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231 > Lecture 30: Hormone control of male and female reproduction > Flashcards

Lecture 30: Hormone control of male and female reproduction Flashcards

1
Q

Describe the hormone control of reproduction

A

GnRH from the hypothalamus causes the release of FSH and LH from the anterior pituitary gland

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2
Q

What is the target organ for LH and FSH?

A

the gonads

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3
Q

LH and FSH act together to affect what two processes?

A

gametogenesis

steroidogenesis

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4
Q

What is gametogenesis (specific to males and females)?

A

sperm production in the testes and ova development in the ovary

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5
Q

What is steroidgenesis?

A

hormone production

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6
Q

What are the two male hormones produced?

A

testosterone and inhibin

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7
Q

What are the three female hormones produced?

A

estrogen, progesterone and inhibin

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8
Q

What does HPG stand for?

A

hypothalamo-pituitary-gonadal

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9
Q

Describe the HPG axis

A

There are GnRH neurons in the hypothalamus which project to the ME where they terminate. Here they release GnRH which stimulates the release of LH/FSH from the anterior pituitary gland. These act on the gonads and cause them to release estrogen, progesterone and testosterone

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10
Q

Do the hormones released from the gonads cause positive or negative feedback to the hypothalamus?

A

it depends

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11
Q

In what way is GnRH released?

A

in a pulsatile way

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12
Q

Inside the scrotum, there is what two things?

A

the seminiferous tubules and the interstitium

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13
Q

What percentage of the scrotum is made up of seminiferous tubules?

A

80%

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14
Q

What percent of the scrotum is made up of the interstitium?

A

20%

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15
Q

What is in the interstitium?

A

Leydig cells

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16
Q

What is the main role of the Leydig cells?

A

to produce testosterone

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17
Q

What is the main role of the seminiferous tubules?

A

to produce sperm

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18
Q

What the support/nursing cell in the seminiferous tubules?

A

the Sertoli cells

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19
Q

The sperm are produced in the seminiferous tubules and stored where?

A

in the epididymis

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20
Q

Describe the process of sperm production

A

There is a precursor (spermatogonium) which differentiates and matured into a spermatocyte, spermatid and spermatozoa

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21
Q

In the hormonal control of male reproduction, which hormone is released from the hypothalamus?

A

GnRH

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22
Q

In the hormonal control of male reproduction, GnRH is released from the hypothalamus and stimulates the release of what from the anterior pituitary gland?

A

LH and FSH

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23
Q

In the hormonal control of male reproduction, what does FSH do?

A

this acts on the Sertoli cells to stimulate the release of inhibin and to stimulate spermatogenesis

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24
Q

In the hormonal control of male reproduction, what does LH do? What is the effect of this?

A

this acts on the Leydig cells and causes them to release testosterone which acts locally on the sertoli cells and enters the blood

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25
Q

What is the effect of inhibin?

A

this acts in a short negative feedback loop to stop the release of FSH from the anterior pituitary gland

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26
Q

What is the effect of testosterone?

  • it locally affects the ____________ cells
  • it is causes a response to testosterone from the ___________ ____________ and other ___________
  • it acts in both a ___________ negative feedback loop to to the release of ___________ from the anterior pituitary gland, and a long negative feedback loop to stop the release of _____________ from the ______________
A
  • it locally affects the Sertoli cells
  • it is causes a response to testosterone from the reproductive tract and other organs
  • it acts in both a short negative feedback loop to to the release of LH from the anterior pituitary gland, and a long negative feedback loop to stop the release of GnRH from the hypothalamus
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27
Q

Describe how LH affects the Leydig cells

A

LH binds to the LH receptor on the Leydig cells and activates a G-protein. There is activation of cAMP which activates PKA and this causes new proteins to be synthesised. This produces new enzymes to be formed that can convert cholesterol to testosterone (in the Leydig cells)

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28
Q

Where does the testosterone produced in the Leydig cells go?

A

it can to the the seminiferous tubules to the Sertoli cells

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29
Q

Describe how FSH affects the Sertoli cells

A

FSH binds to the FSH receptor on the Sertoli cells which activates a G-protein. There is activation of cAMP which activates PKA and this causes new proteins to be synthesised. This produces things like inhibins, ABPs, growth factors and aromatase

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30
Q

What is important about aromatase that is produced by Sertoli cells?

A

They convert the testosterone from the Leydig cells into estradiol

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31
Q

What is the affect of estradiol in the male reproduction?

