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Endocrinology > 3.2 Development and Puberty - GnRH/LH/FSH > Flashcards

3.2 Development and Puberty - GnRH/LH/FSH Flashcards

1
Q
  • what does puberty mean in latin?
  • puberty includes all (3) changes that occur in the growing animal as (3) change from _______ to ________
  • what represents onset of puberty in females vs males?
  • does puberty signify fertility?
A
  • “to grow hairy”
  • includes all physiological, morphological and behavioral changes that occur in the growing animal as gonads/brain/phenotype change from adolescent to adult
  • females: first cycle/menses –> menarche in women
  • males: first ejaculation –> semenarche/spermache
  • both menses and ejaculation DO NOT signify fertility –> bc gonads need to acquire full optimal function first
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2
Q

which axis regulates gonadal development? explain general hormones/schéma

A
  • hypothalamus-pituitary-gonadal axis
    1. hypothalamus is sensitive to environmental factors (photoperiod, temp, light) + physiological factors (nutrition, fat, stress…)
    2. hypothalamus produces GnRH –> sends to pituitary
    3. pituitary produces LH and FSH –> sends to gonads
    4. gonads: deal with gametogenesis, gonadal growth and steroidogenesis (testosterone and estrogen)
    5. testosterone and estrogen have negative feedback on pituitary and hypothalamus
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3
Q

what are the 2 functions of gonads?
1. __________
2._________ –> can control 3 things

A
  1. Gametogenesis: oocytes and sperm
  2. Steroidogenesis (gonads can produce many hormones, but mainly steroid hormones):
    a) reproductive behavior
    b) nutrient metabolism and electrolyte balance
    c) adiposity and muscle mass/muscle function
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4
Q

GnRH
- what type of hormone? size? how many aa?
- how is it produced? released with what?
- synthesized by how many neurons in hypothalamus? neurons from which nuclei?

A
  • very small peptide hormone –> 10 aa cleaved from larger precursor and released with GnRH-associated peptide (GAP)
  • GAP –> slightly larger than GnRH, can be measured but we don’t know its function (not much research done bc not super conserved across species = hard to research)
  • synthesized by about 1000-3000 neurons (considered a small number) in hypothalamus, not organized in a specific nucleus –> spread across multiple nuclei but mainly in arcuate and pre-optic nuclei
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5
Q

what’s special about GnRH neurons?
- where do they terminate?

A

they don’t have axons! they have dendrons –> can carry info in both directions
- GnRH neurons terminate in hypophyseal portal capillaries/ME, BUT can also connect to other brain areas and may affect sexual behavior
- can also receive signal from the ME bc of dendrons (?)
*check recording

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6
Q

how is GnRH secreted? (2 ways ish)

A

2 centers:
1. surge center –> massive release of GnRH, high frequent and high amplitude peaks (peaks add on to each other) in a 6-8h window
2. tonic center –> secretes GnRH in a pulsatile fashion: sharp burst at regulated frequency
*these centers are NOT physical centers –> out of the 3000 neurons, some group of neurons are surge vs some are tonic

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7
Q

from where is GNRH mainly secreted?
- other tissues?

A
  • hypothalamus!
  • also non-hypothalamic tissues –> placenta, gonads (granulosa cells), breast, lymphocytes and pituitary –> but function is unknown
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8
Q
  • _______ mechanism regulate pulsatility of GnRH (adult –> every ____ minutes)
  • pulsatile release of GnRH regulates ________ development
A
  • neuronal mechanism –> every 90 minutes
  • regulates sexual development
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9
Q

pulsatile release of GnRH regulates sexual development
- explain what happens in pre-puberty vs puberty

A
  • GnRH in hypothalamus and LH/FSH in pituitary are present before onset of puberty, but they are not released
  • while GnRH neurons are capable of secreting GnRH (individually), they are not well coordinated before puberty –> no neuronal connection established = no secretion in pulsatile matter
  • in prepubertal monkeys, pulsatile administration of GnRH induces secretion of LH and FSH (already synthesized) which induces menstrual cycle
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10
Q

hypothalamic nuclei are highly sensitive to what feedback before puberty?
- vs at puberty?

