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reproduction Flashcards

1
Q

PGE

A

prostaglandin (eicosanoid) that maintains progesterone production in the CL

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2
Q

PGF2⍺

A

prostaglandin (eicosanoid) responsible for killing the CL (stopping progesterone production by CL)

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3
Q

HPG axis

A
  • GnRH secreted by arcuate nucleus in both M & F
  • GnRH secreted by POA in F only
  • GnRH stimulates gonadotrophs to secrete FSH & LH independently
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4
Q

HPG axis in males vs females

A

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
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5
Q

anatomy of the testes

A
  • predominantly seminiferous tubules → site of spermatogenesis
  • mature semen stored in retes testes
  • tunica vaginalis/tunica albuginea protect testes
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6
Q

anatomy of the ovaries

A
  • 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
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7
Q

peritubular myoid cells

A
  • surrounding seminiferous tubules
  • fx in movement of seminiferous tubules & helping release mature sperm
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8
Q

leydig cells

A
  • surround seminiferous tubules in interstitial space in testicles
  • steroidogenic cells
  • respond to LH & uptake CHO to produce androgens
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9
Q

sertoli cells

A
  • 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
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10
Q

androgen potencies

A
  • diff affinity levels for the androgen receptor
  • dihydrotestosterone (DHT) > testosterone > DHEA
  • need a lot more DHEA to reach 100% occupancy
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11
Q

testosterone & DHT

A
  • 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
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12
Q

theca cell

A
  • synthesis of androgens (steroidogenic cells)
  • respond to LH
  • no aromatase expressed
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13
Q

granulosa cells

A
  • responds to FSH during follicular phase
  • oocyte nourishment
  • conversion of androgens to estrogens
  • produces inhibin which inhibits FSH from anterior pituitary
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14
Q

why do females have a surge center in the POA

A
  • 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
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15
Q

menstrual cycle in endometrium

A
  • 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
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16
Q

menstrual cycle

A
  • early on, as follicles grow: FSH ↑ → responsible for recruiting follicles & promoting growth
  • growing follicles produce
    1. low levels of estradiol → provides ⊖ feedback for both FSH & LH
    2. 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
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17
Q

follicular phase equivalency in estrus cycle

A

proestrus + estrus

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18
Q

luteal phase equivalency in estrus cycle

A

diestrus + metestrus

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19
Q

estrus cycle (cow)

A
  • 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
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20
Q

differences between menstrual cycle & estrus cycle

A
  • 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
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21
Q

secondary effects of testosterone

A
  1. laryngeal development
  2. development of sex accessory glands
  3. proliferation of seminiferous tubules
  4. testicular descent
  5. decreased adiposity
  6. stimulation of spermatogenesis
  7. anabolic effects
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22
Q

secondary effects of dihydrotestosterone (DHT)

A
  • male pattern of facial/body hair
  • hair loss (has genetic predisposition)
  • prostate benign hyperplasia
  • anabolic effects
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23
Q

secondary effects of estradiol (E2)

A
  • epiphyseal closure
  • osteoprotegerin → protecting the bone from resorption by osteoclasts
  • mammary development
  • OT, OTR
  • stimulation of folliculogenesis
  • ovarian fx
  • ovulation
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24
Q

conversion to estradiol (E2)

A

testosterone + aromatase (CYP19)

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25
Q

conversion to dihydrotestosterone (DHT)

A

testosterone + 5⍺-reductase (SRDA1 & SRDA2)

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26
Q

follicular events during luteal phase

A
  • 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)
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27
Q

cumulus granulosa cells

A
  • in direct closed communication w/ oocyte
  • cumulus cells & oocyte exchange factors to promote growth & development
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28
Q

cellular response to LH

A

stimulates steroidogenesis in leydig cells & in theca cells

  • Gs ⍺ subunit activates adenylyl cyclase → converts ATP → cAMP → activates PKA
  • PKA
    1. ↑ expression & translocation of LDLR to membrane to facilitate LDL internalization of CHO
    2. activates CHO esterase to break down ester (CHO mol bound to fatty acid mol) to release free CHO
    3. activates StAR to transport free CHO to mitochondria
    4. activates P450scc to cleave side chain of CHO
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29
Q

cellular response to FSH:

