reproduction Flashcards
PGE
prostaglandin (eicosanoid) that maintains progesterone production in the CL
PGF2⍺
prostaglandin (eicosanoid) responsible for killing the CL (stopping progesterone production by CL)
HPG axis
- GnRH secreted by arcuate nucleus in both M & F
- GnRH secreted by POA in F only
- GnRH stimulates gonadotrophs to secrete FSH & LH independently
HPG axis in males vs females
males & females
- GnRH neurons in Arcuate nucleus
- steroids signal kisspeptin neurons that signal GnRH neurons
- aromatase converts testosterone to estradiol
- testosterone, estradiol, & progesterone inhibit GnRH secretion
- inhibin produced by growing follicles inhibits secretion of FSH from pituitary
females only
- females also express GnRH neurons in POA
- low levels of estradiol block GnRH
- large follicle produces large amounts of estradiol → ⊕ feedback to POA releasing GnRH → LH surge for ovulation
- no FSH surge because of inhibin
anatomy of the testes
- predominantly seminiferous tubules → site of spermatogenesis
- mature semen stored in retes testes
- tunica vaginalis/tunica albuginea protect testes
anatomy of the ovaries
- folliculogenesis in cortex (outer part)
- blood vessels in medulla (inner part)
- tertiary/antral follicle becomes dominant
- graafian follicle → ovulated during LH surge
- CL = follicular cells post ovulation reorganize & produce progesterone
peritubular myoid cells
- surrounding seminiferous tubules
- fx in movement of seminiferous tubules & helping release mature sperm
leydig cells
- surround seminiferous tubules in interstitial space in testicles
- steroidogenic cells
- respond to LH & uptake CHO to produce androgens
sertoli cells
- in seminiferous tubules of testes
- nurse cells → provide nourishment & support of developing spermatogonia
- respond to FSH & convert androgens to estrogens & more potent androgens
- spermatogonia undergo meiosis while moving towards lumen to become spermatozoa
- blood-testes barrier protects developing gametes
androgen potencies
- diff affinity levels for the androgen receptor
- dihydrotestosterone (DHT) > testosterone > DHEA
- need a lot more DHEA to reach 100% occupancy
testosterone & DHT
- testosterone is the main steroid hormone produced by the testes
- ~5% of T is converted to DHT (dihydrotestosterone) → has 30x greater affinity for AR
- testosterone converted to DHT
- via 5⍺-reductase I (SRDA1) in
- hair follicles
- brain
- liver
- skin
- via 5⍺-reductase II (SRDA2) in
- epididymis
- seminal vesicles
- genital skin
- via 5⍺-reductase I (SRDA1) in
theca cell
- synthesis of androgens (steroidogenic cells)
- respond to LH
- no aromatase expressed
granulosa cells
- responds to FSH during follicular phase
- oocyte nourishment
- conversion of androgens to estrogens
- produces inhibin which inhibits FSH from anterior pituitary
why do females have a surge center in the POA
- as the fetus develops, testes produce testosterone that circulates & crosses BBB
- brain cells express aromatase (which converts testosterone to estradiol) ∴ male brain is exposed to high levels of estradiol early in development so surge center is desensitized
- estradiol binds to ⍺FP (alpha fetoprotein) → prevents estradiol from crossing BBB ∴ brain does not see estradiol until later in life ∴ brain is sensitive to estradiol at puberty
menstrual cycle in endometrium
- proliferation of cells during follicular phase (effect of estradiol) preparing to receive an embryo
- secretory phase after ovulation where endometrium is ready to secrete necessary nutrients for embryo survival
- no fertilization: menses = shedding of lining
menstrual cycle
- early on, as follicles grow: FSH ↑ → responsible for recruiting follicles & promoting growth
- growing follicles produce
- low levels of estradiol → provides ⊖ feedback for both FSH & LH
- inhibin that inhibits FSH
- ∴ wave of follicle growth: growing follicles continue to grow but no new follicles grow (won’t have another wave until follicle ovulates)
- large follicle produces ↑ estradiol → ⊕ feedback to POA releasing GnRH → LH surge for ovulation (FSH inhibited by inhibin)
