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Male Repro

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imissyou419's version from 2017-04-02 23:47

Section

Question Answer
What is the reproductive system not responsible for?homeostasis (can take it out and still live)
Urethracommon passage for sperm and urine (in females, it is 2 different passages)
Scotumhold testis; temperature regulation - muscles pull scotum up and down (testis hang out outside of abdominal activity because spermatogenesis needs 35 degrees, countercurrent exchange)
Testisspermatogenesis + hormones
Epididymussperm storage and maturation (metabolic function/ability to fertilize and motility)
Vas deferenstransport sperm
Seminal vesicles Volume, Composition, Why60% volume, alkaline - protect sperm from acidic vagina; fructose (ATP), semenogelin (coagulation - sperm stick together), prostaglandins (smooth muscle contraction - propel into female repro tract)
Prostate gland, Volume, Composition, Why25% volume, acidic; citric acid (ATP), prostate specific antigen (disrupt clot - occurs in female repro tract) - high level of PSA indicate prostate cancer
Bulbourethral Volume, Composition, Why5% volume, alkaline; mucus (lubrication)
Seminiferous tubulesite of spermatogenesis (testis are a sac of these), has Sertoli cells, Leydig cells, developing gametes, made and released into lumen and travel to epididymus
Blood-testis barriersituated within Sertoli cells; barrier (gap junction); on basement membrane side is where spermatogonium is, other side is primary spermatocyte when meiosis starts (spermatogonium yields primary spermatocyte by mitosis though)
Prevent body from killing sperm (when BTB is damaged, antibodies can be generated against sperm)
Cytoplasmic bridgesecondary spermatocytes (n=23) joined together by this, share nutrients/organelles, for X to properly grow, little proteins from X is made that moves to help Y chromosomes
Spermatogoniumstem cell in wall of seminiferous tubules, 2n, either do mitosis to regenerate or starting stage for meiosis, differentiate into primary spermatocyte through mitosis
Leydig cellsperfused by blood, give nutrients and precursors for steroidogenesis and their products move into Sertoli cells
Sertoli cellsnot perfused by blood because of basement membrane
How does spermatogonium become spermatids?spermatogonium (2n=46) -> primary spermatocyte (2n=46) -> 2 secondary spermatocytes (n=23) -> spermatid (n=23), spermatids differentiate (mature/spermiogenesis in epididymus due to fluid pressure movement from Sertoli cells being activated by FSH) and released as sperm; 22 autosomes, 1 X or Y
Meiosis I gives2 secondary spermatocytes (n=23) - cross over before separation so they are genetically different
Meiosis II gives4 spermatids (n=23)
Spermiogenesis (maturation of sperm)
conponents
3 components of sperm: acrosome vesicle (migrates and form cover over nucleus at tip) which contain proteins that digest aspects of ovum prior to fertilization, mitochondria (all secretory parts provide fuel for mitochondria to drive tail), tail;
goes from round cell-like structure to sperm-like structure
Steroidogenesis locationoccurs in mitochondria and ER of Leydig cells
StARrate limiting; key regulating protein involved in getting cholesterol into mitochondria
P450 side chain cleavagefirst enzyme that causes cholesterol to be metabolized, removing the side chain to result in pregnenolone
StAR and P450 action occurs wheremitochondria, rest of process occurs in ER
17-beta-HSDconvert androstenedione to testosterone
5alpha reductaseconvert testosterone to DHT (more potent)
aromataseconvert testosterone to estradiol
How is testosterone produced
Negative feedback
inhibrin
GnRH (pulse generator - active in utero and is shut off, in puberty it is switched on) GnRH rise first then LH and FSH - LH (beta subunit) act on Leydig cells which produce testosterone, FSH act on Sertoli cells
Testosterone negatively feedbacks at at hypothalamus (GnRH) and anterior pituitary (LH and FSH), Sertoli cells make inhibin which negatively feedback onto pituitary gland (decreasing FSH only)
Regulation of testosterone - LH and FSHLH binding to its receptor on Leydig cell -> GPCR activation, increasing cAMP, increases steroidogenesis (upregulate StAR, p450 to increase movement of cholesterol into mitochondria and conversion down pathway to testosterone); cholesterol -> testosterone; FSH bind to its receptor on basolateral membrane, GPCR activation increases: ABP (androgen binding protein), androgen receptor levels, other effects like fluid production to push sperm; testosterone moves to Sertoli cells from Leydig cells and ABP binds to it to keep testosterone concentration high; free testosterone binds to Androgen receptor to increase transcriptional changes;
ABP keeps testosterone high wherein Sertoli cells, in lumen of semniferous tubules, in upper part of epididymus
The entire process of spermatogenesis takes how many days64 days, spermatogenesis preceeds in a regular sequence in any part of seminiferous tubule, human makes 30-100 million sperm/day
Testosterone systemic effectsintrauterine differentiation (penis, scotum, urethra, prostate) - high testosterone week 7; pubertal development (penis, seminal vesicles), sperm production, prostate, beard growth, sebum production; increase RBC, muscle mass, bone, abdominal visceral fat, larynx (male voice), sex drive
Testosterone negative effectscardiovascular (increased viscosity of blood b/c of increased RBC), fertility and testes atrophy (exogenous testosterone shut down GnRH, LH and FSH release -> affect spermatogenesis, testes become smaller), prostate enlargement, breast development (high testosterone gets converted to estrogen = breast develop)
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