A
  • in sertoli (male) & granulosa (female) cells
  • Gs ⍺ subunit
  • short term:
    1. PKA phosphorylates aromatase to convert testosterone to estrogens in males & females
    2. PKA phosphorylates 5⍺-reductase to convert testosterone to DHT in males
  • long-term: ↑ transcription of
    1. androgen-binding proteins in males
    2. aromatase in males & females
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30
Q

function of maternal recognition of pregnancy

A

extend luteal phase to maintain high levels of P4 to maintain uterine quiescence

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31
Q

maternal recognition of pregnancy initiated by

A

embryo

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32
Q

mechanism of maternal recognition of pregnancy in humans

A

embryos produce hCG = human chorionic gonadotropin

  • used in pregnancy test → best test because only produced by embryos (specific to embryo) & produced early on
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33
Q

placenta

A
  1. physical & immune protection ➞ protect female from not recognizing fetus & attacking it
  2. nutrient, gas, & waste exchange between mother & fetus
  3. production of enzymes that inactivate maternal hormones to control fetal exposure
  • does not express P450c17 ∴ there is no conversion of progesterone into androgens
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34
Q

placentation in species w/ hemochorial placenta

A
  • embryonic cells invade endometrium & maternal vasculature in endometrium & myometrium
  • change flow & resistance of maternal spiral arteries to support placental & fetal growth
    • widen artery to maximize flow
35
Q

maternal endocrine changes during pregnancy

A
  1. ↑ cortisol
  2. ↑ insulin
  3. insulin resistance develops during 2nd half of pregnancy
  4. ↑ lipolysis
  5. ↑ total T3 & T4 but free T3 & T4 remain normal because body ↑ production of thyroid-binding proteins
  6. ↑ in RAAS → ↑ aldosterone
  7. anterior pituitary enlarges by 35% due to hypertrophy & hyperplasia of lactotrophs (which produce prolactin)
36
Q

maternal physiologic adaptations to pregnancy

A
  1. volume of uterine cavity ↑ from 10ml to 5L at term
  2. blood volume ↑ throughout preg reaching 40-45% higher at term
  3. plasma volume ↑ to 45-50% due to aldosterone-mediated Na & H2O retention
  4. RBC ↑ 20%
  5. ↑ GFR
  6. ↑ HR, SV, & CO
  7. overall BP does not change significantly dye to ↓ peripheral vascular resistance
37
Q

reproductive steriodogenesis

A
  • DHEA = final steroidogenic product in zona reticularis
    • weak androgen
    • precursor androgen to make more androgens & estrogens
  • 3β-HSD required to convert pregnenolone to progesterone
  • 17β-HSD required to convert androstenedione to testosterone
  • P450arom (aromatase) required to convert testosterone to estradiol
38
Q

enzyme required to convert pregnenolone to progesterone

39
Q

enzyme required to convert androstenedione to testosterone

40
Q

enzyme required to convert testosterone to estradiol

A

aromatase (P450arom)

41
Q

estriol

A

form of estrogen that is only produced during pregnancy due to conversion of 16⍺-hydroxy-DHEAS from fetal origin

  • can use to evaluate fetal health during pregnancy: healthy fetus reduces androgens that are transformed by estriol
  • not used in detecting pregnancy → not early enough in gestation, need a fully formed placenta to convert 16⍺-hydroxy-DHEAS into 16⍺-hydroxy-DHEA via sulfatase
  • potency: estradiol > estrone > estriol
42
Q

maternal-fetal-placental unit: hormones on the maternal side

A
  • uptaking cholesterol
  • requires ↑ LDL & VLDL
  • ACTH helps uptake CHO by putting LDL receptors in membrane
  • steroidogenesis to pregnenolone & DHEAS
  • testosterone & androgens from placenta converted into estradiol (E2) via aromatase
43
Q

maternal-fetal-placental unit: hormones in the placenta

A
  • CHO converted into pregnenolone by P450scc
  • conversion of pregnenolone to progesterone via 3β-HSD
  • progesterone = main product of placenta → goes back to maternal circulation
    • main source for pregnancy
    • placental production replaces CL production upon formation
  • 16⍺-hydroxy-DHEAS converted into 16⍺-hydroxy-DHEA via sulfatase
    • variant of DHEA makes specific form of estrogen (estriol) only produced during pregnancy
  • 16⍺-hydroxy-DHEA converted into androgens via 3β-HSD & 17β-HSD
  • androgens converted into estriol (E3) via aromatase
  • DHEAS from maternal & fetal sides converted into DHEA → converted into T & A4 via 3β-HSD & 17β-HSD
44
Q

