Control of Testicular Function and Sperm Physiology. Flashcards

1
Q

What are the 2 main physiology functions of the testes?

A

1) Production and release of testosterone

2) Spermatogenesis

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2
Q

Explain the hypothalamic GnRH neurones.

A

Cell bodies in the pre-optic area of the hypothalamus extend to the median eminence and release of GnRH to the pituitary portal blood supply.
GnRH is released in regular pulses.

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3
Q

Explain the pituitary and LH/FSH release.

A

Released from the gonadotroph cells in the AP in response to GnRH.
Also released in regular pulses.

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4
Q

What does LH do in males?

A

Stimulates production of testosterone in testes.

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5
Q

What does FSH do males?

A

Stimulates the growth and maturation of the testes and spermatogenesis.

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6
Q

Epididymis?

A

Sperm stored here.

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7
Q

Leydig cells?

A

LH stimulates the synthesis and release of testosterone and other androgens from leydig cells.

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8
Q

What is the main precursor to testosterone?

A

Pregnenolone.

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9
Q

Seminiferous tubules?

A

Spermatogenesis takes place here.

Contains sertoli cells and spermatogonial cells.

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10
Q

Testosterone?

A

Anabolic
Primary and secondary characteristics.
Libido and sexual behaviour
Stimulates spermatogenesis.

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11
Q

What are spermatogonial cells?

A

Produce sperm.

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12
Q

What are sertoli cells?

A

Support, nutrition, protection and regulation.

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13
Q

Explain in brief how sperm are made.

A

Spermatogonial cells….spermatocytes…spermatids….sperm.

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14
Q

Some general details about spermatogenesis?

A

Starts at puberty. Maintains species and introduces genetic variation. Mitosis followed by meiosis. 120,000,000 a dya or 1500 a second.

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15
Q

Explain spermatocytogenesis.

A
Spermatogonial stem cells divide by mitosis to replace themselves and produce spermatocytes, cells that go on to produce sperm.
Type A (d) cells - replicate by mitosis to provide a constant supply of type A (d) and type A (p) cells.

Type A(p) cells divide by mitosis to provide Type B cells.

Type B cells divide by mitosis into primary spermatocytes.

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16
Q

Explain spermatatidogenesis.

A

Primary spermatocytes produce spermatids through meiosis. Produce 4 spermatids (23 chromosomes).

17
Q

What is spermiogensis?

A

A 4 phase process that converts the symmetrical spermatids into mature sperm.

18
Q

What are the 4 phases?

A

Golgi phase
Cap phase
Acrosome phase
Maturation phase

19
Q

Explain the golgi phase.

A

Golgi apparetus creates a vesicle of enzymes around the nucleus.
Mitochondria starts to move to the other side of the cells.
Centriole start to form an axoneme, the cytoskeletal core of the tail.

20
Q

Explain the cap phase.

A

Spermatid DNA is condensed in the nucleus.

The golgi apparatus surround the nucleus and the enzyme vesicle forming the acrosomal cap.

21
Q

Explain the acrosome phase,

A

The axoneme extends to become the tail of the sperm

- temporary cytoskeleton structures called manchettes support the growing tail.

22
Q

Explain the maturation phase.

A

Excess cytoplasm is phagocytosed by sertoli cells to produce mature sperm.

23
Q

Where do sperm gain their motility?

A

Transported from seminiferous tubules to the epididymis where they are stored and gain motility.

24
Q

Explain sertoli cells.

A

Regulated by FSH - essential for spermatogenesis.

  • form the blood testes barrier
  • release androgen binding protein
  • release inhibin for feedback on the pituitary
  • secrete supporting fluid into the lumen
  • phagocytose residual cytoplasm from spermiogensis.
  • release a range of other proteins such as GDNF and anti mullerian hormone.
25
Q

Explain the blood testes barrier.

A

Tight junctions between sertoli cells form a barrier between the lumen of the seminferous tubules and blood vessels.

Allows sertoli cells to control the environment within the lumen.
Protects developing sperm from any toxins.
Seperates the developing sperm from the immune system which othewise would mount an immune response.

26
Q

Explain the androgen binding protein.

A

Spermatogesis requires very high levels of testosterone around the developing system.
ABP binds to testosterone in the lumen, making it less lipophillic - trapping it in the lumen. Concentrates it in the lumen, increasing fertility.

27
Q

What does prolactin do?

A

Released from the AP - also affects male fertility…increases LH receptor expression in Leydig cells…increasing testosterone and spermatogensis.

28
Q

What is ejaculation.

A

Deposition of sperm into the vagina.

29
Q

Role of cervix in sperm transport?

A

Mucous barrier and crypts as sperm reservoirs - sperm motility is important.

30
Q

Role of uterus and fallopian tube?

A

Mild contraction to propel the sperm towards to egg.

31
Q

Where does fertilisation occur?

A

In the ampullary region of the tube.

32
Q

Explain sperm capacitation

A

Takes place in the uterus.
Cholestrol and glycoproteins are removed from the sperm surface by enxymes such as heparin.
Switching on of sperm though increase Ca++ influc.
Hyperactivity - increased motility.

33
Q

Explain the acrosome reaction.

A

Triggered by contact with oocyte.
Interaction with ZP3 protein on oocyte membrane prevents cross-species fertilisation.
Acrosome releases enzymes (hyaluronidase and acrosin) to break through the egg coating allowing fertilisation.

34
Q

What happens following feritlisation?

A

Cortical granules are release - oocyte membrane becomes impermeable to other sperm. Formation of male and female pronuclei.

35
Q

Klinefeiter syndrome?

A

47XXY - hypogonadism, decreased fertility.

36
Q

Kallman syndrome?

A

Mutation in olfactory means GnRH neurones dont develop.

No reproductive function and no sense of smell.

37
Q

Hyperprolactinaemia?

A

High [prolactin].
Pituitary tumors
Side effects of vaious perscription drugs that affect dopamine.
Decrease libido and fertility.

38
Q

Androgen insensitivity syndrome

A

Genetic defect in androgen receptor - decrease sensitivity.

Female body development.

39
Q

What factors affect sperm production?

A

Hormones - steroids suppress GPG axis and decrease fertility

Non-hormonal; heat, environment, radiation, air pollution, food chain pollution and stress.