A

it affects the Leydig cells to affect testosterone production

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32
Q

How does testosterone affect the cell?

A

Testosterone enters the cell and is converted to the more potent 5α-dihydrotestosterone (5α reductase) inside the cell. This binds to an androgen receptor. Two of these complexes join together and enter the nucleus to get protein expression

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33
Q

How does the testosterone secretion change throughout the day?

A

it is pulsatile throughout the day but it the mean level is higher between midnight and noon

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34
Q

How does the testosterone secretion change in a lifetime?

A

The embryo produces a little bit and then it increases which reflects the masculinisation of the embryo. Then it drops off before birth. There is a post-natal spike and then at puberty it vastly increases and is held steady until about 60yrs when it begins to decline

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35
Q

Is testosterone produced by the sertoli cell?

A

no

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36
Q

Is testosterone synthesised from cholesterol?

A

yes

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37
Q

Are testosterone levels constant throughout the life of a male?

A

no

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38
Q

Can testosterone be converted to an estrogen?

A

yes

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39
Q

What is the main reproductive organ of the female?

A

the uterus

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40
Q

What is the role of the uterus?

A

for protection of the embryo and for nutritional support

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41
Q

Where does the oocyte (if fertilised) implant?

A

in the endometrium

42
Q

Describe the follicular development

A

Each 2 million primordial follicle contains one oocyte. This matures into a primary, secondary and finally a tertiary follicle

43
Q

Describe the tertiary follicle

A

It is one oocyte surrounded by granulosa and theca cells

44
Q

What happens to the follicle after ovulation occurs?

A

the corpus luteum forms

45
Q

How many primordial follicles are reserved at menarche?

A

300,000

46
Q

Of the 300,000 primordial follicles that are reserved at menarche, how many of them undergo atresia?

A

about 270,000

47
Q

What is atresia?

A

it is programmed cell death

48
Q

Of the 30,000 primordial follicles that develop into primary, secondary or tertiary follicles, how many of them undergo atresia?

A

Just under 30,000

49
Q

After all the atresia, how many follicles are left to be dominant follicles?

A

about 450

50
Q

After ovulation, the follicle _________ and the ________ cells enlarge to form the _______ ______________

A

collapses
granulosa
corpus luteum

51
Q

The corpus luteum secretes what three hormones?

A

estrogen, progesterone and inhibin

52
Q

If fertilisation does not occur, what happens to the corpus luteum?

A

it degenerates which takes about 10 days

53
Q

Corpus luteum degeneration leads to what?

A

menstruation

54
Q

What are the two phases and what happens in each of these phases?

A

the follicular phase when the follicle develops

the luteal phase when the corpus luteum is active

55
Q

Is the follicular phase before or after ovulation?

A

it is before

56
Q

Is the luteal phase before or after ovulation?

A

it is after

57
Q

Describe the hormonal control of ovarian function during early and middle follicular phase

A

The hypothalamus secretes GnRH which causes the release of FSH and LH from the anterior pituitary gland. FSH affects the granulosa cells and causes them to release inhibin. LH affects the theca cells and causes them to release oestrogen which impacts the granulosa cells and the reproductive tract and other organs

58
Q

What is the effect of inhibin?

A

it is part of a short negative feedback loop which stops the release of FSH from the anterior pituitary gland

59
Q

What is the effect of estragen?

A

it is part of a short negative feedback loop which stops the release of LH from the anterior pituitary gland, and is part of a long negative feedback loop which stops the secretion of GnRH from the hypothalamus

60
Q

What happens when LH binds to a theca cell?

A

The binding of LH onto a receptor on a theca cell activates a G-protein. This activates cyclic AMP which causes the conversion of cholesterol to pregnenolone. This is then converted to progesterone and them to an intermediate and then to androstenedione and then to testosterone

61
Q

Why can estradiol not be made in the theca cell?

A

because there is no aromatase to convert testosterone to estradiol or convert androstenedione to estradiol (via estrone)

62
Q

Where does the androstenedione go from the theca cell? What happens to it?

A

it travels to the granulosa cell to be converted into testosterone or estradiol

63
Q

What happens when LH binds to the GRANULOSA cell?

A

When LH binds to the granulosa cell, there is activation of a G-protein which activated PKA which converts cholesterol to pregnenelone and then this is converted to progesterone.

64
Q

Why can androstenedione not be made from progesterone in the granulosa cells?

A

Because there is no 17-α hydroxylase enzyme to make this conversion

65
Q

Aromatase synthesis to convert androstenedione to estradiol is facilitated by which hormone?