maternal-fetal-placental unit: hormones on the fetal side

A
  • pregnenolone from placenta converted to pregnenolone sulfate via sulfotransferase
  • pregnenolone sulfate converted to DHEAS in forming fetal adrenal gland
  • DHEAS converted into 16⍺-hydroxy-DHEAS in liver → only happens in fetal liver
  • testosterone & androgens from placenta converted into estrone (E1) via aromatase
45
Q

maternal-fetal-placental unit

A
  • placenta + fetal adrenal glands + maternal adrenal glands
  • collaboration between placenta & fetal & maternal adrenal glands to produce progesterone & estrogens necessary for successful pregnancy
  • androgens:
    • testosterone (T)
    • androstenedione (A4)
    • dehydroepiandrosterone (DHEA)
  • estrogens:
    • estradiol (E2)
    • estrone (E1)
    • estriol (E3)
46
Q

hormones produced by the placenta

A
  1. progesterone (progestational steroid hormone)
  2. estrogens (estrone, estradiol, estriol, esterol)
  3. human chorionic gonadotropin (hCG)
  4. placental lactogen (hPL)
  5. placental growth hormone (GH2)
  6. human chorionic corticotropin (hCC)
47
Q

progesterone fxs

A
  • progestational steroid hormone
  • maintenance of pregnancy
  • inhibits uterine contractility → uterine quiescence
  • substrate for fetal synthesis of glucocorticoids & mineralocorticoids
  • immunomodulation: create barrier so female immune system does not attack fetus b/c fetus is not exactly “self”
  • preparation of mammary tissue for lactation: alveolar duct branching & alveolar differentiation
    • sustained exposure to high levels of P4 inhibits terminal differentiation of mammary gland & lactogenesis ∴ need a drop of progesteron & estrogen to initiate lactation
48
Q

estrogens & their fxs

A
  • estrone, estradiol, estriol, esterol
  • stimulate uptake of LDL, VLDL, & HDL for cholesterol availability by the placenta
  • increase uteroplacental blood flow
  • preparation of mammary tissue for lactation
  • proliferation of mammary epithelial cells during puberty
  • stimulates synthesis of OTR receptors in uterus
  • epiphyseal closure
  • stimulates OPG that binds ODF & inhibits its binding & activation of osteoclasts ∴ ↓ rate of bone resorption
49
Q

human chorionic gonadotropin (hCG)

A
  • produced by placenta
  • similar fx to LH → utilizes LH receptors to initiate steroidogenesis pathway to progesterone in CL
  • maternal recognition of pregnancy & progesterone synthesis
  • stimulates differentiation of cytotrophoblasts into syncytiotrophoblasts (future placental cells)
50
Q

placental lactogen (hPL)

A
  1. provides fetus w/ a constant supply of nutrients ➞ strong stimulant of IGF-1 production
  2. promotes maternal insulin resistance & ↑ lipolysis ➞ important to redirect glucose for fetal development from maternal circulation
  • similar to GH & PRL → binds to their receptors ∴ boosts effects of GH & PRL
51
Q

placental growth hormone (GH2)

A
  • stimulates IGF-1 production
  • at term: 85% of GH in maternal circulation is GH2
52
Q

human chorionic corticotropin (hCC)

A
  • ACTH-like peptide hormone produced by placenta
  • stimulated by cortisol in a ⊕ feedback loop
  • placental also produces CRH-like hormone to produce local stimulation of hCC
53
Q

enzymes produced by the placenta

A
  • 11β-HSD converts cortisol to cortisone
  • 17β-HSD converts estradiol to estrone
  • DI3 inactivates TH
  • MAO/COMT inactivates catecholamines
  • placenta has filtering fx to stop increased hormone levels in mother from getting to fetus
54
Q

parturition from a fetal perspective

A
  • activated CRH release & HPA axis ➞ ↑ fetal cortisol
  • ↑ NE & EPI
  • glucose homeostasis usually normalizes w/in 5-7d
  • Ca homeostasis normalizes w/in 1-2w
55
Q

an increase in fetal production of NE & EPI stimulates

A
  1. ↑ BP & inotropic effects
  2. ↑ glucagon & ↓ insulin secretion
  3. ↑ thermogenesis in BAT (β-adrenergic receptor mediated)
56
Q

