female repro phys

what ovarian structures produce estrogen?

estrogen production requires coordination of both theca and granulosa cells

what ovarian structure produces progesterone?

luteal cells (corpus luteum)

gonadotropin-independent follicular development

• from primordial follicle up to secondary follicle

• can occur at any time, including before birth

• if insufficient gonadotropin signaling is present, follicles will undergo atresia

  • no gonadotropin before puberty → secondary follicle = most developed follicle possible pre-puberty

• cohort/wave of primordial follicles is recruited in a cycle

gonadotropin-dependent follicular development

• secondary follicle → mature/graafian follicle

  • follicular phase of the estrous cycle

• only possible after puberty, during specific periods of the estrous cycle

what controls development during the gonadotropin-independent stage?

local growth factors

receptors in secondary vs. mature follicle

• secondary: contains LH, FSH, and estrogen receptors

  • LH receptors only on theca cells (more external cells)

• mature follicle: contains LH, FSH, and estrogen receptors

  • LH receptors on both theca and granulosa cells (allow mature follicle to respond to LH surge)

• FSH and estrogen receptors on granulosa cells (inner cells) in both stages

what are the general effects of estrogen during the follicular phase?

• preparing for mating & fertilization

  • follicle/gamete maturation

  • induce ovulation

  • open cervix

  • contraction of oviduct to move fertilized eggs along

  • environmental changes in uterus and vagina to increase survival and transport of sperm

    • ex. cornification of vaginal cells,

• behavior: estrus (receptive for mating)

• -/+ feedback on HPG aixs

how does the dominant follicle suppress growth of the rest of the cohort?

dominant follicle develops faster and becomes independent of FSH → secretes inhibin and estrogen → negative feedback suppresses FSH and deprives other follicles of FSH → other follicles undergo atresia

(“kick down the ladder”)

superovulation

• rescue the rest of the follicles in the cohort before they undergo atresia at the gonadotropin-dependent stage by providing FSH

• allows multiple “dominant” follicles for LH surge

what effects does the LH surge have on mature follicle(s)?

1. permits continued oocyte maturation

   • resumes meiosis, then arrests again → formation of secondary oocyte

   • cytoplasmic maturation

2. triggers ovulation

3. initiates formation of corpus luteum

what is LH’s effect on corpus luteum?

LH works on both small and large luteal cells to increase progesterone production; some LH required for function of corpus luteum

luteotrophic hormones

• LH (& prolactin — in rodents and dogs)

  • relative importance of luteotrophic hormones varies with species

• regulate function of corpus luteum

• note: progesterone is a product of CL → not a luteotrophic hormone

metestrus

stage of the luteal phase in which the corpus luteum is not fully functioning (corpus hemorrhagicum)

diestrus

stage of the luteal phase in which the corpus luteum is fully functional

what hormones are produced by the corpus luteum?

• progesterone (dominant)

• estrogens

• relaxin

what are the general effects of progesterone during the luteal phase?

• coordinating physiology for potential pregnancy

  • reduce contraction of oviduct

  • uterus: increase nutrition secretion, suppress immune system

  • close cervix

  • inhibit estrogen actions in vagina (make inhospitable for sperm)

• behavior: stop estrus behaviors

• HPG axis: only negative feedback

why must luteolysis occur before the next wave of follicles can mature?

• CL produces progesterone (P4) → suppresses HPG axis

• apoptosis of luteal cells → rapid loss of P4 → HPG axis negative feedback removed → FSH/LH increases → maturation of next wave of follicles

what triggers luteolysis?

• PGF-2a (most species)

  • two different sources:

    • uterus (ruminants; other species)

    • corpus luteum due to decreased LH (primates)

• programmed demise (dog)

  • CL dies of old age

how is ovulation induced in spontaneous ovulators?

high levels of estrogen in late follicular phase cause GnRH/LH surge, which triggers ovulation

induced/reflex ovulators

• no positive feedback of estrogen

• GnRH/LH surge triggered by cervical stimulation

what advantages do induced/reflex ovulators have?

• no luteal phase if not mated → do not waste time with luteal phase; can start developing new follicles sooner

• ovulation timed with arrival of sperm

control of corpus luteum formation

• option 1: most spontaneous ovulators → fully functional CL

  • luteotropic support (i.e. LH) is adequate regardless of a mating stimulus (e.g. ruminants, primates, equids)

• option 2: rodents → poorly functioning CL if not mated (need LH + mating-induced PRL)

what is prolactin’s (PRL) role in corpus luteum formation (rodents)?

• cervical stimulation causes reflex release of PRL

  • PRL inhibits conversion of progesterone to a weaker form

• in the absence of mating, corpus luteum produces weak progesterone

PGF2a

prostaglandin produced by the uterus or corpus luteum responsible for destruction of corpus luteum (luteolysis)

control of luteolysis

• uterus secretes PGF2a

  • ruminants: special relationship between uterine vein and ovarian artery

  • horse: release into systemic circulation

• decreased LH (primates)

  • uterus not involved; CL produces PGF2a

  • functional decrease in LH availability → increases PGF2a in CL (self-destruct)

• programmed demise (in canids, CL dies of old age)

  • lifespan of CL in non-pregnant and pregnant females is almost the same