Flashcards in Lecture 6 - Male Reproductive Tract II Deck (16):
Testicular Changes in puberty?
marked increase in proliferation of spermatagonia, cords develop lumen and become seminiferous tubules, sperm production
Spermatogenesis - mitotic division?
reactivated germ cells (spermatogonial stem cells) mitose, one undifferentiated to maintain population, one into spermatagonia which continues to divide, move from sertoli to seminiferous tubule adluminal compartment -> primary spermatocytes
Spermatogenesis - meiotic division?
primary spermatocyte undergoes meiosis I to become secondary (chr 46 -> 23), meiosis II into 4 spermatids (23)
Spermatogensis - cytodifferentiation?
androgen dependent - spermatids shed residual cytoplasm as residual body, move to lumen
released from ant. pituitary following GnRH stimulation from hypothalamus, stimulates testosterone release from Leydig cells, DHT most potent sort for secondary sexual characteristics (short and long negative feedback loop)
released from anterior pituitary following GnRH stimulation from hypothalamus, simulate sertoli cells to release androgen binding protein, transports testosterones around body (inhibin release negatively feeds back short loop)
Secondary sexual characteristics?
aggresiveness, libido, hair growth, baldness
Continuous sperm production?
segmental progression of spermatogensis along tubule
concentrate semen 100x fold with spern, stereocilia for reabsorption, sperm gain ability for motility and fertilisation
major storage site of sperm, three muscular layers: inner and outer longitudinal and middle circular, simple lumen at epididymal end then enlarged w crypts for greater sperm storage at the ampulla (prostate end)
Seminal vesicle funtion?
secrete alkaline fluid via excretory duct, with Semenogelin that causes semen clotting post ejaculation (I and II types, also with fibronectin)
surrounds prostatic urethra, secretes acidic fuid containing PSA (used in out of NZ cancer screening)
central (not prone to carcinoma), peripheral (prone to carcinoma), transition (site of benign hyperplasia), anterior (muscle no glands)
parasymp. release of Ach, inducing NO release by corpora endothelial cells, inducing cGMP production causing vasodilation, corpora relax and fill with blood, venous outflow reduced leading to erection
blocks type V phosphodiesterase, reducing cGMP metabolism, causing vasodilation - useless for parasympathetic nerve damage as no NO causing cGMP production