A
  • highly sensitive to negative feedback from gonadal steroids (estrogen and testosterone) before puberty
  • as puberty increases, negative feedback of steroids decrease = GnRH is more and more released
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11
Q
  • surge and tonic centers in both females and males?
  • at onset of puberty, levels of GnRH rise/decrease? (both ______ and ______ of the pulses increase/decrease)
  • increase/decrease in GnRH pulses is caused by increased/decreased sensitivity of tonic center to negative/positive feedback from what?
  • vs surge center?
A
  • surge only in females. tonic in both males and females
  • levels of GnRH rise: both amplitude and frequency of pulses
  • increase in GnRH pulses caused by DECREASED sensitivity of tonic center to negative feedback from gonadal steroids
  • surge center in female does not change sensitivity. before puberty, estrogen levels are not high enough to stimulate surge release (surge center is inactivated in males
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12
Q
  • before puberty, GnRH neurons of tonic center for both males and females release GnRH?
  • after puberty in female, the tonic center controls _______ levels of GnRH but they are lower/higher than in prepubertal female bc of what?
  • The surge center controls ___________ surge of GnRH.
  • Male has surge center?
A
  • yes! release low amplitude and low frequency pulses of GnRH
  • tonic center controls basal levels of GnRH but levels are higher than in prepubertal female bc pulse frequency increases
  • surge center controls preovulatory surge of GnRH
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13
Q

at puberty, increase in (2) support spermatogenesis and folliculogenesis?

A
  • increase in pulses of LH/FSH
  • increase in levels of steroids
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14
Q

what is the sexual dimorphism in regards to surge vs tonic centers in hypothalamus?
*potential exam question

A

FEMALES:
- estradiol produced by fetal ovary cannot cross blood brain barrier BECAUSE estradiol binds to alpha-fetoprotein (produced by fetal liver and binds to steroids/toxins/lipid soluble substances)
- aFP has high binding affinity to estradiol –> cannot cross BBB –> absence of estradiol allow for organization of surge center
- female retains surge center + tonic center to control LH/FSH after puberty
MALES:
- testosterone produced by testis freely enters brain (bc aFP doesn’t have high affinity to testosterone)
- in brain, testosterone converted to estradiol through aromatase enzyme
- estradiol inhibits development of surge center –> defeminization of surge center
- male only has tonic center to control LH/FSH post-puberty

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15
Q
  • what hormone (what kind) regulate pulsatile secretion of GnRH, through which receptor (what kind?)
  • (hormone) neurons come from where?
  • (hormone) neurons are inhibited and activated by what?
A
  • Kisspeptin (KISS1) = peptide hormone (expressed as big protein and cleaved) –> regulate pulsatile secretion of GnRH through KISS1 receptor (KISS1R) (GPCR)
  • from anteroventral periventricular nuclei (AVPV) and arcuate nuclei (ARC)
  • KISS1 neurons in ARC are inhibited by steroid feedback (estradiol or testosterone) and regulate tonic center
  • KISS1 neurons in AVPV are activated by estradiol feedback and regulate surge center
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16
Q

KISS1 act as mediators btw what and what?
- they are also sensitive to signals like (2) which can modify what?

A
  • btw GnRH neurons and steroid hormones
  • like feeding behavior and light –> can modify GnRH neuron secretion
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17
Q
  • LH and FSH are ___________
  • are secreted by __________
  • basic structure?
  • how are they secreted? in response to what? through which receptor?
A
  • gonadotropins
  • gonadotrophs (of anterior pituitary)
  • a-chain (common btw LH, FSH and TSH) + b-chain (unique to each hormone)
  • secreted in pulsatile fashion about every 60 minutes in response to GnRH pulses
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18
Q
  • actions of FSH: females, males vs both sexes?
  • actions of LH: females vs males
A

FSH:
- females: development of ovarian follicles and estradiol secretion from follicles
- males: spermatogenesis and estradiol secretion from sertoli cells
- both: secretion of inhibit (Negative feedback on FSH)
LH:
- females: steroidogenesis in follicles (estradiol), induction of ovulation, maintenance of steroidogenesis by corpus luteum
- males: stimulation of testosterone production in Leydig cells

