Sexual Differentiation in Mammals
Role of Sex
sex (XX or XY) is determined by the type of sperm (X-bearing or Y-bearing) that
fertilizes the egg.
gonads have potential to be either ovaries and testes for ~6 weeks
region of the Y chromosome (SRY) is a gene producing a protein which causes the
middle of the neuter gonads to become testes.
testes develop, they begin to produce androgens like testosterone.
this gene is not present, the outside of the neuter gonads turn into ovaries.
of SRY gene from Yà XY mouse develops as a
SRY gene to X à XX mouse develops as a male
§After Gonad Development, the
remainder of sexual development depends on hormone environment.
§Normal sources of sex
l Testes and ovaries
l Adrenal cortex
Effects of Hormones
all begin with ducts, genitals and brains which can go either way (male or
of male ducts, genitals, & brain depends on action of androgens
(testosterone & dihydrotestosterone (DHT)).
differentiation requires no hormones.
fact, in males, development of female ducts must be actively inhibited by
release of another hormone: Mullerian
inhibiting hormone (MIH), usually in 2nd & 3rd month of
of gonads, genitals, ducts, and brain occurs at different (but overlapping)
time periods during gestation.
newly formed testes begin producing androgens about week 7-8 beginning the
masculinization of genitals but penis may not be visibly distinct until 3rd or
4th month & not complete until ~5th month.
also have defeminizing and masculizing effects on developing brain.
Exposure to androgens “program” the hypothalamus for the fairly constant sex
hormone secretions seen in males vs the cyclic hormone secretion of females
is some evidence that masculinization of brain occurs later than
masculinization of body.
Nucleus (SDN) of Preoptic Region of Hypothalamus
Differences in the Brain
- part of medial preoptic hypothalamus shows testosterone-related size
differences; ventromedial hypothalamus
important in females
dimorphic nucleus” is larger in males
and testosterone-treated females and smaller in females and castrated
LeVay- 3rd interstitial nucleus of the anterior hypothalamus (INAH3) in humans
is larger in heterosexual males and smaller in females and gay males
other regions show sex differences – e.g. females have more neurons in
Wernicke’s area and more axons in corpus callosum
Another of Mother
rats testosterone entering the brain is turned into estradiol by the process of
“aromatization” and estradiol, in turn, triggers the “masculinization” of the
brain (e.g. SDN and medial preoptic hypothalamus).
estrogens present during pregnancy do not masculinize the brain because they
bind to alpha-fetoprotein and can’t get past the BBB.
if excess estrogens are present, some do get into brain and do bias behavior in
a male direction.
perinatal testosterone in males or testosterone treatment of females has
induced same sex preferences and changes in sex-typical patterns of sexual
behavior in a wide range in species (rats, hamsters, ferrets, pigs, finches,
dogs, sheep etc.).
is correlational data from both men and women suggesting that early hormone
environment may also affect sexual orientation in humans.
Other Evidence for
a Biological Basis of Sex Orientation
l identical twins - 52% of
l fraternal twins - 22% of
l adopted brothers - 11% of
l Identical twins - 48%
l fraternal twins - 16%
l adopted sisters - 6%
baby whose body can’t respond to androgens due to lack of androgen receptors:
“androgen-insensitivity” - baby has female genitalia, feels female
baby exposed to more androgens than usual - body & brain masculinized;
“androgenization of females”, e.g. congenital adrenal hyperplasia or
of DHT – female genitalia until puberty, then penis & scrotum develops.
Assumes male identity despite 10+ years of “female experience”
also may be due to unusual prenatal hormone exposure (decreased masculinization
of brain), as may cases of gender identity disorder
that 1 out of 100 has some degree of genital ambiguity.
Case of John/Joan – unsuccessful rearing as female
deficiency – despite years as a female, easy switch to male identity at puberty.
both cases brain would be masculinized by early testosterone.
in life hormones have an organizational
effect on body and brain.
amount and timing of hormones will have a life-long effect on physiology and
in hormones during critical sensitive periods of prenatal development are the
likely cause of variations in sex preference.
Puberty and Beyond
puberty both males & females need hormones to develop secondary sexual
that point on, hormones have an activational rather than organizational effect,
influencing sexual motivation rather than sex preference.
drive in females seems more closely related to androstendione than to estrogen-
ovariectomy does not decrease drive
of the feedback mechanisms (body-> brain), taking hormone supplements
commonly leads to decreased production of natural hormones.
testosterone like drugs (anabolic steroids) can cause atrophy of testes and
breast development due to conversion to estrogen