Spermatogenesis and Spermiogenesis Flashcards

1
Q

What is represented by the arrows?

A
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2
Q

What are the 2 major compartments of the testes?

A
  • Seminiferous tubules
  • Interstitial spaces
  • Both compartments are separate: blood-testis barrier
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3
Q

Describe the components of the seminiferous tubules.

A
  • ~250m total length
  • Developing germ cells
  • Sertoli cells
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4
Q

Describe the components of the interstitial spaces in the testes.

A
  • Leydig cells (synthesise androgens)
  • Blood and lymph vessels
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5
Q

What is the role of the blood-testis barrier?

A
  • Prevents immune reaction to spermatozoa
  • Separated fluids of different composition
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6
Q

What are the stages of spermatogenesis?

A
  • Production of mature spermatozoa from undifferentiated germ cells (primordial germ cell) occurs in 3 stages:
    • Mitotic proliferation
    • Meiotic divisions
    • Cell modelling (spermiogenesis)
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7
Q

Where is the blood-testis barrier created?

A

Between neighbouring sertoli cells by tight junctions.

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8
Q

How long is the spermatogenic cycle?

A
  • ~74 days (from the first mitotic division to the release of spermatozoa).
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9
Q

Describe the cycle of spermatogenesis.

A
  • The spermatogenic cycle is ~74 days (from first mitotic division to the release of spermatozoa).
  • Spermatogenesis occurs in waves, initiated every 16 days.
  • Rate of each developmental stage is not uniform:
    • Spermatogonium → primary spermatocytes = 25 days.
    • Meiotic division 1 → secondary spermatocytes = 9 days.
    • Development → spermatids = 19 days.
    • Differentiation → spermatozoa = 21 days.
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10
Q

What is spermiogenesis?

A

The transition from the spermatocyte to the more recognisable mature sperm cell.

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11
Q

Describe the end of differentiation.

A
  • At end of differentiation:
    • Cytoplasmic links are broken
    • Spermatozoa are released into tubule lumen
    • Sperm are virtually immobile
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12
Q

Describe the movement of spermatozoa from the seminiferous tubules.

A
  • Fluid secreted by Sertoli cells flushes spermatozoa from the seminiferous tubules, through the rete testis into the epididymus:
    • Capacity for motility by the time they reach the tail of the epididymus.
    • Motility is suppressed by epididymal fluid.
    • Instead movement through the reproductive tract is aided by peristaltic muscle contractions.
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13
Q

Describe sperm maturation.

A
  • If ejaculated spermatozoa are placed with oocytes in vitro fertilisation does not occur immediately.
  • They need to undergo the process known as capacitation:
    • Normally occurs in the female reproductive tract (2-6h)
  • Glycoprotein coat gained in the epididymis is stripped.
  • This results in two changes:
    • Head acquires the capacity to initiate acrosome reaction.
    • Hyperactivation (ingreased flagellar beats).
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14
Q

What is the quality of human sperm like?

A
  • Poor
  • Only 4-14% of sperm show normal morphology under a microscope.
  • If normal morphology drops below 4% fertilisation rates obtained with IVF are reduced.
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15
Q

How is infertility in men primarily diagnosed?

A
  • Infertility in men is primarily diagnosed by semen analysis comprising of:
    • Determination of sperm concentration / total count
    • Motility
    • Morphology
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16
Q

What is oligozoospermia?

A

Reduced sperm count (<15 million / mL)

17
Q

What is azoospermia?

A

Absence of sperm in the ejaculate

18
Q

What is asthenozoospermia?

A

Reduced sperm motility (<50% moving)

19
Q

What is teratozoospermia?

A

Reduced percentage of sperm with normal morphology

20
Q

What are antisperm antibodies?

A

Abnormal immune response to sperm

21
Q

What is the role of the hypothalamus and pituitary gland?

A
  • Secretion of hormones by the hypothalamus, pituitary and testes are regulated by complex feedforward and feedback loops.
  • Pulsatile secretion of gonadotrophin-releasing hormone (GnRH) from the hypothalamus stimulated the anterior pituitary gonadotrophs.
  • The pituitary gonadotrophins, leuteinizing hormone (LH) and follicle stimulating hormone (FSH) control testicular functions.
22
Q

What are the functions of LH and FSH?

A
  • Leydig cells in the testes have receptors for LH.
    • Stimulated synthesis and secretion of testosterone.
  • If LH secretion is too low, testosterone is low.
    • Spermatogenesis halts.
  • However, LH and testosterone cannot maintain spermatogenesis at its normal level without FSH.
  • FSH is required for maximum sperm production.
    • Acts of Sertoli cells.
23
Q

Describe the hormonal regulation of spermatogenesis.

A
24
Q

Describe the effects of FSH on sertoli cells.

A
25
Q

Which hormones are synthesised by the testes?

A
  • Testosterone (steroid)
  • Estrogens (steroid)
  • Inhibins (peptide hormone)
  • Oxytocin (peptide hormone)
26
Q

Describe the production of testosterone in the testes.

A
  • Steroid produced by Leydig cells.
    • In some tissues, testosterone does not exert direct effects, but are converted to dihydrotestosterone or estrogens.
27
Q

Describe the production of estrogens in the testes.

A

Steroid produced by Sertoli and Leydig cells.

28
Q

Describe the production of inhibins in the testes.

A
  • Peptide hormone produced by sertoli cells.
    • Feedback loop to control hormone levels.
29
Q

Describe the production of oxytocin in the testes.

A
  • Peptide hormone synthesised by leydig cells.
    • Contraction of smooth muscle of the genital tract.
30
Q

What is the role of testosterone?

A
  • Essential for spermatogenesis:
    • If production of testosterone is prevented, spermatogenesis ceases.
    • Blocked when primary spermatocytes enter meiotic prophase.
  • If blood (testosterone) is low then fewer stem cells will begin cell division but the whole proess will still take 74 days.
31
Q

What are the most common causal diagnoses of male infertility?

A
  • Only 28% of men are provided a causal diagnosis.
    • Most consist of previous gonadotoxic chemo- or radio- therapy for the treatment of malignant disease (10%).
    • Testosterone abuse or other chronic diseases (e.g. diabetes) (~14%).
    • Genetic disorders (e.g. Kleinfelter’s syndrome, Karyotype 47, XXY or microdeletions on the Y-chromosome) (~4%).
  • Genes involved in the migration and function of GnRH neurons or their upstream regulators have been discovered that may be mutated in patients with congenital hypogonadotrophic hypogonadism with or without anosmia.