A

FSH when it binds to the granulosa cells

66
Q

How long is the follicular phase?

A

about 15 days

67
Q

What does the follicular phase start with?

A

the menstrual phase

68
Q

During which phase is the endometrium thickening?

A

in the follicular phase to it is highest during the luteal phase (and then shed during the menstrual phase)

69
Q

Describe the hormonal control of the menstrual cycle at the beginning of the follicular phase

A

there is low estrogen which means that the levels of LH and FSH increase and multiple follicles develop

70
Q

After many follicles develop, what rises?

A

the oestrogen level

71
Q

After the oestrogen level rises, what does the dominant follicle do?

A

it secretes oestrogen and inhibin

72
Q

What does the increase oestrogen and inhibin from the dominant follicle do?

A

it reduces the FSH

73
Q

What does reduced FSH cause?

A

oestrogen being switched to positive feedback

74
Q

When oestrogen is positively feeding back, what happens?

A

there is an LH surge and ovulation

75
Q

What happens after ovulation?

A

the corpus luteum forms

76
Q

What does the corpus luteum secrete?

A

it secretes oestrogen and progesterone

77
Q

What does the oestrogen and progesterone secreted from the corpus luteum do?

A

it inhibits FSH and LH

78
Q

When FSH and LH are inhibited, the corpus luteum degenerates. What does this cause?

A

oestrogen and progesterone levels decrease

79
Q

What do the decreased levels of oestrogen and progesterone cause?

A

FSH and LH to rise and the cycle starts again

80
Q

What cells are involved in the oestrogen switch to positive feedback?

A

Kisspeptin cells

81
Q

What does the pill contain?

A

synthetic oestrogen and progesterone

82
Q

What is the purpose of the pill?

  • prevent ________ by maintaining _________ feedback
  • make the __________ less likely to accept ___________
  • thicken the ___________ in the cervix
A
  • prevent ovulation by maintaining negative feedback
  • make the uterus less likely to accept implantation
  • thicken the mucus in the cervix
83
Q

What 5 things might oral contraceptives influence?

A

coagulation, increase the risk of deep vein thrombosis, pulmonary embolism, stroke and myocardial infarction

84
Q

After fertilisation, there is cleavage of the conceptus. This means that all cells are what?

A

totipotent

85
Q

At which stage (day 4-7) do cells begin to differentiate?

A

the blastocyst stage

86
Q

What is a trophoblast?

A

The outer cell layer which will be involved in nutrition and secretion of hormones

87
Q

If there is an inner cell mass and fluid filled cavity, the inner cell mass becomes the what?

A

the embryo and then the foetus

88
Q

After how many days does implantation occur?

A

day 7

there is embedding of the blastocyst into the endometrium

89
Q

How long does a normal human pregnancy last?

A

40 weeks

90
Q

During the last weeks of pregnancy, the cervix becomes soft and flexible due to what?

A

the breakup of the collagen fibres

91
Q

Coordination of contractions is possible because of what?

A

gap junctions between smooth muscle cells that greatly increase near the end of pregnancy

92
Q

Which hormone is responsible for milk synthesis?

A

prolactin

93
Q

Which hormone is responsible for milk ejection?

A

oxytocin

94
Q

How is the secretion of prolactin controlled after suckling?

A

Due to suckling, there is activation of neurons and via the spinal cord, there is a nervous long-loop negative feedback system. This means that this nervous input inhibits the tubero-infundibular dopamine neurons so that no dopamine is released an this allows prolactin to be released from the anterior pituitary gland which stimulates milk synthesis

95
Q

Describe the milk ejection reflex

A

Due to suckling, there is activation of neurons and via the spinal cord, there is a nervous long-loop positive feedback system. This activates neurons in the SON/PVN which causes the release of oxytocin from the posterior pituitary gland to stimulate milk ejection

96
Q

What is cholesterol converted to in the theca cells?

A

testosterone

97
Q

What is cholesterol converted to in the granulosa cells?

A

estradiol

98
Q

What two hormones can the granulosa cell bind to?

A

LH and FSH

99
Q

What happens to the progesterone made in the granulosa cells?

A

it can travel to the theca cell and help with production of testosterone

100
Q

Which cell can progesterone not be converted into testosterone? Why is this?

A

In the granulosa cell because it doesn’t contain the 17-α hydroxylase enzyme which converts progesterone to androstenedione (which then can go on and become testosterone)

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