sex differentiation and determination Flashcards
chromosomal sex
XX= female XY= male
determined by sex determination: fertilization of ovum by sperm bearing a X or Y chromosome
point at which an individual develops as a male or female
gonadal sex
presence of ovaries (F) or testes (M)
germinal ridge
primordial gonad that is indifferent/bipotential–> aka it has the potential to develop into either an ovary OR testis
hormonal sex
sex of an individual determined by the concentration/ratio of androgens to estrogens
morphological sex
sex determined by body form
- accessory sex organs/internal structures
- external genitalia
- secondary sex characteristics
Mullerian duct system
develops into FEMALE accessory sex organs (fallopian tubes, vagina, cervix, uterus)
**development of Mullerian progresses w/o presence of local testosterone, and lack of MIH
Wolffian duct system
develops into MALE accessory sex organs (vas deferens, seminal vesicles, epididymis, prostate)
- *development of Wolffian dependent on LOCAL TESTOSTERONE (masculinization)
- *regression of Mullerian (F) dependent on MIH (defeminization)
male external genitalia development
- *blood borne testosterone, 5a reductase
- *testosterone–> DHT
- *DHT needed for male penile and scrotal development
female external genitalia development
**lack of androgens/absence of testosterone–> labia and clitoris
Turner syndrome
XO
- female external appearance
- limited ovarian development, gonads not fully developed
- do not produce steroid hormones
- hormone therapy needed to undergo puberty
- short, webbed neck
Klinefelter syndrome
XXY
- externally and internally masculinized
- SRY gene activation from the Y chromosome–> masculinization
- sterile b/c of decreased sperm production
- tall, long
- underdeveloped penis
- gynecomastia: boob growth
gynecomastia
boob growth seen in individuals with Klinefelter’s syndrome
Jacob’s syndrome
XYY
- male, may be sterile
- associated with increased aggressiveness
- taller, lesser intelligence
- elevated testosterone
congenital adrenal hyperplasia
XX
- enzyme deficiency: 21-hydroxylase
- continuous secretion of androgens–> early androgen exposure (blood borne–because there is no Y chromosome, there is no testis–> no local testosterone–> no Wolffian development; and with no MIH, Mullerian system develops normally)
Mullerian system develops normally
external genitalia: because of elevated blood borne androgen in the adrenal cortex–> genitalia will be AMBIGUOUS
21-hydroxylase role
cholesterol–> pregnenolone–> progesterone–> aldosterone and cortisol (mineral corticoid and glucocorticoid steroid hormones)
–progesterone–> ald. and cort. via 21-hydroxylase
cholesterol–> progesterone–> androgens
21-hydroxylase deficiency implications
if 21-hydroxylase isn’t working, there will be no negative feedback on CRH (corticotropin releasing hormone) and ACTH from the anterior pituitary–> increased levels of CRH and ACTH–> increased stimulation of the adrenal cortex (trying to produce glucocorticoids and mineral corticoids)–> increased synthesis of ANDROGENS–> masculinize and defeminize the fetus
androgen insensitivity syndrome= testicular feminization
- XY
- lack of androgen receptors (you have androgens, but there are not going to produce a biological effect)
- MIH: regression of the Mullerian system
- testosterone but no receptors: regression of Wolffian
- no internal structures
- b/c there are no androgen receptors–> feminized external genitalia
- female behavior
- infertile (often discover they have AIS because they do not have a period)
5-a reductase deficiency
- 5a reductase implicated in conversion of testosterone–> DHT (directly responsible for male external genitalia development)
- XY–> SRY gene–> testes–> testosterone–> Wolffian
- NORMALLY: testosterone–> DHT (penis and scrotum); but w/ deficient 5a reductase, genitalia are AMBIGUOUS
- MIH: regression of Mullerian system
- increased testosterone production during puberty–> masculinization
- can lead to hypospadias
hypospadias
urethral opening that is not at the tip of the penis
-seen during puberty in ind w 5a reductase deficiency
organization/activational hypothesis
in development (during a critical period), sex hormones “organize”/program the nervous system and structures needed for male and female behaviors
Organization: occurs early during a critical period in development, is permanent and irreversible
in adulthood, sex hormones activate/inhibit/modulate the function of neural circuits
Activation: occurs peri-pubertal or later, is short term and is reversible
early hormone environment during a critical period ORGANIZES the brain, hormones in adulthood ACTIVATE brain and behavior
(lordosis requires activation by estrogen and progesterone, mounting requires activation by testosterone)
Young experiment
Question: how are behavioral differences in hormonal responses between males and females mediated?
Hypothesis: Hormonal events early in development are responsible for the induction of male and female behavioral patterns
procedure:
- injection of testosterone propagate into pregnant guinea pigs during pregnancy
- adulthood: androgen exposed males and females (as well as control males and females) gonadectomized and injected with estrogen and progesterone
results
-females who had been treated with androgens had DECREASED LORDOSIS, INCREASED MOUNTING
(androgen exposure programmed male behaviors)
-males treated with androgens were not impacted (normal mounting, no lordosis)
conclusion: prenatal action of hormones in causing differentiation/organization of neural substances for behavior
feminization, masculinization
feminization: absence of exposure to gonadal steroids
masculinization: begins when testis produces androgens during a critical period
gonadal hormones increase in adulthood–> promotion of sex difference sin behavior by acting on a neural substrate that was organized during the CP
LH release in male and female rats
GnRH (hypo)–> LH (AP)
During ovulation, a surge of estrogen–> surge of GnRH–>surge of LH and FSH–> ovulation via positive feedback mechanisms
anosmic
cannot smell
