In humans, having only one sex chromosome—a single X—results in a condition called Turner’s
syndrome . These individuals appear to be female , in keeping with the fact that in the absence of
gonadal secretions the body will develop in a feminine pattern. Individuals with Turner’s syndrome have
recognizable ovaries , which is what would be expected in the absence of Sry protein .
Human females may be exposed to early androgens as a consequence of overproduction of androgens by
the adrenals ; this condition is known as congenital adrenal hyperplasia . CAH women have
been exposed to levels of androgens intermediate between those of females and males and
often have intersexual genitalia. Such people have normal ovaries , and the müllerian system is fully
developed. CAHaffected individuals are sometimes described as tomboys; most report heterosexual
orientation as adults.
In androgen insensitivity syndrome, a defect in the sole copy of a male’s androgen receptor gene,
causes the body to be completely unresponsive to androgens. The gene for the androgen receptor is carried
on the X chromosome. Wolffian ducts fail to sense testosterone and thus regress▯ external genital
tissue form labia and clitoris. Shallow vagina, lack of ovaries or uterus. Look like women. Normal testes.
Androgeninsensitive XY individuals develop testes due to the presence of Sry protein , and
consequently they also secrete AMH , which causes the müllerian derived feminine structures to
regress. However, since their tissues are insensitive to androgen, the wolffian system also regresses. Due
to the insensitivity of the genital skin to androgens, the external genitalia develop into a clitoris and labia, but
the vagina is shallow .
Androgeninsensitive XY individuals look and behave like normal women. They are usually attracted to and
marry men, and even after they learn of the disorder they still categorize themselves as women. They may
therefore be characterized as male with respect to their genes, female with respect to their brains, male
in their gonads, and female with respect to their genitals. This illustrates the problems inherent in selecting
criteria for classifying people as male or female.
Exposing female rat pups to testosterone during a period that spans from before birth to ten days
following birth greatly reduces their lordosis responsiveness as adults. Conversely, male rats that were
castrated during the first week of life readily display lordosis behavior when treated with ovarian
hormones in adulthood.
An ovariectomized adult female guinea pig given the proper regime of ovarian steroids will display normal
lordosis (sexual reflex) in response to mounting by a male. This is an example of an activational effect
of steroids; such effects are generally transient . Castrated adult males given the same treatment will
not display the same behavior.
In order for a male rat to display mounting behavior in adulthood, he must be exposed to testosterone during
the perinatal period and then have circulating levels of androgens in adulthood (either from the testes or
by injection). A female treated with testosterone in adulthood may display some mounting behavior. If she receives such treatments before and after birth and again in adulthood, she can show the entire pattern
of male copulatory behavior, including mounting, intromissions, and ejaculation .
In experiments on the role of aromatization in the copulatory behavior of male rats, male rat pups were
castrated at birth and given the androgen dihydrotestosterone (DHT), a potent metabolite of
testosterone that has virilizing effects on the genitalia. DHT cannot be aromatized to estradiol. When
the treated animals reached adulthood, they had male genitalia but failed to achieve intromissions even
when treated with testosterone.
However, males castrated at birth and given early estrogen treatments, followed by testosterone
treatments in adulthood, showed normal male copulatory behavior despite having sma