- as follicle ovulates, estrogen levels ↓ b/c CL produces progesterone to prepare for pregnancy
- no fertilization: body senses no embryo & sends signals to regress CL & ↓ progesterone levels to restart LH & FSH
follicular phase equivalency in estrus cycle
proestrus + estrus
luteal phase equivalency in estrus cycle
diestrus + metestrus
estrus cycle (cow)
- LH surge causing ovulation
- progesterone levels ↑ after ovulation
- estradiol levels ↓ after ovulation
- FSH increases until follicle produces inhibin, then when follicles stop being functional FSH ↑ again
- low until pre-estrus phase when it starts increasing again until it peaks at estrus
- 2 waves of follicle growth
- estrus = ovulation
- diestrus = luteal phase
- proestrus = CL stops producing progesterone
differences between menstrual cycle & estrus cycle
- in menstrual: follicular & luteal phases
- in estrus: no menses b/c no shedding of endometrial cells
- estrus = ovulation
- diestrus = luteal phase
- proestrus = CL stops producing progesterone (before estrus)
- proestrus + estrus = follicular phase
- diestrus + metestrus = luteal phase
secondary effects of testosterone
- laryngeal development
- development of sex accessory glands
- proliferation of seminiferous tubules
- testicular descent
- decreased adiposity
- stimulation of spermatogenesis
- anabolic effects
secondary effects of dihydrotestosterone (DHT)
- male pattern of facial/body hair
- hair loss (has genetic predisposition)
- prostate benign hyperplasia
- anabolic effects
secondary effects of estradiol (E2)
- epiphyseal closure
- osteoprotegerin → protecting the bone from resorption by osteoclasts
- mammary development
- OT, OTR
- stimulation of folliculogenesis
- ovarian fx
- ovulation
conversion to estradiol (E2)
testosterone + aromatase (CYP19)
conversion to dihydrotestosterone (DHT)
testosterone + 5⍺-reductase (SRDA1 & SRDA2)
follicular events during luteal phase
- granulosa cells become large luteal cells (LLC)
- responsible for producing P4
- LLC don’t express P450c17: cannot convert P4 into androgens ∴ only possible route for pregnenolone conversion is P4
- P4 synth stimulated by LH (acquire LH receptors in new LLC)
- theca cells become small luteal cells (SLC)
- less than LLC
- responsible for production of androgens & estrogen
- can aromatize androgens into estrogens ➞ converting androgens to estrogen also occurs in CL (not as pronounced)
cumulus granulosa cells
- in direct closed communication w/ oocyte
- cumulus cells & oocyte exchange factors to promote growth & development
cellular response to LH
stimulates steroidogenesis in leydig cells & in theca cells
- Gs ⍺ subunit activates adenylyl cyclase → converts ATP → cAMP → activates PKA
- PKA
- ↑ expression & translocation of LDLR to membrane to facilitate LDL internalization of CHO
- activates CHO esterase to break down ester (CHO mol bound to fatty acid mol) to release free CHO
- activates StAR to transport free CHO to mitochondria
- activates P450scc to cleave side chain of CHO
cellular response to FSH:
- in sertoli (male) & granulosa (female) cells
- Gs ⍺ subunit
- short term:
- PKA phosphorylates aromatase to convert testosterone to estrogens in males & females
- PKA phosphorylates 5⍺-reductase to convert testosterone to DHT in males
- long-term: ↑ transcription of
- androgen-binding proteins in males
- aromatase in males & females
function of maternal recognition of pregnancy
extend luteal phase to maintain high levels of P4 to maintain uterine quiescence
maternal recognition of pregnancy initiated by
embryo
mechanism of maternal recognition of pregnancy in humans
embryos produce hCG = human chorionic gonadotropin
- used in pregnancy test → best test because only produced by embryos (specific to embryo) & produced early on
placenta
- physical & immune protection ➞ protect female from not recognizing fetus & attacking it
- nutrient, gas, & waste exchange between mother & fetus
- production of enzymes that inactivate maternal hormones to control fetal exposure
- does not express P450c17 ∴ there is no conversion of progesterone into androgens