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19
Q
  • inhibin: what type of hormone?
  • regulates which gonadotropin(s)?
A
  • peptide hormone
  • negative feedback on FSH
  • NO role in LH regulation –> that’s why LH secretion is tightly coordinated with GnRH secretion (no mediation from inhibit)
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20
Q
  • LH acts on which cells (in ovary vs testis) + which pathways?
  • FSH acts on which cells (in ovary vs testis) + which pathways?
A

LH:
- thecal cells and leydig cells
- GPCR: adenylate cyclase –> PKA AND phospholipase C –> DAG + IP3 –> PKC
FSH:
- granulosa cells and sertoli cells
- GPCR: adenylate cyclase –> PKA

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21
Q

actions of LH and FSH:
- promote (2) of which type of cells in gonads
- regulate ___________
- increase of intracellular _____A_____
- transport of _____A______ from where to where using which enzyme?
- conversion of _____A______ to ________ by which enzyme?

A
  • promote proliferation and differentiation of somatic cells of gonads
  • regulate steroidogenesis
  • increase of intracellular cholesterol (+ local synthesis is also possible)
  • transport of cholesterol from outer mitochondria/cytoplasm to inner mitochonrial membrane by steroidogenic acute regulatory protein (StAR)
  • conversion of cholesterol to pregnanolone by CYP11A1
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22
Q

LH and FSH
- target cells in testis + what do the target cells produce?
- target cells in ovaries + what does target cells produce?

A

TESTIS:
- LH acts on Leydig cells (testosterone + estradiol)
- FSH on sertoli cells (estradiol)
OVARIES:
- LH –> steroidogenic act on theca interna (testosterone)
- FSH –> steroidogenic act on granulosa cells (estradiol)
- LH also acts on granulosa cells (estradiol) and luteal cells (progesterone)

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23
Q

negative or positive feedback:
- testosterone on pituitary and hypothalamus
- testosterone on sertoli cells
- inhibin on FSH/LH?
- estradiol and progesterone on pituitary and hypothalamus

A
  • testosterone on pituitary and hypothalamus –> NEGATIVE
  • testosterone on sertoli cells: POSITIVE
  • inhibin on FSH/LH: ONLY NEGATIVE ON FSH, no effect on LH
  • estradiol and progesterone on pituitary and hypothalamus: POSITIVE OR NEGATIVE (?)
24
Q

Where does spermatogenesis occur?
- 3 different cell types of importance?
- which cells surround the main cells that become spermatids?

A
  • in testis!
  • spermatogonia (differentiate into spermatids) + sertoli cells + leydig cells
  • sertoli cells surround spermatogonia
25
Q

androgen synthesis in testis
- 2 main androgens?
- 95% produced from _______ vs 5% produced from _______
- how much mg per day?
- what percentage is bound to what (3)
- main hormone acts on (3)
- receptor for androgens?

A
  • dehydroepiandrosterone (DHEA) and testosterone
  • 95% from testis, 5% from adrenal gland
  • 3-10mg per day
  • 98% bound to albumin, globulin and sex-hormone binding globulin (SHBG)
  • testosterone acts on reproductive tract, genitalia development and muskulo-skeletal growth
  • androgen receptors! –> present in lots of cell types: muscle, heart, adipose tissue…
26
Q

schéma: how to synthesize DHEA and testosterone?
- enzymes!

A
  1. cholesterol = precursor –> enters inner mitochondria using StAR enzyme
  2. cholesterol –> pregnenolone via CYP11A1
  3. prenenolone –> 17-OH pregnenolone –> DHEA
    - both rxns catalyzed by CYP17A1
    3.1 DHEA –> androstenedione via HSD3B2
    3.2 androstenedione –> testosterone via HSD17B
  4. pregnenolone –> progesterone via HSD3B2
    4.1 progesterone –> 17OH-progesterone –> androstenedione
    - both rxns catalyzed by CYP17A1
    4.2 androstenedione –> testosterone via HSD17B
    *DHEA can also –> DHEAS via SULT2A1
27
Q

action of androgens in males
- a powerful ________ hormone
- young children produce androgens? –> consequence?
- as puberty hits, testosterone has 7 functions

