Male Reproductive System I

Question 1

Overview of the sperm journey?

Answer 1

1. testis (high speed manufacturing)
2. epididymis head & body (finishing steps)
3. epididymis body (warehouse and shipping)
4. accessory sex glands (final alterations & packaging)
5. penis (delivery system)

Question 2

Function of the testis?

Answer 2

High speed manufacturing
- 1-25x10^9 spermatozoa/day (35,000-200,000 per second)
- “plant” must be air conditioned

Question 3

Function of the epididymis head & body?

Answer 3

finishing shops
- fluid absorption
- 8-25x10^9 spermatozoa (mb changes, nuclear & flagellar stabilization, motility, cytoplasmic droplet translocation)

Question 4

Function of the epididymis tail?

Answer 4

warehouse & shipping
- storage (10-50x10^9 spermatozoa)
- spermatozoa for 5-10 ejaculations
- smooth muscle contractions upon sexual stimulation

Question 5

Function of the accessory sex glands?

Answer 5

final alterations & packaging (remove inhibitory signals on sperm & feed them)
- metabolic substrates
- surface coatings
- transport for spermatozoa

Question 6

Function of the penis?

Answer 6

delivery system (with accessory sex glands)
- erection
- protrusion
- emission
- ejaculation

Question 7

Testis tissue has to be how much cooler than body temperature for normal sperm production?

Answer 7

4-6 degrees C

Question 8

Cooling is a function of:

Answer 8

• cremaster muscle, scrotal skin, tunica dartos, vascular counter current
• move the testis closer & further from the body as needed
• bottom of the scrotum is a lot cooler

Question 9

what is the pampiniform plexus?

Answer 9

venous network wrapped around the testicular artery

Question 10

What is the pampiniform plexus effective in?

Answer 10

• heat exchange
• pulse pressure reduction
• transfer of testosterone

Question 11

What is the pulse pressure in the spermatic cord?

Answer 11

• there is a difference in pulse pressure in the testicular artery above & below the pampiniform plexus
• the mechanism & functional significance for this reduction is not clear
• potentially b/c testicular artery becomes more elastic?
• testicular artery @ bottom has same mean pressure as @ top but waay smaller fluctuations in pressure (hypothesized to prevent damage)

Question 12

How temperature sensitive is the scrotum?

Answer 12

resp rate is 10x higher w/ 10 degree increase in temperature applied to scrotum

Question 13

Where are the rete testis located in Sw & bulls?

Answer 13

• centrally

Question 14

Where are the rete testis located in Eq & humans?

Answer 14

• more superficial

Question 15

What are Leydig (interstitial endocrine) cells?

Answer 15

• produce testicular androgens (& lots of estrogen in Se & Eq)
• occupy approximately: 1% in Rams, 5% in bulls, & 20-30% in Sw of the volume of the testis
• display typical steroid producing cell features (a lot of lipids)
• large polymorphous acidophilic cells w/ round nucleus

Question 16

What are the 3 distinct populations of Leydig cells during testicular development?

Answer 16

1. Fetal Leydig cells (from sex determination to shortly after birth)
2. Infantile/Early Postnatal Leydig cells (only in some spp - primates, sw, bull; very short lived)
3. Adult Leydig Cells (from puberty through adult life; remain & produce testosterone for that animal)
   These populations come & go and then are replaced by the next one

Question 17

What are seminiferous cords & tubules?

Answer 17

• convoluted double-ended loops (total ~2 m in mice, ~ 5 km in bulls)
• consist of lamina propria, Sertoli cells, & spermatogenic cells
• lamina propria is made up of a basal lamina (collagen & other ECM) surrounded by peritubular cells
• cords are immature, lack a lumen, ~70-90 micrometers in diameter, & are made up of Sertoli & gonocytes
• tubules are more developed, have a lumen, ~150-300 micrometers, & are made up of Sertoli & multiple generations of germ cells

Question 18

What are peritubular myoid cells?

Answer 18

• 1-5 layers of contractile cells that surround the basal lamina
• contain abundant actin filaments & cytoskeleton proteins
• resemble myofibroblasts (ex: in bull) or smooth muscle fibers (ex: in boar)
• their contractile action assists in the propulsion of sperm & testicular fluid along the lumen of seminiferous tubules toward rete testis

Question 19

What are Sertoli (sustentacular) cells?

