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ANAT322 > Dr. Bernard Reproductive system > Flashcards

Dr. Bernard Reproductive system Flashcards

1
Q

where are LH and FSH neurons secreting?

A

in median eminence in hypothalamus

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2
Q

what direct estradiol’s effect?

A

its interaction and affinity with receptors, not its circulating level

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3
Q

what happens during each phase of menstrual cycle?

A

Follicular phase: follicles grow
ovulation: egg release triggered by LH
luteal phase: corpus luteum grows and is maintained
menstruations: corpus luteum degenerates

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4
Q

what hormone is only present during pregnancy? what does it trigger?

A

HCG; thickens uterine, stimulates testosterone production

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5
Q

what is caused by a lack of GnRH?

A

no puberty, infertility

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6
Q

how long is GnRH precursor? how many cleavages for activation?

A

92 amino acids; 2 cleavages

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7
Q

where are GnRH cells located and where do they project? what’s a special feature?

A

in SON and MBH mediobasal hypothalamus;
project to median eminence;
dendron

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8
Q

what is HH and what causes it?

A

hypogonadotropic hypogonadism, cause by a 1 bp insertion in GnRH1 gene that keeps from producing GnRH

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9
Q

is HH dominant or recessive?

A

it is an autosomal recessive condition

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10
Q

what happens to hypogonadal mice reproductive organs?

A

super small

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11
Q

where and how is GnRH released?

A

in pulses in median eminence

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12
Q

what is kallman’s syndrome?

A

GnRH neurons fail to migrate in the brain (GnRH deficiency)

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13
Q

how are GnRH/LH pulses throughout the menstrual cycle?

A

follicular phase: more but smaller pulses
luteal phase: less but bigger pulses

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14
Q

where is the pulse generator?

A

in MBH mediobasal hypothalamus and arcuate nucleus

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15
Q

what happens to gonadotropins when arcuate nucleus is lesioned

A

no more LH or FSH secretion

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16
Q

what happens when GnRH is continuously secreted?

A

it downregulates LH and FSH

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17
Q

what are the KNDy neurons?

A

kisspeptin, dynorphin, and neurokinin neurons in the arcuate nucleus exhibiting pulsatile activity

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18
Q

what are dynorphin and neurokinin’s role?

A

dynorphin inhibits kisspeptin release, neurokinin stimulates kisspeptin release

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19
Q

what is GPR54 and where is it found?

A

kisspeptin (kiss1) g-protein-coupled receptor on hypothalamic GnRH neurons, in pituitary, placenta, pancreas, spinal cord

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20
Q

what happens to GPR54 KO mice?

A

inhibited kisspeptin secretion -> inhibited GnRH secretion but not production -> super small ovaries, no gonadotropins release

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21
Q

what are the 3 forms of kisspeptin?
where are they expressed?

A

kisspeptin-10, -13, -14;
placenta, testis, small intestine, brain (Arc)

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22
Q

what does kisspeptin do?

A

stimulates LH release in women

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23
Q

how does estradiol do negative feedback?

A

inhibits GPR54/kiss1 expression in GnRH arcuate nucleus neurons and inhibits KNDy neurons pulsatile activity (inhibits kisspeptin production and secretion)

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24
Q

what happens to ERalphaKO mice?

A

knocked out estradiol receptor suppresses the estradiol negative feedback = too much estradiol = infertility

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25
Q

what cells express ERalpha?

A

kisspeptin neurons

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26
Q

can you cancel the effect of ERalphaKO by giving estradiol?

A

no because the estradiol receptors still don’t work

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27
Q

what is the same between ovariectomized and ERalphaKO mice?

A

increased KNDy pulsatile activity leading to infertility. due to lack of estrogen feedback

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28
Q

how does estradiol positive feedback work?

A

estradiol activates AVPV ERalpha receptor -> stimulates kiss1 expression in AVPV anteroventral periventricular nucleus and in rostral periventricular area of 3rd ventricle -> stimulates POA GnRH neurons

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29
Q

How can estrogen stimulate Kiss1 in the AVPV/RP3V while at the same time inhibiting Kiss1 in the ARC?

A

ERalpha must bind to DNA to stimulate kiss1 in AVPV.
ERalpha inhibition on kiss1 in Arc is DNA-independent.
the promoters/enhancers are also different

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30
Q

what drive the GnRH/LH surge?

A

the stimulatory input from AVPV/RP3V kisspeptin neurons

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31
Q

the amplitude of LH and FSH release is mediated by what?

A

by the pituitary

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32
Q

in addition to the hypothalamus, estrogen has a negative and positive feedback effect where else? (on gonadotropins)

A

on pituitary

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33
Q

what effect does elevated estrogen levels have on the pituitary?

A

increases pituitary sensitivity to GnRH

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34
Q

what hormone acts the most to slow down LH pulses and regulates (amplifies) LH surge amplitude?

