What are gonads, and how do they affect behavior?
The gonads are endocrine glands that secrete sex hormones in all mammalian species. In males, the gonads are the testes, which secrete sex hormones called androgens; in the female, the gonads are the ovaries, which secrete estradiol and progesterone. These sex hormones, which are released into the bloodstream, have effects on the formation of both internal and external reproductive organs during prenatal development; later, they have important behavioral effects, particularly in the expression of sexual behaviors. They are also implicated in maternal and aggressive behaviors.
In the prenatal period, as the embryo is developing, the gonads are the first sex organs to differentiate into male and female organs. Prior to the seventh week of human gestation, the gonads are identical for the two sexes. If the embryo is genetically male, the gonads differentiate into male testes at the seventh or eighth week of development. If the embryo is female, the gonads differentiate into ovaries at around the tenth or eleventh week. This differentiation is controlled by a protein called the sex-determining region Y (SRY) protein, which is encoded by a gene on the Y chromosome known as the SRY gene. When the SRY protein is present, it will stimulate the formation of testes. If it is absent, ovaries will automatically develop several weeks later.
Once the sexual differentiation of the gonads has occurred, a sequence of events takes place that will determine the sexual dimorphism of both the internal and the external reproductive organs, and therefore the sex of the individual. This is known as the organizational effect of the gonads. If the gonads have differentiated into testes, the testes will begin to secrete androgens, primarily testosterone, which have a masculinizing effect and cause the development of internal male structures such as the prostate, the vas deferens, and the epididymis. If there is an absence of androgens, the female uterus, fallopian tubes, and inner two-thirds of the vagina will develop instead. A genetic disorder called Turner syndrome illustrates how the absence of androgens results in the development of female structures. In this disorder, the individual has only one X chromosome, which prevents the development of functioning ovaries, and no Y chromosome, which precludes the secretion of androgens; in their absence, the individual’s other internal female sexual organs develop normally.
The external or visible genitalia develop in much the same way, governed by the presence or absence of androgens. The embryos of both sexes begin with undifferentiated genitals that are capable of becoming characteristically male or female, depending on androgen exposure. If there is androgen exposure, the primordial phallus will differentiate into the glans or head of the penis, the genital swelling will become the scrotum (into which the testes will eventually descend from the abdominal cavity), and the genital tubercle will differentiate into the shaft or main body of the penis. If there is no androgen exposure, then the primordial phallus will become the clitoris, the genital swelling will become the labia majora, and the genital tubercle will become the labia minora and the outer one-third of the vagina. Again, regardless of the genetic sex of the embryo, the absence of stimulation of primordial genital tissue by androgens will result in female structures. The presence of androgens is required for masculine development. In the example of Turner syndrome, the external genitalia are those of a normal female even though she lacks ovaries.
At birth, the infant has his or her primary sex characteristics: testes or ovaries and both internal and external sexual organs characteristic of males or females. It is not until puberty that an individual’s gonadal hormones begin to determine further development. Puberty begins with the secretion of hormones by the hypothalamus and the pituitary, located in the brain; the hormones travel via the bloodstream to the testes or ovaries, causing the production of the gonadal hormones that will direct the development of sexual maturation and the emergence of secondary sexual characteristics. The ovaries begin to produce estradiol, while the testes secrete testosterone. Estradiol causes enlargement of the breasts, growth in the lining of the uterus, widening of the hips, changes in the deposition of fat, and maturation of the female genitalia. Testosterone is responsible for growth of facial hair, deepening of the voice, masculine muscular development, and growth of the male genitalia.
Estradiol secretion in the female is also responsible for the onset of the first menstrual cycle. The cycle begins when an ovarian follicle is stimulated by hormones from the pituitary and thereby matures. It then secretes estradiol, which causes growth in the lining of the uterus in preparation for implantation of a fertilized ovum. It also causes ovulation, in which the follicle ruptures, releasing an ovum. During the second half of the cycle, the follicle itself becomes the corpus luteum, which produces both estradiol and progesterone. The latter hormone is responsible for maintaining the lining of the uterus during pregnancy. If the ovum is not fertilized, the production of both estradiol and progesterone decreases and the uterine lining is sloughed off in menstruation.
The influence of gonadal hormones has been studied in relation to the activation of sexual, maternal, and aggressive behaviors. The effects of gonadal hormones on behavior can be subdivided into organizational and activational influences, with the former occurring during prenatal development and the latter occurring after puberty.
Psychologists have studied the ways in which prenatal exposure or insensitivity to androgens organizes sexual behavior. In adrenogenital syndrome, the adrenal glands secrete unusually high levels of androgens, to which the developing embryo is exposed. If the embryo is male, normal development will occur. If the embryo is female, masculinization will occur, with enlargement of the clitoris and possibly fused labia. Researchers at the Johns Hopkins University studied thirty young women with adrenogenital syndrome to determine whether androgenization (exposure of the developing embryo to male sex hormones) affected their sexual orientation. The women described themselves as homosexual or bisexual at approximately four times the rate that occurs naturally in random populations of women. This hints that exposure of the developing female fetus to androgens may affect sexual orientation, possibly by altering the organization of the brain in ways that are not yet understood. A similar finding has occurred in primate research. When androgens were injected into monkeys pregnant with female fetuses, these androgenized infants became significantly different from their nonandrogenized peers in displaying more malelike behaviors, such as engaging in attempted mountings of other females.
