Abstract
The purpose of this paper is to describe the process of sexual development and maturity, the physiological basis of sexual development and orientation and to examine the interaction between hormones, the body, and behavior, including sex differences in brain morphology and the hormonal control over sexuality. The affects of the environment on sexual development and orientation will be considered as to the maternal and paternal causes and effects.
Sexual Development and Orientation
A person’s chromosomal sex is determined at the time of fertilization (Carlson, 2007). All cells of the human body (other than sperms or ova) contain 23 pairs of chromosomes. The genetic information that programs the development of a human is contained in the DNA that constitutes these chromosomes. The production of gametes (ova and sperms; gamein means “to marry”) entails a special form of cell division. This process produces cells that contain one member of each of the nine pairs of chromosomes. The development of a human begins at the time of fertilization, when a single sperm and ovum join, sharing their 23 single chromosomes to reconstitute the 23 pairs (Carlson, 2007). A person’s genetic sex is determined at the time of fertilization of the ovum by the father’s sperm. 22 of the twenty-three 23 pairs of chromosomes determine the organism’s physical development independent of its sex. The last pair consists of two sex chromosomes, which determine whether the offspring will be a boy or a girl (Carlson, 2007 ).
When considering sexual maturation, the onset of puberty occurs when cells in the hypothalamus secrete gonadotropin-releasing hormones (GnRH), which stimulate the production and release of two gonadotropic hormones by the anterior pituitary gland. The gonadotropic (“gonad-turning”) hormones stimulate the gonads to produce their hormones, which are ultimately responsible for sexual maturation (Carlson, 2007). The two gonadotropic hormones are folliclestimulating hormone (FSH) and luteinizing hormone (LH), named for the effects they produce in the female (production of a follicle and its subsequent luteinization). However, the same hormones are produced in the male, where they stimulate the testes to produce sperms and to secrete testosterone. If male and female pituitary glands are exchanged in rats, the ovaries and testes respond perfectly to the hormones secreted by the new glands (Harris and Jacobsohn, 1951-1952). In response to the gonadotropic hormones (usually called gonadotropins), the gonads secrete steroid sex hormones. The ovaries produce estradiol, one of a class of hormones known as estrogens (Carlson, 2007). The testes produce testosterone, an androgen. Both types of glands also produce a small amount of the hormones of the other sex. The gonadal steroids affect many parts of the body. Both estradiol and androgens initiate closure of the growing portions of the bones and thus halt skeletal growth. Estradiol also causes breast development, growth of the lining of the uterus, changes in the deposition of body fat, and maturation of the female genitalia. Androgens stimulate growth of facial, axillary (underarm), and pubic hair; lower the voice; alter the hairline on the head (often causing baldness later in life); stimulate muscular development; and cause genital growth (Carlson, 2007 ).
The physiological basis of early sexual development and orientation is the same for all primates. Early in embryonic development, the internal sex organs are bisexual; that is, all embryos contain the precursors for both female and male sex organs. However, during the third month of gestation, only one of these precursors develops; the other withers away. The precursor of the internal female sex organs, which develops into the fimbriae and Fallopian tubes, the uterus, and the inner two-thirds of the vagina, is called the Müllerian system. The precursor of the internal male sex organs, which develops into the epididymis, vas deferens, and seminal vesicles, is called the Wolffian system (Carlson, 2007). The gender of the internal sex organs of a fetus is determined by the presence or absence of hormones secreted by the testes. If these hormones are present, the Wolffian system develops. If they are not, the Müllerian system develops. The Müllerian (female) system needs no hormonal stimulus from the gonads to develop; it just normally does so. In contrast, the cells of the Wolffian (male) system do not develop unless they are stimulated to do so by a hormone. Thus, testes secrete two types of hormones. The first, a peptide hormone called anti- Müllerian hormone, does exactly what its name says: It prevents the Müllerian (female) system from developing. It therefore,has a defeminizing effect. The second, a set of steroid hormones called androgens, stimulates the development of the Wolffian system (Carlson, 2007 ).
