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BIOL 432 Final > Male and Female Reproduction > Flashcards

Male and Female Reproduction Flashcards

1
Q

What two types of cells are found in the testes?

A
  1. Leydig cells

2. Sertoli cells

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2
Q

What kind of cells are leydig cells and what do they secrete?

A
  • they are interstitial cells (major endocrine tissue)

- they secrete testosterone

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3
Q

Where are sertoli cells located and what are their functions?

A
  • part of seminiferous tubules
    1. spermatogenesis
    2. form blood-testis barrier
    3. secrete androgen-binding protein
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4
Q

What does androgen-binding protein do?

A

facilitates spermatogenesis

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5
Q

How is testosterone, estradiol and dihydrotestosterone synthesized (major pathway)?

A
  1. Cholesterol
  2. Pregnenolone
  3. 17 alpha-hydroxypregenolone by 17 alpha-hydroxylase
  4. dehydroepiandrosterone
  5. androstenediol
  6. testosterone
  7. a) estradiol by aromatase
  8. b) dihydrotestosterone by 5 alpha-reductase
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6
Q

How is testosterone synthesized (minor pathway)

A
  1. Cholesterol
  2. pregnenolone
  3. progesterone
  4. hydroxyprogesterone by 17 alpha-hydroxylase
  5. androstenedione
  6. testosterone
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7
Q

What is dihydrotestosterone?

A

a more potent androgen than testosterone

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8
Q

What is the pathway that makes estradiol without testosterone?

A
  1. cholesterol
  2. 17 alpha-hydroxypregnenolone
  3. dehydroepiandrosterone
  4. androstenedione
  5. estrone
  6. estradiol
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9
Q

What is the testosterone axis?

A
  1. gonadotropin releasing hormone (hypothalamus)
  2. luteinizing hormone (pituitary)
  3. testosterone (leydig cells in testes)
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10
Q

What are testosterone’s functions?

A
  • normal spermatogenesis
  • secondary sexual characteristics
  • anabolic effects on muscle, liver and kidney
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11
Q

What do testosterone levels in blood depend on?

A
  • steroidogenic abilities of individual Leydig cells
  • total number of Leydig cells per testes
  • luteinizing hormone levels
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12
Q

In the blood, what is testosterone bound to?

A
  • albumin (38%)

- or sex hormone binding globulin (60%)

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13
Q

Where is sex hormone binding globulin synthesized?

A

in the liver

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14
Q

What is testosterones action on target cells?

A
  • circulates bound
  • enters cell once free
  • is reduced to dihydrotestosterone by 5 alpha-reductase or aromatized to estradiol
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15
Q

What type of enzyme is aromatase?

A

it is a cytP450 type enzyme

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16
Q

How can aromatase be upregulated?

A

upregulated by EDC (endocrine disrupting chemicals)

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17
Q

What do testosterone and dihydroxytestosterone have in common?

A

they bind the same receptor

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18
Q

How are leydig cells involved in the Hyp-Pit-Testicular Axis?

A
  1. luteinizing hormone binds luteinizing hormone receptor
  2. adenylyl cyclase increased
  3. cAMP increased
  4. StAR increased
  5. testosterone syntheis and release stimulated
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19
Q

What gives feedback for the leydig cells involved in the Hyp-Pit-Testicular Axis?

A
  1. Negative feedback from estradiol and testosterone

2. positive feedback by activin to increase follicle stimulating hormone

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20
Q

How are the sertoli cells involved in the Hyp-Pit-Testicular Axis?

A
  1. Follicle stimulating hormone binds follicle stimulating hormone receptor
  2. adenylyl cyclase increased
  3. cAMP increased
  4. androgen-binding protein increased
  5. increase in concentration of intratubular testosterone
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21
Q

What gives feedback for the sertoli cells in the Hyp-Pit-Testicular axis?

A
  1. Negative feedback by testosterone, dihydroxytestosterone, estradiol, and inhibin to decrease follicle stimulating hormone
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22
Q

What receptor is used by luteinizing hormone and follicle stimulating hormone?

A

GPCR Galpha s

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23
Q

What family are inhibin and activin in?

A

TGF-beta (transforming growth factor) with mullerian inhibiting factor

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24
Q

What is inhibin’s function?

A

inhibits follicle stimulating hormone secretion from the pituitary

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25
Q

Where is inhibin produced?

A

produced by the sertoli cells (male) late granulosa (inhibin B) and corpus luteum (inhibin A) (female)

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26
Q

What is inhibin made up of?

A

heterodimers of alpha and beta subunit

27
Q

What is activin’s function?

A

activates follicle stimulating secretion and binding

28
Q

Where is activin produced?

A

produced by leydig cells (male) early granulosa cells or late corpus luteum (female)

29
Q

What is activin made up of?

A

hetero and homodimers of beta subunits

30
Q

What is the function of follistatin?

A

binds activin, decreases bioavailability, and decrease follicle stimulating hormone synthesis

31
Q

What two types of cells are present in the ovaries?

A
  1. Granulosa cells

2. Theca cells

32
Q

What is produced in the granulosa cells?

A
  1. estradiol (has aromatase)
  2. activin
  3. granulosa-lutein (in luteal phase)
  4. progesterone
  5. inhibin
33
Q

What is not produced in the granulosa cells and why?