initiation of labor

A
  • final stage of preg leading to initiation of preg depends on a drop in progesterone levels &/or a drop in progesterone activity
  • estrogen receptors become more abundant in uterus → allows for ↑ production of prostaglandins & oxytocin receptors critical for initiating uterine contractions
  • prostaglandins (PGE1 & PGE2⍺) are potent inducers of labor
    • induce uterine contractions
    • treat postpartum hemorrhage
    • prostaglandin inhibitors used to prevent preterm labor
57
Q

oxytocin in parturition

A
  • second stage of labor
  • ↑ estrogen:progesterone → ↑ OTR in myometrial cells → ↑ tissue response to OT = coordinated & strong myometrial contractions
  • estrogen stimulates synthesis of OTR receptors in uterus
58
Q

stage 2 of labor

A

fetal expulsion

  • ferguson reflex: ⊕ feedback loop → cervical/vaginal dilation stimulates release of OT
  • OTR more abundant in uterine fundus
59
Q

an increase in fetal production of cortisol stimulates production of

A
  1. lung surfactant → maturation of lungs
  2. PNMT → conversion of fetal NE to EPI
  3. DI2 in liver → conversion of fetal T4 to T3
60
Q

hypothalamic-prolactin axis

A
  • lactotrophs produce PRL in anterior pituitary
  • lactotrophs mostly respond to ⊖ signal from dopamine neurons in arcuate nucleus
  • dopamine inhibits PRL secretion
  • PRL stimulates dopamine secretion
  • secondary stimulatory signals for PRL:
    1. TRH produced by PVN
    2. GnRH from Arc & POA (in females)
    3. estradiol from gonads
61
Q

inhibitors of PRL

A
  • dopamine
  • cortisol (stimulates dopamine & also inhibits PRL directly)
62
Q

secondary stimulatory signals for PRL

A
  1. TRH produced by PVN
  2. GnRH from Arc & POA (in females)
  3. estradiol from gonads
63
Q

rhythm of PRL secretion outside of pregnancy

A

circadian rhythm: PRL secretion peaks during sleep hours (amplitude is larger in females than males)

  • PRL secretion peaks during sleep hours (amplitude is larger in females than males)
  • in seasonal animals: PRL is controlled by day length
    • ↓ duration of light ↓ PRL secretion
    • seasonal influences
64
Q

prolactin (PRL)

A
  • polypeptide hormone secreted by lactotrophs in adenohypophysis
  • first described as an essential hormone for milk prod/lactation
  • fx: promote proliferation & differentiation of mammary epithelial cells & synthesis of milk
  • same family as GH/placental lactogen → very similar structure
  • binds to PRLR in mammary epithelial cells but some PRL is uptaken by the cell & released into milk
    • may have role in neonatal development
65
Q

metabolic effects of PRL

A

PRLR are present in β cells of endocrine pancreas → stimulates insulin synthesis & β cell proliferation

66
Q

immunologic effects of PRL

A

PRL stimulates proliferation of T & B immune cells (role of PRL in leukocyte differentiation is less clear)

67
Q

PRL effects in hair, skin, & sweat glands

A
  • PRL modulates hair growthby controlling keratin expression
    • mutation in PRL gene results in hairy phenotype that changes conformation of PRL gene ➞ major defects in lactation
    • mutation in the PRLR gene results in sleek hair phenotype that shortens PRLR (no effects on lactation)
      • cattle w/ PRLR mutation have sleek hair & more thermotolerant
  • sweat glands have similar structure to mammary alveoli (definitive role of PRL in sweat glands TBD)
68
Q

PRL effects on parental behavior

A
  • nest-building, gathering, grouping, cleaning, nursing
  • effects result from synergistic activity of elevated steroid hormones progesterone + estradiol + PRL
  • contact w/ pups induces expression of PRLR in brain of female & male rats
69
Q

prolactin receptor

A

cytokine receptor = jak/stat signaling pathway → involves activation of STAT1, STAT3, & STAT5