The fact that the internal sex organs of the human embryo are bisexual and could potentially develop as either male or female is dramatically illustrated by two genetic disorders: androgen insensitivity syndrome and persistent Müllerian duct syndrome. Some people are insensitive to androgens; they have androgen insensitivity syndrome, one of the more aptly named disorders (Money and Ehhartardt, 1972). T he cause of androgen insensitivity syndrome is a` genetic mutation that prevents the formation of functioning androgen receptors. (The gene for the androgen receptor is located on the X chromosome.) The primitive gonads of a genetic male fetus with androgen insensitivity syndrome become testes and secrete both anti-Müllerian hormone and androgens. The lack of androgen receptors prevents the androgens from having a masculinizing effect; thus, the epididymis, vas deferens, seminal vesicles, and prostate fail to develop. The second genetic disorder, persistent Müllerian duct syndrome, has two causes: either a failure to produce anti-Müllerian hormone or the absence of receptors for this hormone (Warne and Zajan, 1998). When this syndrome occurs in genetic males, androgens have their masculinizing effect but defeminization does not occur. Thus, the person is born with both sets of internal sex organs, male and female. The presence of the additional female sex organs usually interferes with normal functioning of the male sex organs.
The interaction between hormones, the body, and behavior, including sex differences in brain morphology and the hormonal control over sexuality can be seen in cycles. The reproductive cycle of female primates is called a menstrual cycle (from mensis, meaning “month”). Females of other species of mammals also have reproductive cycles, called estrous cycles. Estrus means “gadfly”; when a female rat is in estrus, her hormonal condition goads her to act differently from when she does at other times. Menstrual cycles and estrous cycles consist of a sequence of events that are controlled by hormonal secretions of the pituitary gland and ovaries. These glands interact, the secretions of one affecting those of the other. A cycle begins with the secretion of gonadotropins by the anterior pituitary gland. These hormones (especially FSH) stimulate the growth of ovarian follicles, small spheres of epithelial cells surrounding each ovum. Women normally produce one ovarian follicle each month; if two are produced and fertilized, dizygotic (fraternal) twins will develop. As ovarian follicles mature, they secrete estradiol, which causes the growth of the lining of the uterus in preparation for implantation of the ovum, should it be fertilized by a sperm.
The LH surge causes ovulation: The ovarian follicle ruptures, releasing the ovum. Under the continued influence of LH, the ruptured ovarian follicle becomes a corpus luteum (“yellow body”), which produces estradiol and progesterone. The latter hormone promotes pregnancy (gestation). It maintains the lining of the uterus, and it inhibits the ovaries from producing another follicle. Meanwhile, the ovum enters one of the Fallopian tubes and begins its progress toward the uterus. If it meets sperm cells during its travel down the Fallopian tube and becomes fertilized, it begins to divide, and several days later it attaches itself to the uterine wall. If the ovum is not fertilized or if fertilized too late to develop sufficiently by the time it gets to the uterus, the corpus luteum will stop producing estradiol and progesterone, then the lining of the walls of the uterus will slough off. At this point, menstruation will commence.
Male sexual behavior is quite varied, although the essential features of intromission (entry of the penis into the female’s vagina), pelvic thrusting (rhythmic movement of the hindquarters, causing genital friction), and ejaculation (discharge of semen) are characteristic of all male mammals (Carlson, 2007). After ejaculating, the male refrains from sexual activity for a period. Most mammals will return to copulate again and again, showing a longer pause, called a refractory period, after each ejaculation. (The term comes from the Latin refringere, “to break off.”) Sexual behavior of male rodents depends on testosterone, a fact that has long been recognized (Bermant and Davidison, 1974). If a male rat is castrated (that is, if his testes are removed), his sexual activity eventually ceases. However, the behavior can be reinstated by injections of testosterone. Other hormones play a role in male sexual behavior. Oxytocin is a hormone produced by the posterior pituitary gland that contracts the milk ducts and thus causes milk ejection in lactating females and is also produced in males, where it obviously plays no role in lactation. Oxytocin is released at the time of orgasm in both males and females and appears to contribute to the contractions of the smooth muscle in the male ejaculatory system and of the vagina and uterus (Carter, 1992) .
The mammalian female has been described as the passive participant in copulation, that in some species the female’s role during the act of copulation is merely to assume a posture that exposes her genitals to the male. This behavior is called the lordosis response (from the Greek lordos, meaning “bent backward”). The female will also move her tail away (if she has one) and stand rigidly enough to support the weight of the male. However, the behavior of a female rodent in initiating copulation is often very active (Carlson, 2007). Sexual behavior of female rodents depends on the gonadal hormones present during estrus: estradiol and progesterone. In rats, estradiol increases about 40 hours before the female becomes receptive; just before receptivity occurs, the corpus luteum begins secreting large quantities of progesterone (Feder, 1981).