A
  • powerful anabolic hormone
  • occasional pulses of LH and FSH in young children (mainly nocturnal) = production of steroid hormones –> level high enough to produce secondary sex characteristics at puberty
    1. spermatogenesis
    2. skeletal muscle growth
    3. larynx development
    4. hair growth
    5. behavioral changes
    6. epiphyseal fusion (completion of bone growth)
    7. change in excretion of sebaceous gland (acne)
28
Q

female reproductive endocrinology
1. as ovary differentiates, ______ cells undergo _______ (name of cell?)
2. oocyte surround by single layer of ________ to form ________ follicles
3. then 1st meiotic division (arrested at __________) begins to form several _______ oocytes
4. oocytes remain in _________ until ovulated –> then continues meiosis 2 (arrested at ________)

A
  1. germ cells undergo mitosis (oogonia)
  2. granulosa to form primordial follicles
  3. prophase I –> several million oocytes
  4. remain in prophase I until ovulated –> arrested at metaphase 2
29
Q
  • number of primordial follicles set at what moment in life? –> peak!
  • how many oocytes at birth?
  • until puberty, (2) occur BUT insufficient (?) to cause final maturation
  • at puberty, how many oocytes?
  • how many ovulations in lifetime? –> success rate in ovulation = ____%
A
  • set at around 5th month of embryonic development –> 7 million ish
  • 1.5 million
  • follicular growth and atresia (cell death) –> follicular growth –> secretes estradiol but not enough for positive feedback of GnRH –> insufficient FSH/LH to cause final maturation
  • at puberty: 300 000
  • 400-500 ovulations in lifetime –> 0.000036% success in ovulation
30
Q

can ovaries contain primary follicle, secondary follicle and corpus luteum at the same time?
- polyovulators vs monoovulators?

A
  • yes! at any given time, ovary contains many many different structures
  • polyovulators: ie mice: release 15 oocytes at once VS mono-ovulators (cows, humans) release 1 oocyte at a time
31
Q

explain steroidogenesis (which hormone) in follicles
hint: 2 cells - 2 gonadotropins

A
  1. LH acts on theca internal cells (outside basement membrane of antral follicle) –> GPCR –> activates CYP17A1 to convert cholesterol to testosterone
    *testosterone travels to granulosa cell
  2. FSH acts on granulosal cell –> GPCR –> activates CYP19A1 to convert testosterone to estradiol
    *estradiol goes into bloodstream
32
Q

antral follicle:
CYP17A1 expressed in which cells? vs CYP19A1
- regulated by which hormone?

A

CYP17A1 = theca cells –> LH
CYP19A1 = granulosa cells –> FSH

33
Q

effect of estradiol
- on brain (1)
- on reproductive tract (6)

A

BRAIN:
- libido/sexual behavior
REPRODUCTIVE TRACT:
- increase: blood flow + edema of tissues + secretion (mucus) + leukocytes + smooth muscle motility + growth of uterine glands

34
Q
  1. hypothalamus produces ______ –> acts on ____A______ to produce (2)
  2. these (2) –> act on ______B_______
    - ____B____ produces (2)
  3. both hormones produced by __B___ have negative feedback on what?
    - one of the hormones produced by ___B___ has positive feedback on what?
A
  1. hypothalamus –> GnRH –> acts on pituitary to produce LH and FSH
  2. LH and FSH act on follicle
    - follicle produces inhibin and estradiol
  3. both inhibin and estradiol have negative feedback on FSH (pituitary)
    - Estradiol has positive feedback on surge center in pituitary –> if strong enough –> leads to oculation
35
Q

_______ changes (4 ish) regulate ovarian steroid secretion
- ovarian steroid secretion regulates/acts upon (2 changes)

A

ovarian changes (follicular growth and maturation –> ovulation –> corpus luteum –> luteolysis) regulate ovarian steroid secretion
- acts upon uterine changes and vaginal changes

36
Q

describe the 4 phases ish of uterine changes

A
  1. menstruation (beginning of cycle)
  2. proliferative phase: endometrial glands do not secrete anything (before ovulation
  3. secretory phase (after ovulation): endometrial glands secrete stuff like carbs
  4. pre-decidual phase (before menstruation, unique to species who menstruate): decidualization = endometrial layer goes through complex physiological changes
37
Q

what are the vaginal changes before and after ovulation?

