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Behavioral Endocrinology > sex differentiation and determination > Flashcards

sex differentiation and determination Flashcards

1
Q

chromosomal sex

A 
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

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2
Q

gonadal sex

A

presence of ovaries (F) or testes (M)

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3
Q

germinal ridge

A

primordial gonad that is indifferent/bipotential–> aka it has the potential to develop into either an ovary OR testis

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4
Q

hormonal sex

A

sex of an individual determined by the concentration/ratio of androgens to estrogens

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5
Q

morphological sex

A

sex determined by body form

  • accessory sex organs/internal structures
  • external genitalia
  • secondary sex characteristics
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6
Q

Mullerian duct system

A

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

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7
Q

Wolffian duct system

A

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)
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8
Q

male external genitalia development

A
  • *blood borne testosterone, 5a reductase
  • *testosterone–> DHT
  • *DHT needed for male penile and scrotal development
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9
Q

female external genitalia development

A

**lack of androgens/absence of testosterone–> labia and clitoris

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10
Q

Turner syndrome

A

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
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11
Q

Klinefelter syndrome

A

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
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12
Q

gynecomastia

A

boob growth seen in individuals with Klinefelter’s syndrome

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13
Q

Jacob’s syndrome

A

XYY

  • male, may be sterile
  • associated with increased aggressiveness
  • taller, lesser intelligence
  • elevated testosterone
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14
Q

congenital adrenal hyperplasia

A

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

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15
Q

21-hydroxylase role

A

cholesterol–> pregnenolone–> progesterone–> aldosterone and cortisol (mineral corticoid and glucocorticoid steroid hormones)

–progesterone–> ald. and cort. via 21-hydroxylase

cholesterol–> progesterone–> androgens

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16
Q

21-hydroxylase deficiency implications

A

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

17
Q

androgen insensitivity syndrome= testicular feminization

A
  • 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)
18
Q

5-a reductase deficiency

A
  • 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
19
Q

hypospadias

A

urethral opening that is not at the tip of the penis

-seen during puberty in ind w 5a reductase deficiency

20
Q

organization/activational hypothesis

A

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)

21
Q

Young experiment

A

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

22
Q

feminization, masculinization

A

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

23
Q

LH release in male and female rats

A

GnRH (hypo)–> LH (AP)
During ovulation, a surge of estrogen–> surge of GnRH–>surge of LH and FSH–> ovulation via positive feedback mechanisms

24
Q

anosmic

A

cannot smell

25
Q

uterine position and early androgen exposure effects

A

exposure to androgen secreted by male littermate MASCULINIZES and DEFEMINIZES female pups

0M and 2M have the same reproductive capacity BUT…

  1. intrafemale aggression: 2M>0M
  2. time males spend with females: 0M>2M
  3. length of ovarian cycle: 2M>0M
  4. ease of inhibition of cycle by other females: 0M>2M
26
Q

estradiol and aromatization

A

testosterone–> estradiol via aromatase

-masculinizing effects of testosterone exerted through the brain by conversion by aromatase into enzymes

27
Q

a-fetoprotein

A

binds to estradiol so that it cannot enter the brain and exert masculinizing effects

28
Q

DNMT

A

testosterone removes ___–> removal of a methyl group–> gene transcription–> masculine behaviors in adulthood

lack of testosterone–> methylated proteins (DNMT NOT REMOVED)–> silencing of gene transcription

29
Q

DNA methylation

A

epigenetic mechanism of gene regulation whereby methyl groups are added to DNA to decrease gene transcription

if females are given DNMT inhibitors… NO METHYL–> gene transcription allowed–> masculinized behavior in adulthood

conclusion: masculinization requires DEmethylation, feminization requires METHYLation

30
Q

sexually dimorphic nucleus of POA

A

males: SNN-POA much larger b/c testosterone/estradiol protects neurons from apoptosis

females treated prenatally w/ androgens have a much larger SDN-POA

males castrated prenatally/during CP–> F-sized SDN-POA

Behavioral Endocrinology (12 decks)

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