What controls a person’s sexual orientation, that is, the gender of the preferred sex partner? Many studies have examined the levels of sex steroids in male homosexuals (Meyer-Bahlburg, 1984), and the vast majority of them found these levels to be similar to those of heterosexuals. A few studies suggest that about 30% of female homosexuals have elevated levels of testosterone (but still lower than those found in men) (Carlson, 2007). If these differences are related to a biological cause of lesbianism or whether differences in lifestyles may increase the secretion of testosterone is not yet known. A more likely biological cause of homosexuality is a subtle difference in brain structure caused by differences in the amount of prenatal exposure to androgens. Perhaps, then, the brains of male homosexuals are neither masculinized nor defeminized, those of female homosexuals are masculinized and defeminized, and those of bisexuals are masculinized but not defeminized (Carlson, 2007 )
Evidence suggests that prenatal androgens can affect human social behavior and sexual orientation, as well as anatomy. In a disorder known as congenital adrenal hyperplasia (CAH), the adrenal glands secrete abnormal amounts of androgens. (Hyperplasia means “excessive formation.”) The secretion of androgens begins prenatally; thus, the syndrome causes prenatal masculinization. Boys born with CAH develop normally; the extra androgen does not seem to have significant effects. However, a girl with CAH will be born with an enlarged clitoris, and her labia may be partly fused together.
When considering the environmental factors of sexual development, one must consider the parental factors. Although most research on the physiology of parental behavior has focused on maternal behavior, some researchers are now studying paternal behavior shown by the males of some species of rodents. Then the human paternal behavior is very important for the offspring of our species, but the physiological basis of this behavior has not yet been studied.
Most sexually dimorphic behaviors are controlled by the organizational and activational effects of sex hormones. Maternal behavior is somewhat different in this respect. First, no evidence exists that organizational effects of hormones play a role. Second, although maternal behavior is affected by hormones, the behavior is not controlled by them. Most virgin female rats will begin to retrieve and care for young pups after having infants placed with them for several days (Wiesner and Sheard, 1939). Although hormones are not essential for the activation of maternal behavior, many aspects of maternal behavior are facilitated by hormones. Nest-building behavior is facilitated by progesterone, the principal hormone of pregnancy. Voci and Carlson (1973)found that hypothalamic implants of prolactin as well as progesterone facilitated nest building in virgin female mice. Presumably, nest building can be facilitated by either hormone: progesterone during pregnancy and prolactin after parturition. Prolactin, produced by the anterior pituitary gland, is responsible for milk production. Unlike many other peptides, special mechanisms transport this hormone from the blood into the brain (Carlson, 2007 ).
References
Bermant, G., and Davidson, J. M. Biological Bases of Sexual Behavior. New York: Harper &
Row, 1974.
Carlson, N. R. (2007 ). Physiology of Behavior, Ninth Edition. Boston: Allyn and Bacon.
Carter, C. S. Hormonal influences on human sexual behavior. In Behavioral Endocrinology,
edited by J. B. Becker, S. M. Breedlove, and D. Crews. Cambridge, Mass.: MIT Press,
1992.
Feder, H. H. Estrous cyclicity in mammals. In Neuroendocrinology of Reproduction, edited by
N. T. Adler. New York: Plenum Press, 1981.
Harris, G. W., and Jacobsohn, D. Functional grafts of the anterior pituitary gland. Proceedings of
the Royal Society of London [B], 1951– 1952, 139, 263– 267.
Meyer- Bahlburg, H. F. L. Psychoendocrine research on sexual orientation: Current status and
future options. Progress in Brain Research, 1984, 63, 375– 398.
Money, J., and Ehrhardt, A. Man & Woman, Boy & Girl. Baltimore: Johns Hopkins University
Press, 1972.
Warne, G. L., and Zajac, J. D. Disorders of sexual differentiation. Endocrinology and
Metabolism Clinics of North America, 1998, 27, 945– 967.
Voci, V. E., and Carlson, N. R. Enhancement of maternal behavior and nest behavior following
systemic and diencephalic administration of prolactin and progesterone in the mouse.
Journal of Comparative and Physiological Psychology, 1973, 83, 388– 393.
Wiesner, B. P., and Sheard, N. Maternal Behaviour in the Rat. London: Oliver and Brody, 1933.