A

BEFORE OVULATION:
- high pH watery mucus conducive to sperm survival
- high E2 and low progesterone
AFTER OVULATION:
- low pH viscous mucus inimical/not helpful to sperm survival
- bc of high progesterone

38
Q

describe the basic functioning of follicle waves

A
  1. primordial follicles grow and become responsive to FSH = become antral/go through follicular wave
  2. primary/antral follicles start growing together
  3. one follicle is selected to grow = dominant follicle –> only that dominant follicle is capable of ovulation if preovulatory surge
  4. the rest of the growing follicles become subordinate follicles
  5. if the dominant follicle doesn’t ovulate (bc not enough estradiol to have positive feedback on surge center), dominant follicle dies off = end of wave
39
Q
  • what technology allowed to understand how follicles develop in a wave-like fashion?
  • what is the name of the menstrual cycle for cows?
A

ultrasonography
- estrous cycle

40
Q

explain follicular waves with the hormonal profiles
9 steps ish

A
  1. small increase in FSH stimulates growth of follicles
  2. simultaneous growth of many follicles –> 1 becomes the dominant
  3. follicles (mainly the dominant one) produce estradiol –> E2 = negative feedback to FSH –> FSH decreases
  4. bc no FSH, non-dominant follicle go through atresia (bc need FSH to grow) –> becomes subordinate follicle
  5. dominant follicle doesn’t die off bc it has granulosa cells that express LH receptors –> tonic LH levels are enough to make it grow more
  6. bc progesterone is high, E2 cannot peak = LH cannot surge = dominant follicle goes through atresia
  7. E2 decreases = no negative feedback on FSH anymore –> FSH increases –> induces 2nd follicular wave
  8. progesterone levels follow growth/degradation of corpus luteum very closely. when CL dies off/luteolysis, progesterone decreases
  9. low progesterone –> estradiol can increase a lot –> induces LH peak + FSH peak –> leads to ovulation
41
Q

a) what is the only source of progesterone during the estrous cycle?
b) why is it that only the dominant follicle can ovulate?
c) what (2) induces LH surge?
d) is it possible to stimulate more than 1 follicle to become dominant?
e) the dominant follicle is dependent on what for its growth?

A

a) corpus luteum!
b) bc only the dominant follicle has LH receptors! can respond to LH surge
c) increase in estrogen + low progesterone
d) yes! if you inject enough FSH
e) dependant on tonic levels of LH! NOT dependant on FSH

42
Q

what are the 3 main things that happen at ovulation/caused by preovulatory LH surge?

A
  1. follicular wall ruptures and oocyte exits
  2. luteinization –> granulosa cells become luteal cells
  3. oocyte maturation –> continues meiosis
43
Q

which 3 hormones are produced at preovulatory LH surge?
leads to what? –> leads to 2 main things –> ovulation

A
  1. increase prostaglandin E2 –> increase blood flow to ovary and mainly around dominant follicle –> edema –> increase follicular pressure
  2. increase prostaglandin F2a
    2.1 PGF2a leads to increase contraction of ovarian smooth muscle –> increase follicular pressure
    2.2 PGF2a leads to increase release of lysosomal enzymes –> follicle wall weakens
  3. shift form E2 to P4 by dominant follicle (switch machinery of steroid genesis: no testosterone and estradiol anymore –> granulosa cells become luteal cells and produce progesterone)
    3.1 increase P4 –> increase collagenase (induces breakdown of basement membrane btw granulosa cells and theca cells) –> follicle wall weakens
    OVERALL: increase follicular pressure + follicle wall weakens = ovulation
44
Q

how does preovulatory LH surge induce oocyte maturation?
- explain oocyte maturation: 4 steps

A
  • gap junction breakdown btw granulosal cells and oocyte
    1. removing the gap junction = removal of meiotic inhibition
    2. meiosis continues –> results in 1 large daughter cell + first polar body (dies off)
    3. 1 large haploid oocyte –> continues meiosis –> gets arrested at metaphase II
    4. only if fertilization that meiosis II completes and forms the 2nd polar body
45
Q

ovulation if brought about by (3 physiological things ish)

A
  1. elevated blood flow (increase follicular pressure)
  2. breakdown of connective tissue (follicle wall weakens)
  3. ovarian contractions (induced by PGF2a)
46
Q
  • usually ________ _________ separates granulosa and theca cells
  • this (A) ruptures –> formation of ___B___ ___B____ = ______________
  • (B) survives with tonic __C__ secretion –> ___C___ stimulates (B) to secrete _____
    *what maintains basal levels of (C)
A
  • basement membrane
  • basement membrane ruptures –> formation of corpus luteum = luteinization
  • corpus luteum survives with tonic LH secretion –> stimulates CL to secrete progesterone
  • tonic center produces GnRH –> maintains basal levels of LH
47
Q

