each of these 12 gates vary. The developmental "gates" that involve anatomical development have narrow, specific temporal "windows" (i.e., times during development when primordial, unspecialized tissues can respond to developmental stimuli) At other "gates," especially those involving behavior, the timing of development is less restricted and may even extend over years. The outcome of development at a specific developmental gate may be one dimensional (i e, the outcome of that aspect is either-or, male or female). Development at other gates has a two-dimensional outcome that results from two concurrent processes, one process defeminizing a particular aspect of sexual development by overriding the inherent tendency of some structures to develop in the female path, while a second simultaneous process masculinizes other related structures.

Table 1. The 12 "Gates" of Psychosexual Development

Prenatal Gate	Temporal Window	Dimensional Character
1. Genetic sex	When sperm and egg unite	Either XX female or XY male
2. Gonadal sex	Weeks 6 to 12	Either ovaries or testes
3. Hormonal sex	Second month of pregnancy through death	Two-dimensional combination of masculinizing and feminizing hormones
4. Internal sexual anatomy	Second month of pregnancy through death	Two-dimensional some structures being masculinized while others are feminized
5. External sexual anatomy	Third month of pregnancy	One-dimensional, either a penis and scrotum or clitoris and labia
6. Encoding of neural tendency	Second half of pregnancy through death	Two-dimensional combination of masculine and feminine tendencies and traits, somewhat flexible in some behavioral areas; gender orientation tendencies
7. Gender assignment	Usually occurs at birth; later reassignment possible	One-dimensional: "It's a boy" or "It's a girl "
8. Gender scripting	From birth onward	Multi-dimensional, culturally flexible combination of masculine or feminine scripts
9. Gender	From early infancy throughout life	Multidimensional, flexible combination of masculine or feminine roles and behaviors
10. Gender identity	Believed to be irreversibly set by age 3	One-dimensional, either "I'm a male" or "I'm a female "
11. Gender orientation	Believed to be irreversibly set by age 5, definitely by late childhood	Oriented to persons of the same gender, other gender, or both genders
12. Adult gender identity-role	Usually set by the time of puberty, but elaborated on throughout life	Gender identity set as either male or female, with more or less flexibility in gender role behaviors

In the higher animals (mammals), there exists an inherent or default tendency for the sexual and reproductive organs and brain tissues of all embryos to follow the female path through the 12 gates of psychosexual development. This inherent or default tendency does not depend on any genetic and hormonal stimulus or control, except that two X chromosomes are required for development of fertile ovaries. Development of the male organs and male psyche, on the other hand, is said to be additive or cumulative because they depend on two factors, one genetic and the other hormonal. In the second month of pregnancy, the Testes Determining Factor (TDF) gene carried on the Y chromosome directs development of the testes, which then produce three hormones: testosterone, dihydrotestosterone (DOT), and a Müllerian inhibiting hormone (MIH). The critical balance and interaction of these three hormones direct full male development. (See Genetics and Sex.)

Gates 1 and 2: Chromosomal (or Genetic and Gonadal) Sex

Chromosomal (or genetic) sex is determined at fertilization (see Genetics and Sex). Four weeks later, development of the sexual and reproductive system begins with formation of gonadal ridges on the surface of paired intermediate (metanephric) kidneys inside the embryo's thoracic-abdominal cavity and the migration of primordial germ cells from the primitive yolk sac outside the embryo to these ridges. During the sixth week, the sexually undifferentiated gonads may begin developing along a path that will result in testes, which produce a male balance of sex hormones and, after puberty, sperm. If the gonads are not stimulated to become testes in the sixth week, they will wait a few weeks to differentiate into ovaries, capable of producing a female balance of sex hormones and, with puberty, eggs (ova). At this early stage, some cells in the gonads develop to nourish and support development of the eggs and sperm. These are follicular cells in the ovaries and Sterol cells in the testes.

The either/or development of the undifferentiated gonads into ovaries or testes depends on the fetal genetic constitution established at fertilization. If the cells of the embryo's body contain the TDF gene (usually carried on a Y chromosome), the tissues of the gonadal ridges form seminiferous (sperm-producing) tubules and associated ducts during the sixth week. In week seven, some cells sandwiched between the seminiferous tubules develop into the cells of Leydig and begin producing testosterone, a hormone that will stimulate and direct further differentiation of the reproductive and sexual structures.