A

progesterone

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35
Q

what differs between LH and FSH?

A

the beta subunit

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36
Q

what is LH’s half life? what cells does it target? what phenomenons does it regulate?

A

20 min
theca/mural granulosa and Leydig cells.
regulates ovulation and androgens synthesis

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37
Q

what is FSH’s half life? what cells does it target? what phenomenons does it regulate?

A

3-4 hours
ovary granulosa and testis sertoli cells
regulates follicle development, estrogen synthesis, spermatogenesis

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38
Q

at what menstrual cycle stage are LH and FSH levels respectively higher?

A

FSH high during early follicular phase, both LH and FSH peak at ovulation

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39
Q

what cells produce LH and FSH? what stimulates those cells to secrete?

A

gonadotropes
GnRH

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40
Q

what does continuous GnRH secretion cause?

A

down-regulation of gonadotropin (LH, FSH) secretion

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41
Q

what pulse frequency favors each gonadotropin?

A

high GnRH pulse frequency favors LHbeta.
low GnRH pulse frequency favors FSHbeta.

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42
Q

what decodes the GnRH pulses?

A

gonadotropes (GnRH pulse frequency decodor)

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43
Q

so which gonadotropin is more sensitive to GnRH?

A

FSH

44
Q

however, does GnRH pulse frequency mediate gonadotropins release through the cycle? how do we know?

A

no, pulse frequency doesn’t change during the follicular phase. It slows down during luteal phase only due to high estrogen negative feedback

45
Q

when is each inhibin made during menstrual cycle?

A

Inhibin B is mainly secreted during follicular phase
Inhibin A is mainly secreted during luteal phase

46
Q

where is each inhibin produced?

A

Inhibin B is a product from proliferating granulosa cells of growing follicles.
Inhibin A is a product of corpus luteum.

47
Q

what is inhibin’s role?

A

inhibits only FSH secretion

48
Q

what are inhibins and activins?

A

structurally related TGFbeta ligands with opposing effects on FSH

49
Q

what are inhibin’s structure?

A

same alpha subunit + betaA or betaB subunit

50
Q

what are activin’s structure?

A

combination of betaA and/or betaB subunits

51
Q

how and where do activins work?

A

activins work on the pituitary to stimulate only FSH production

52
Q

what’s different about inhibins in primates vs rodents?

A

in primates, corpus luteum makes inhibin A.
In rodents, preovulatory follicles make inhibin A

53
Q

in rodents, what do the LH/FSH surges during proestrus do?

A

suppress ovarian inhibin A and B synthesis

54
Q

what happens when you knock out even just type 2 activin receptor? what consequence does that have

A

can’t make FSG -> can’t make estrogen -> no estrogen feedback -> increase in LH

55
Q

why are ovaries small in animals who can’t make FSH?

A

no FSH = no estrogen stimulation of endometrial cells in uterus

56
Q

what is inhibin’s effect on activin? how does it affect activin receptor?

A

inhibins act as endogenous competitive receptor antagonist (alpha subunit binds to betaglycan co-receptor to block activin type 2 receptor)

57
Q

what happens to inhibin A and B effect in mice that lack betaglycan and TGFBR3L co-receptor?

A

no more suppression of FSHbeta from inhibins

58
Q

what do betaglycan and TGFBR3L bind to respectively?

A

betaglycan: inhibin A and B
TGFBR3L: inhibin B only

59
Q

how are each inhibin’s level through menstrual cycle?

A

inhibin A increases during luteal phase.
inhibin B increases during follicular phase (cus follicles increase)

60
Q

basically what 2 phenomenons stimulate FSH production right at the beginning of the follicular phase?

A
  1. loss of estrogen negative feedback on GnRH increases GnRH
  2. loss of inhibin A negative feedback increases activin
61
Q

what does the increase of FSH at the beginning in follicular phase cause related to inhibins?

A

increase in inhibin B levels

62
Q

why is there an FSH decrease during follicular phase? what does it cause?

A

because some follicles don’t have enough FSH to grow due to estrogen neg feedback -> causes a decrease in inhibin B

63
Q

what cells have FSH receptors?

A

granulosa cells

64
Q

what is recruitment? what controls it?

A

follicle growth: oocytes get bigger and pre-granulosa cells differentiate into granulosa cells.
don’t know what triggers!

65
Q

when do follicle start responding to FSH?

A

when antrum (fluid-filled space) forms and granulosa cells start expressing FSHR

66
Q

more specifically how does FSH work?

A

activates PKS -> triggers granulosa cell proliferation and differentiation, aromatase production, and LH receptor production

67
Q

what are LH’s main effects?

A

androgen synthesis by theca cells,
support of dominant follicles,
ovulation

68
Q

where is the LH receptor expressed?