PROGESTERONE (P4)
- negative feedback on (4 ish)
- positive feedback on (1)

A

NEGATIVE:
- on GnRH neurons of hypothalamus –> GnRH, LH and FSH are suppressed + little estrogen is produced
*also P4 is through to decrease # of GnRH receptors on anterior pituitary
- P4 inhibits myometrium –> reduces its contractibility and tone
POSITIVE:
- on endometrium of uterus –> uterine glands secrete material (nutrients!) into the uterine lumen

48
Q
  • what happens to corpus luteum is NO fertilization?
  • how does it happen in ruminants?
A
  • luteolysis!
    1. oxytocin and E2 stimulate endometrial cells in uterus (that have receptor for oxytocin and E2) to produce PGF2a
    2. close association between uterine veins and ovarian artery –> PGF2a travel really fast from uterus to ovary through this close association
    3. PGF2a in ovary helps corpus luteum break down
49
Q

why is the close association btw uterus and ovary important during luteolysis?

A
  • because PGF2a is very short lived! 1 passage into the lungs/general circulation will metabolize it by 80% –> only 20% left after
50
Q

explain luteolysis in primates

A
  • oxytocin –> increases PGF2a in ovary = luteolysis –> decrease P4 and E2 –> stimulates endometrial synthesis of PGF2a –> vasoconstriction of endometrial arterioles –> endometrial necrosis and sloughing/menses
51
Q

luteolysis in ruminants vs primates
* can humans have menstrual cycle even if no uterus? vs cows?

A

RUMINANTS:
- PGF2a produced by uterus + goes to ovary through close association btw uterine veins and ovarian artery
PRIMATES
- oxytocin produced in pituitary but also in ovary!
- PGF2a appears to come from ovary itself! but still not super clear
*humans can have menstrual cycle even if hystorectomy (remove uterus) but NOT COWS! bc they need uterus to make PGF2a

52
Q

bovine study: _______ is the origin of luteolytic signal: describe lifespan of CL:
a) normal uterus
b) total hysterectomy
c) contralateral hysterectomy (opposite side)
d) ipsilateral hysterectomy (same side)

A
  • endometrium!
    a) CL normal lifespan (normal 21 day cycle)
    b) CL lifespan longer! similar to gestation length –> bc no PGF2a
    c) CL normal lifespan bc horn of uterus of same side can produce PGF2a
    d) CL lifespan longer –> slight increase in CL life (>35 days): 1 horn is enough to produce PGF2a but it has to enter general circulation to get to other horn = longer time
53
Q

describe maternal recognition of pregnancy in cow and ewe
- 3 steps

A
  1. embryo produces interferon-tao (IFN-T)
  2. IFN-T inhibits oxytocin receptor expression –> receptor needed to signal production of PGF2a
  3. IFN-T also stimulates endometrial gland to make nutrients (ie protein) –> stimulates growth of embryo –> increase IFN-T = positive loop
54
Q

describe maternal recognition of pregnancy in sow (pig)
- compare non-pregnant sow with pregnant sow

A
  • no interferon tao
    NON-PREGNANT SOW:
  • oxytocin produced –> makes endometrial cells produce PGF2a –> PGF2a goes to blood supply to reach ovary and makes CL go through luteolysis
    PREGNANT SOW:
  • sow’s blastocyst produces estradiol –> diverts PFG2a into uterine lumen, instead of blood supply
  • so CL in ovary doesn’t get PGF2a = no luteolysis
55
Q

knowing about ovarian functions/reproductive science can be useful in (name a few of the 13)

A
  • gamete preservation
  • endangered species
  • pharmaceuticals
  • companion animals
  • lactation and nursing
  • human medicine (Ob/Gyn)
  • reproductive health (disease)
  • genetics
  • assisted reproductive technologies
  • veterinary medicine
  • domestic animals (food)
  • molecular biology
  • endocrinology (hormones)

Endocrinology (14 decks)

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