Androgen insensitivity syndrome prevents male fetuses from being androgenized properly. These genetically male individuals will develop female genitalia and, if reared as females, will easily assume female sexual identities and overwhelmingly prefer male sexual partners. There is some possibility, then, that prenatal androgenization encourages a preference for female sexual partners, while lack of such exposure results in a preference for male sexual partners, regardless of genetic sex. It should be remembered, however, that this remains quite speculative, and conclusive research has not yet been conducted.
The activational effects of gonadal hormones on adult sexual behavior have also been of interest to psychologists. While estradiol and progesterone strongly influence the sexual behaviors of lower animals, these hormones do not seem to influence human female sexual behavior. For example, while both estrogen and progesterone levels fluctuate considerably over the menstrual cycle, women can become aroused at any time in the cycle and are not more easily aroused when these hormones are especially high or low. Further, when a woman’s ovaries are surgically removed or cease to produce hormones after menopause, sexual activity and interest are not affected.
There is some evidence that androgens, either present in small amounts secreted by the adrenal glands or ingested in the form of synthetic male hormones, will cause greater sexual desire in females and more frequent instigation of sexual activity but will have no effect on an already-established sexual orientation. The influence of androgens on male animals is direct: All male mammals respond to the presence of testosterone with increased sexual desire. Without testosterone, sperm production and copulatory ability cease.
Much aggressive behavior among animals takes place within the context of reproductive behavior. It comes as no surprise, then, that aggressive behaviors in both sexes are also strongly influenced by gonadal hormones, particularly androgens. Male offensive attacks and competitive behaviors, as well as interfemale aggressiveness and maternal aggression, are increased by exposure to androgens in most mammals.
One of the most stable behavioral differences between males and females is aggression; males display higher levels of aggression at all ages and in all forms. Because this sex difference has been observed in toddlers, before strong socialization influences have had their impact, it is speculated that prenatal exposure to androgens is partly responsible for these behavioral differences. This same relationship holds for all other mammalian species: the greater the prenatal androgenization, the more aggressive the subsequent behavior.
The relationship between aggressive behavior and testosterone levels has been studied in a variety of ways. One avenue of research has been to examine the testosterone levels of males who display different levels of aggressive behavior. For example, the testosterone levels of male prisoners with histories of violent crime have been compared with the frequency of their violent behavior while incarcerated. No relationship between the androgen levels and current aggressive expression has been found; however, androgen levels have been positively correlated with the frequency of these prisoners’ aggressive behaviors in adolescence. Perhaps by adulthood, learning had intervened to modulate this relationship, with some high-testosterone males able to exert control over their aggressive impulses while some men with lower testosterone levels have learned to vent their aggressiveness.
With regard to the effects of gonadal hormones on maternal behavior, the findings are clear in most lower animals. In laboratory rats, for example, sequences of progesterone followed by estradiol will facilitate nest-building behaviors. No such relationship, however, seems to hold for humans. It seems that maternal behavior is determined largely by learning and by an early bonding between mother and infant and that caretaking behaviors are not influenced by hormonal activation.
Research concerning the effects of gonadal hormones on behavior is one of the many avenues of investigation into the development of gender identity, an individual’s sense of being a man or a woman. There are many determinants of such identity: one’s genetic makeup, prenatal sex hormone exposure, one’s internal and external genitalia, the gender to which one is assigned at birth, and socialization—learning about culturally appropriate gender behaviors through interaction with parents and peers. Most often, these determinants are consistent with one another, and the individual develops a clear, stable sense of gender identity. When this is not the case, such inconsistencies may lead to an individual experiencing gender dysphoria.
Future research concerning gonadal hormones will continue in two major directions: the effects of gonadal hormones on the sexual differentiation of the brain and the interaction between sex hormones and adult sexual behaviors. Most research on sexual differentiation of the brain has been conducted with nonhuman species. For example, it has been found that testosterone “masculinizes” the brains of birds to produce typical male birdsong and produces male or female sexual behaviors in laboratory animals. The way in which this masculinization occurs is somewhat paradoxical: Inside the brain of the male embryo, testosterone is converted to estrogen, the hormone that actually produces the masculinization. In females, on the other hand, a protein exists in the neurons of the brain that prevents estrogen from effecting such masculinization.
In humans, it is known that the absence of prenatal androgen exposure sets the brain in a female pattern, which causes the pituitary to function in a cyclical manner, thus creating the menstrual cycle. Some interesting initial research with humans suggests that as a result of prenatal hormone exposure, there is greater lateralization of male brains than of female brains. Therefore, there is more specialization of the two cerebral hemispheres in males and more crossover of functions across the two hemispheres in females. This observation remains speculative and will be subject to considerable scrutiny.
Research interest will continue to be directed toward discovering the role of gonadal hormones in adult sexual behavior. More recent areas of study concern the question of prenatal hormonal determinants of sexual orientation. Studies will also continue to be focused on the question of sexual motivation in general to determine the levels and kinds of sex hormones that either enhance or depress sexual interest.
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