A

in theca cells and mural granulosa cells of mature follicles

69
Q

how is LH secretion during follicular phase?

A

constant pulses

70
Q

on what cells does the LH surge act on? what does it trigger?

A

mural granulosa cells -> secrete epidermal growth factor EGF to cumulus cells -> myotic maturation

71
Q

what is the main androgen made by theca cells?

A

androstenedione

72
Q

how are androgens made?

A

communication of enzymes between theca and granulosa cells. needs both LH and FSH

73
Q

what does the corpus luteum respond to? what does it secrete?

A

responds to LH, produces progesterone, estradiol, inhibin A

74
Q

what happens to corpus luteum during pregnancy?

A

HCG acts through LHR to maintain corpus luteum when LH can’t anymore

75
Q

what is LH and FSH’s effect in males

A

they both drive spermatogenesis.
only LH drives testosterone production

76
Q

what inhibin do males have?

A

only inhibin B

77
Q

where do steroidogenesis and spermatogenesis take place?

A

testis sertoli cells

78
Q

what drives testosterone pulses?

A

LH pulses (driven by GnRH pulses)

79
Q

what is the difference between testosterone and estrogen release?

A

testosterone is released in pulses, not estrogen

80
Q

what brain region works as the pulse generator?

A

arcuate

81
Q

what is affected in GnRH in Gpr54/kiss1 KO mice?

A

GnRH secretion! not it’s production

82
Q

what is the effect of castration?

A

loss of T neg feedback = increased KNDy neurons activity, increased kiss1 expression in Arc

83
Q

what is testosterone? what does it become

A

a prohormone.
5alpha-reductase transforms it into dihydrotestosterone DHT
aromatase transforms it into estradiol

84
Q

what is DHT? what does it do?

A

an androgen.
downregulates kiss1 (less efficient than estradiol tho)
Gets converted to estrogen by aromatase.

85
Q

where does inhibin B come from in males?

A

testis

86
Q

where do inhibins work?

A

directly on pituitary

87
Q

what happens to male LHbeta KO mice?

A

decreased testis weight
no mature sperm
decrease plasma and testicular T
infertility

88
Q

what happens to male FSHbeta KO mice?

A

decreases testis weight
decreased sperm count (but they still have some, compared to LHbeta KO)
normal T level
fertile

89
Q

what happens to people with LHbeta inactivation mutation?

A

low T, high FSH, undetectable LH.
caused by missense mutation blocking dimer assembly.
FSH can be stimulated by GnRH, not LH

90
Q

how did we treat patient with LHbeta inactivation mutation?

A

intramuscular T: still small testis and no sperm
then, HCG treatment: increased testis volume and now made sperm

91
Q

what happens to a patient with inactivating FSHbeta mutation?

A

infertile, normal T level, small testis, can’t make sperm (mice can make sperm without FSH, humans can’t).
caused by nonsense mutation preventing dimeric FSH production.

92
Q

what is LH and FSH effect in males?

A

LH -> leydig cells -> testosterone production
FSH -> sertoli cells -> inhibin B and androgen binding protein ABP production

93
Q

what are leydig and sertoli cell’s equivalent in females

A

leydig = theca cells
sertoli = granulosa cells

94
Q

signalling cascade triggered by LH

A

LHR -> cAMP -> PKA phosphorylates StAR -> StAR brings cholesterol in mitochondria -> testosterone release

95
Q

what is androgen binding protein ABP?

A

binds T to increase it’s concentration in testis
(necessary for spermatogenesis)

96
Q

can testosterone be stored in cells?

A

no

97
Q

where are sertoli cells?

A

seminiferous tubule

98
Q

is T necessary for spermatogenesis and spermiation?

A

no

99
Q

what happens to sertoli cell androgen receptor knockout mice?

A

slightly smaller testis,
spermatocytes can’t mature to spermatids

100
Q

what is one thing that dictates how much sperm can be made?

A

amount of sertoli cells

101
Q

do males have estradiol positive feedback?

A

no. males loose the AVPV/RP3V kiss1 expressing cells. estradiol only inhibits LH in males.

102
Q

how is the brain feminized/masculanized?

A

increase of T production around birth defeminizes male brains

103
Q

how can you reverse masculinization of the brain?

A

neonatal castration reverses kiss1 expression in AVPV/RP3V

104
Q

how can you reverse feminization of the brain?

A

neonatal estrogen exposure reverses kiss1 expression in AVPV/RP3V

105
Q

what does the high aromatase level in the placenta do?

A

converts systemic androgens into estrogen

106
Q

what is the protein that protects female from defeminizing effects of estrogen?

A

alpha-fetoprotein. Necessary for LH surges

107
Q

what drives the positive estrogen feedback in primates?

A

the pituitary. more than AVPV/RP3V kisspeptin expression (that’s more in rodents)

ANAT322 (10 decks)

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