Answer 19

• have oval nucleus w/ a prominent nucleolus near base
• adult cells differ from fetal/early postnatal & lose mitotic capability
• large elongated cells w/ irregular outlines touching basal mb, & laterally & apically fill space among germ cells
• evenly spaced in tubule (~20 cells per cross section)
• provide nutrients & signals to dividing germ cells
• move germ cells along to lumen
• secrete testicular fluid into lumen for sperm transport
• phagocytize faulty germ cells & their excess cytoplasm
• produce chemical mediators to regulate spermatogenesis

Question 20

What 2 types of specialized junctional complexes do Sertoli cells form?

Answer 20

• SERTOLI-SERTOLI TIGHT JUNCTION btwn adjacent cells (S1 & S2) forms BLOOD-TESTIS BARRIER & divides tubules into BASAL & ADLUMINAL COMPARTMENTS
• it opens like a zipper to allow germ cells to pass from basal to adluminal compartment before meiosis to protect them from the immune system
• SERTOLI-SPERMATID JUNCTIONAL specialization w/ spermatid nucleus (S2 & N)
• both characterized by bundles of microfilaments

Question 21

What is a gonocyte?

Answer 21

part of male germline stem cells (germ cells that come after primordial germ cells (PGCs) & before spermatogonial stem cells (SSCs)

Question 22

What is the origin of gonocytes?

Answer 22

• 1st appear @ ~13.5 dpc in rodents & 7 wk of gestation in human embryos (their development is hormone independent)
• they appear when testis cords are formed & PGCs have lost alkaline phosphatase (AP) activity & adopted male germ cell fate

Question 23

How are gonocytes classified?

Answer 23

1. mitotic fetal gonocytes = multiplying (M)-prospermatogonia
2. quiescent gonocytes = primary transitional (T1)-prospermatogonia
3. mitotic postnatal gonocytes = secondary transitional (T2)-prospermatogonia

Question 24

What are mitotic fetal gonocytes?

Answer 24

multiplying (M)-prospermatogonia
- immediately after PGCs & before mitotic arrest
- proliferate from 13.5 to 18 dpc in rodents or @ 18 wk of gestation in human embryos
- then become quiescent

Question 25

What are quiescent gonocytes?

Answer 25

primary transitional (T1)-prospermatogonia
- distinctively large round cells. w/ 1 or 2 nucleoli in a prominent nucleus
- in transition to A-spermatogonia but in the center of cords
- start after mitotic arrest & until 1-2 days (rodents) or wk/mo after birth (depending on spp)

Question 26

What are mitotic postnatal gonocytes?

Answer 26

secondary transitional (T2)-prospermatogonia
- in transition to A-spermatogonia, residing @ basement mb
- T1-prospermatogonia develop pseudopods, migrate to the basement mb, resume mitosis, & differentiate into T2-prospermatogonia
- failing to develop pseudopods lead to apoptosis & potentially even testicular cancer in young men
- start @ 1-4 days postnatally in rodents or ~8 wk after birth in infant boys

Question 27

How does gonocyte mal-development lead to testicular cancer?

Answer 27

• Testicular germ tumours (TGTs) are derived from in situ germ cell neoplasia (GCNIS) previously called in situ carcinoma (CIS)
• TGTs are thought to be caused by a combination of negative environmental & genetic factors (multifactorial & polygenic)
• key pathogenic element is inadequate masculinization & deterioration of fetal somatic testicular (Leydig & Sertoli cells) fxns
  Normal development pathway:
  PGC -> migration -> in fetal testis: Gonocyte w/ normal Sertoli & Leydig cell fxn -> birth -> in prepubertal testis: spermatogonia -> puberty -> (in adult testis: spermatocytes -> spermatids)
  Impaired development pathway:
  PGC -> migration -> (in fetal testis: gonocyte w/ impaired Sertoli or Leydig cell fxn due to environmental insults or gene mutations -> arrest) -> birth -> (in prepubertal testis: delayed gonocyte “pre-GCNIS” -> “adaptation”: genomic aberrations) -> puberty -> (in adult testis: GCNIS w/ invasive capacity -> (proliferation -> SEMINOMA) OR (re-programming -> EC (epididymal cyst) somatic differentiation -> NONSEMINOMAS)