A
  • androgens are not produced here because there is no 17 alpha-hydroxylase
  • also lacks luteinizing hormone receptor
34
Q

What is produced in the theca cells?

A

androstenedione (has 17 alpha-hydroxylase)

35
Q

What is not produced in the theca cells and why?

A
  • estradiol is not made here because theca cells lack aromatase
  • there are also no follicle stimulating hormone receptors
36
Q

What does estrogen do to the body?

A

produces secondary sex characteristics, stimulates the uterus and ovary size and development

37
Q

What acts to synthesize in granulosa cells and in theca cells?

A
  • granulosa cells: follicle stimulating hormone

- theca cells: luteinizing hormone

38
Q

What is SF-1?

A
  • steroidogenic factor 1
39
Q

What is StAR?

A
  • steroidogenic acute regulatory protein
40
Q

What changes in the corpus luteum part of the two cell hypothesis?

A
  • luteinizing hormone now acts to synthesis progesterone in the granulosa cells
41
Q

What are the three phases in the menstrual cycle regulation?

A
  1. Follicular phase
  2. Luteal phase
  3. Cessation
42
Q

What stimulates expression of follicle stimulating hormone and luteinizing hormone?

A
  • hypothalamic release of gonadtropin releasing hormone
43
Q

What does estradiol do to the brain?

A

increases the sensitivity of the the pituitary to gonadtropin releasing hormone

44
Q

What happens with gonadotropin releasing hormone in the follicular phase?

A
  • initially a slow pulse frequency

- stimulates follicle stimulating hormone (favoured if increase in activin) and luteinizin hormone

45
Q

What happens with follicle stimulating hormone in the follicular phase?

A
  • increase in estradiol from granulosa cells

-

46
Q

What does the increase in estradiol from follicle stimulating hormone in the follicular phase cause?

A
  • provides negative feedback to the hypothalamus and pituitary
  • initially decrease in amount of gonadotropin releasing hormone
  • later results in increased gonadotropin releasing hormone pulse frequency
  • decrease follicle stimulating hormone relative to luteinizing hormone
47
Q

What happens with insulin-like growth factors during the follicular phase?

A

enhance response to follicle stimulating hormone

48
Q

What happens with luteinizing hormone during the follicular phase?

A
  • increase in estradiol
  • increase sensitivity of pituitary to gonadotropin releasing hormone
  • increase in luteinizing hormone
  • ovulation
49
Q

What happens during the luteal phase?

A
  • increase in progesterone (negative feedback on gonadotropin releasing hormone
  • increase inhibin A (decreases follicle stimulating hormone)
  • later, higher luteinizing levels (relative)which increases activin and increases follicle stimulating hormone to restart cycle
50
Q

What happens during cessation (no implant)?

A
  • luteolysis

- decrease in estradiol, progesterone, and inhibin (luteinizing hormone receptor down regulation in folicular cells)

51
Q

What causes menstruation during cessation?

A

prostaglandins cause vasoconstriction and relaxation resulting in menstruation

52
Q

What is the cycle driven by?

A
  • alterations in gonadotropin releasing hormone pulsation which favor the production of different gonadotropins
53
Q

What does follicular development result in?

A
  • estradiol production

- then causes positive feedback to produce luteinizing hormone surge

54
Q

After ovulation, what does the corpus luteum produce?

A
  • produces progesterone

- causes slowing of gonadtropin releasing hormone pulse and decrease in luteinizing hormone

55
Q

What is essential for the maintenance of the menstrual cycle?

A
  • the characteristic periodic secretion of gonadotropin releasing hormone from the hypothalamus at an average rate of one pulse an hour
56
Q

What causes the pulses of gonadotropin releasing hormone?

A
  • oscillations in the electrical activity of the gonadotropin releasing hormone pulse generator
57
Q

What influences the gonadotropin releasing hormone pulse generator?

A
  • assortment of interactions of multiple neural, hormonal and environmental inputs to the hypothalamus
  • conditions like stress, light changes, exercises and sleep
  • specific metabolic signals meant for energy homeostasis
58
Q

What is tightly regulated for maintenance of reproductive cycles as well as an intrinsic property of gonadotropin releasing hormone cells?

A
  • pulsatile gonadotropin releasing hormone release
59
Q

What do gonadotropin releasing hormone neurons exhibit?

A

spontaneous action potentials that are associated with Ca2+ oscillations and hormone secretion

60
Q

What appears to stimulate gonadotropin releasing hormone release and how?

A
  • increased cAMP levels in neurons by activation of cAMP-gated cation channels (cyclic nucleotide-gated ion channels)
61
Q

What does the activation of cyclic nucleotide-gated ion channels correlate with?

A
  • increased neuronal excitability and calcium oscillations
62
Q

How are these cAMP levels potentially decreased?

A
  • potential negative feedback pathways by inhibiting adenylyl cyclase V and activating a phosphodiesterase
63
Q

Why must gonadotropin-releasing hormone be pulsatile?

A
  • if not pulsatile then luteinizin hormone ad follicle stimulating hormone becomes desensitized

BIOL 432 Final (14 decks)

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