  1. PRL binds to cytokine receptor
  2. jaks cross-phosphorylate each other on tyrosines
  3. activated jaks phosphorylate receptors on tyrosines → allows STATs to bind
  4. STATs dock on phospho-tyrosines → jaks phosphorylate them
  5. phosphorylated STATs dissociate from receptor & dimerize
  6. translocate to nucleus to bind to promoter regions & response elements
  7. transcription/translation of
    1. keratin (K14, K15)
    2. casein
    3. alpha-lactoalbumin
70
Q

effects of PRL in mammary development & lactation

A
  • mammogenesis = development of mammary gland
  • lactogenesis = milk synthesis
  • galactopoiesis = maintenance of milk production
71
Q

development of mammary system

A
  • at birth: gland is formed but ducts are rudimentary
    • born with primary mammary buds & fat pads
  • from birth to puberty: isometric growth = mammary gland is growing at the same rate as the rest of the body
    1. duct elongation
    2. differentiation of myoepithelial cells
  • around puberty: allometric growth = mammary gland is developing faster than other systems → expansive proliferation
    • GH, IGF-1, & estrogen stimulate
      1. fat pad accumulation
      2. proliferation of epithelial mammary tree
  • during reproductive cycle: progesterone stimulates duct branching
  • during pregnancy: P4, PRL, estrogen, placental hormones, & IGF-1 stimulate branching & alveolar duct differentiation → maturation of system to prepare for lactation
72
Q

development of mammary system during pregnancy

A

P4, PRL, estrogen, placental hormones, & IGF-1 stimulate branching & alveolar duct differentiation → maturation of system to prepare for lactation

73
Q

development of mammary system during reproductive cycle

A

progesterone stimulates duct branching

74
Q

development of mammary system during puberty

A
  • allometric growth = mammary gland is developing faster than other systems → expansive proliferation
    • GH, IGF-1, & estrogen stimulate
      1. fat pad accumulation
      2. proliferation of epithelial mammary tree
75
Q

development of mammary system during pre-pubertal growth

A
  • isometric growth = mammary gland is growing at the same rate as the rest of the body
    1. duct elongation
    2. differentiation of myoepithelial cells
76
Q

development of mammary system at birth

A
  • gland is formed but ducts are rudimentary
  • born with primary mammary buds & fat pads
77
Q

lactogenesis

A
  • milk synthesis
  • PRL stimulates:
    1. synthesis of milk protein casein & ⍺-lactoalbumin
    2. synthesis of milk sugar lactose
    3. uptake of glucose & AA by mammary epithelial cells
  • myoepithelial cells have OTR → squeeze alveolus during contraction to release milk that was produced & stored in alveolus
  • alveoli = group of secretory epithelial cells that express PRLR
78
Q

hormones involved in mammary development

A
  • estrogens: proliferation of mammary epithelial cells
  • progesterone & PRL: duct branching & alveolar differentiation
  • ↑ progesterone & estrogen inhibits terminal differentiation & lactogenesis ∴ need a drop in P4 & estrogens for lactation to begin
  • cortisol & insulin promote lactation
79
Q

maternal prolactin levels during lactation

A
  • follows circadian rhythm: levels at night > day
  • declines gradually over course of lactation
  • levels will remain high for as long as mother breastfeeds
  • levels rise w/ suckling: more feedings = higher level of serum prolactin
  • in absence of breastfeeding: levels fall to basal w/in 7d of birth
  • normal lactation: levels remain elevated for several months
80
Q

suckling stimulus

A
  • inhibits dopamine secretion from TIDA neurons → removes ⊖ inhibitor of PRL
  • stimulates TRH
  • may stimulate other prolactin-releasing factors (PRF) secretion from hypothalamus & posterior pituitary
81
Q

release of OT & PRL in response to suckling stimulus

A
  • PRL has pulsatile secretion pattern
  • maintenance of high levels requires freq breastfeeding
  • PRL stimulates OT neurons in lactating females through PRLR located in these neurons
82
Q

peripartum oxytocin & PRL secretion & during lactation

A
  • OT secreted at high levels 2 times: birth & placental expulsion
    • then small pulsatile secretions in response to suckling stimuli
  • PRL levels rise until birth then high pulsatile release gradually decreasing over time
83
Q

where is testosterone converted to DHT via 5𝛼-reductase I (SRDA1)

A
  • hair follicles
  • brain
  • liver
  • skin
84
Q

where is testosterone converted to DHT via 5𝛼-reductase II (SRDA2)

A
  • epididymis
  • seminal vesicles
  • genital skin

NPB 130 (5 decks)

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