If the embryo's body cells do not contain the TDF gene, the undifferentiated gonads do not begin developing until week 12 when, by default, the inherent tendency of the embryo to develop as a female is activated. This inherent tendency has been named the Eve Plan. Development of fertile ovaries requires two X chromosomes in the embryo's body cells. By week 16, the primitive female germ cells are incorporated into millions of primary ovarian follicles. Most of these degenerate during pregnancy, leaving only one million or two million primary oocyte (developing eggs) at birth. These primitive eggs begin the two-stage meiosis, or reduction, cell division that will produce an egg with half the normal number of chromosomes in the body cells. But the cell division stops in what geneticists term "prophase arrest " They remain in this arrested state until cell division resumes sometime after puberty. This phenomenon of arrested egg development increases the risk of abnormalities in the number of chromosomes in the egg and thus in an embryo. (See Genetics and Sex for discussion of Turner and Klinefelter syndromes)

As the temporary (mesonephric) kidneys degenerate and are replaced functionally by the developing definitive kidneys, the ovaries or testes shift out of the thoracic-abdominal cavity to assume their final position in the pelvic cavity.

Gate 3: Hormonal Sex

In the third month of gestation, the testes begin producing three hormones: (1) testosterone and its derivative, (2) DHT, and (3) MIH. These hormones direct development of the male sexual and generative anatomy and establish behavioral tendencies in the neural pathways of the brain. As these hormones circulate throughout the fetal body, specific transfer enzymes on selective target cells and organs allow these hormones to enter those cells and organs, including the brain. Testosterone and DHT are androgenic (or masculinizing) hormones; MIH has a defeminizing effect on the embryo, blocking the inherent tendency of the embryo to develop as a female. Estrogens, which are produced by both the ovaries and testes, do not appear to be involved in sexual differentiation until puberty. At that time, estrogens stimulate development of secondary sexual characteristics of the female and have some minor effects on the secondary sexual characteristics of males.

Gate 4: Internal Sexual Anatomy

In both male and female embryos, a pair of ducts drain urine from the two temporary kidneys (mesonephros) and carry it to the cloaca for excretion into the amniotic sac. Parallel with these Wolffian (mesonephric) ducts are two Müllerian (or paramesonephric) ducts. The Müllerian ducts move toward the midline as they approach the cloaca, fusing into a single tube which ends at the cloaca without opening into the urogenital sinus.

By the eleventh week, Sertoli cells in the testes are producing MIH. In the male embryo, MIH "defeminizes" by triggering degeneration of the Müllerian ducts. This prevents the Eve Plan from coming into play; in the Eve Plan, the Müllerian ducts would develop into the vagina, uterus, and Fallopian tubes. MIH may also initiate the testes to descend about the time of birth and produce as yet undetected effects of neural pathways late in pregnancy. After birth, MIH has no known function.

In the developing male embryo, during the third month, the cells of Leydig in the testes produce the hormone testosterone, which causes the Wolffian ducts to develop. The portion of these tubes near the testes becomes highly twisted to form the epididymis The rest becomes the vas deferens, ejaculatory duct, and the seminal vesicles of the male duct system. Tissue surrounding the ejaculatory ducts where they join the urethra forms the prostate gland. The outer urethra and penis develop from the open urogenital sinus as part of the external development described in Gate 5 below. The paired bulbourethral (or Cowper's glands) develop below the prostate from outpocketings of the urethra

In a fetus that lacks the TDF gene and does not develop threshold levels of masculinizing hormones and MIH in the critical period between weeks 6 and 12, development of internal and external sexual organs—and neural templates—follows the Eve Plan. With no testosterone to stimulate their development into male structures, the Wolffian ducts degenerate and disappear. The absence of MIH allows the Müllerian ducts to develop according to their inherent genetic tendencies in the female path. The portion of the Müllerian ducts near the ovaries become the Fallopian (or uterine) tubes. The remaining caudal portion of the Müllerian ducts fuses in the eighth week, with the medial septum disappearing about week 12. This primordial becomes the uterus, cervix, and vagina. The outer muscles of the uterus and vagina develop from surrounding tissue.

Because the internal sexual system (excluding the gonads) originates from parallel primordial ducts for the male (Wolffian) and the female (Müllerian) systems, anomalous development can result. The internal sexual duct system may, for instance, be masculinized by testosterone, but not defeminized due to a lack of MIH. This would leave the fetus with both internal male and female sexual structures (as discussed below). A second variation, androgen insensitivity (or testicular feminization) syndrome, is caused by a single defective gene (see Genetics and Sex). In this condition, the fetus is defeminized by MIH but not masculinized because none of the body cells can recognize the masculinizing message of the testosterone and DHT. It therefore lacks both male and female internal systems