L11 Flashcards
How many sperm in an mL? How much is ejaculated at once?
- 60-100mill sperm/mL
2. 3-5mL
What is capacitation and decapacitation
Capacitation is series of events that enable spermatozoon to fuse with fertilize ovum.
To prevent from occurring early, spermatozoa/sperm are kept in decapacitated state
7 fxns of sertoli cells
- Site of peripheral conversion of T into Estradiol (aromatase)
- T and FSH required for spermatogenesis
−receptors on Sertoli cells (T is steroid so nuclear or cytoplasmic receptors; FSH peptide hormone so surface receptors) - Maintain high local T conc (w/in testes and seminiferious tubules)
–androgen binding protein (identical to SHBP, which is incirculation) - Secrete fluid
–bathes developing sperm and aids their movement - Engulf residual bodies (leftover cytoplasm from cytoplasmic bridge upon release of spermatozoon)
- Produce AMH
- Produce inhibin/activin
2 fxns of leydig cells
- Synthesise and acquire (from LDL) cholesterol
−produce T (can go into sertoli cells where it’ll be converted to DHT by aromatase, or seminiferious tubule) - Close proximity to seminiferous tubules
−local high T - Produce T in response to LH.
- LH binds to LHR
- LHR is GPCR (coupled to Ga)
- Ga will activate cAMP pathway -> activation of PKA -> activation of TFs -> Gene products required for T synthesis
Maturation of sperm in epididymis encompasses what 3 components
- Motility
- Metabolism
- Morphology
What occurs for maturation of sperm in epididymis
- Progressive inc in forward MOTILITY
- Inc ability to FERTILIZE
- Maturation of ACROSOME
- Molecular reorganization of PM:
- Lipids (stabilization of PM)
- Proteins (shedding as well as acquisition of new proteins) - Ability to bind to zona pellucida
- Acquisition of receptors for proteins of zona pellucida
- Inc disulfide bonds btwn cysteine residues in sperm nucleoproteins
- Topographic regionalization of glycosidic residues
- Accumulation of mannosylated residues on periacrosomal PM
- Dec cytoplasm and cell volume
Describe conc of T over lifespan and compare it to sperm production
Developing fetus: T important for intrauterine differentiation thus T lvls high in utero. Mullarian degeneration, elevation in T and DHT lvls leads to intrauterine differentiation of male and primary and secondary sex structures.
Birth: Remain low until puberty.
Puberty ~12-13. As T lvls rise, sperm production rise. Sperm lags just behind T conc at puberty. No andropause (equivalent to menopause) but there is senescence. No stoppage or halting spermatogensis, but after ~60, cause of dec T, sperm count tends to go down (spermatogenesis not occurring optimally) and quality dec (not as many, not as motile). Senescence analogous to menopause but not same. Fall off in androgen lvls w/time and resulting in fall off of spermatogenesis.
Hypothalamic-pituitary-gonadal axis for males
- Parvocellular hypothalamic neurons secrete GnRH
- AP releases LH and FSH
- LH acts (primarily) on Leydig cells to cause T production
- FSH acts (primarily) on Sertoli cells to concentrate [T] and convert to estradiol and DHT
What are the 3 main feedback routes in the HPG axis in males?
3 main feedback routes:
- Circulating androgens (i.e T) inhibit pulsatile GnRH release
- Circulating androgens (T) inhibits AP
- Inhibin (Sertoli cells) inhibits AP/FSH
Hormonal Disturbances
- LH acts on Leydig cells that produce T
- FSH acts on Sertoli cells that produce Androgen Binding Protein (ABP), which concentrates T in the seminiferous tubules
- 100X concentration required for maintenance of testes and spermatogenesis
- Anabolic steroids enhance protein content of muscle fibres (hypertrophy)
Anabolic steroids enhance negative feedback resulting in lower LH levels, reduced T levels and lower intracellular T
-> Enhanced muscle mass but smaller testes and reduced spermatogenesis
Describe how an erection is caused and the neurovascular component
- Erection occurs when spaces in erectile tissue fill w/blood
- Various erectile autonomic inputs:
3 motor pathways and a sensory pathway
a) PNS, S2-S4; pelvic nerve
b) SNS, TL spinal cord; hypogastric nerve
c) Somatic fibres from sacral spinal cord; pudendal nerve (striated penile muscles)
d) Afferent (sole): dorsal nerve (pudendal)
Describe anatomy of penis
- Penis is composed of 3 erectile bodies (right corpus cavernosum, left corpus cavernosum, and corpus spongiosum)
- The end of the penis is glans penis. On the posterior side of the glans, an indentation called the frenulum is thought to be the most sensitive part of the penis
Describe how an erection is caused and the neurovascular component
Ejaculation involves:
- emission (peristalsis); movement of seminal fluid into prostatic urethra)
- ejaculation (spinal reflex)
- afferent/sensory impulses reach sacral spinal cord and trigger efferent activity in somatic motor neurons (pelvic floor/ ischiocavernosus/bulbospongiosus muscles)
Using a flow diagram show how erection is neurovascular event
Slide 12
Sexual stimulation (tactile, visual, auditory, psychic) -> Cavernous nerve -> NO -> NO activates guanylyl cyclase. In vascular smooth muscle of helicine arteries, GTP is converted into cGMP by guanylyl cyclase. -> cGMP converted into GMP by phosphodiesterase OR leads to relaxation -> Inc blood flow into sinusoidal cavernous spaces -> Collapse of venous return from cavernous spaces
Sexual stimulation can also lead to -> contraction of muscles around base of penis -> collapse of venous return from cavernous spaces
Describe the physiological and psychological factors with erectile dysfxn
Physiological
- Risk factors: age, high BP, high cholesterol, diabetes, alcohol, smoking, obesity, nerve damage
- Treatment: Constriction ring; Viagra/Cialis
Psychological
- Performance anxiety, stress, mental health conditions
- Treatment: Generally treated with therapy
