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Reproductive Cyclicity - Follicular Phase - Coggle Diagram
Reproductive Cyclicity - Follicular Phase
driving force for the initiation of the follicular phase is luteolysis
negative feedback by progesterone on the hypothalamus is removed and GnRH is released at higher amplitudes and frequencies than during the preceding luteal phase
2-cell, 2-gonadotropin model describes estrogen synthesis
binding of LH to its receptos acctivates a sascafe of intracellular events
major effects of estradiol on the reproductive tract
change in tissue electrical conductivity
leukocytosis
increased mucosal secretion
genital swelling
initiation of uterine gland growth
increase blood flow
elevated myometrial tone
cervix and cranial vagina respond to estradiol by producing mucus:
lubricate the vagina and cervix in preparation for copuation
flush foreign material such as bacteria out of the tract following copulation
low viscosity mucus provides "privileged pathways" for spermatozoa to traverse the cervix and enter the uterus
leukocytosis: influx of leukocytes into the tissue and the lumen of the reproductive tract
estradiol causes increased tone and motility of the muscularis in all regions of reproductive tract
proestrus and estrus:
during follicular phase four significant event take place
follicular preparation for ovulation
sexual receptivity (estrus)
gonadotropin release from the anterior lobe of the pituitary
ovulation
gonadotropin release is controlled by ovarian estrogen and hypothalamic GnRH
follicular phase is governed by the hypothalamus, anterior lobe of the pituitary and the vary through the secretion of estradiol isn the absence of progesterone
produces GnRH
hypothalamic nuclei
ventromedial nucleus
arcuate nucleus
episodic profile:
surge center: responsible for the preovulatory release of GnRH that stimulates a surge of LH, causing ovulation
anterior hypothalamic area
suprachiasmatic nucleus
preoptic nucleus
GnRH secretion from the tonic center appears to be spontaneous but is influenced by progesterone
folliculate dynamics is controlled by FSH and LH and involves both growth and death of these follicles
dynamics of antral follicles
dominance
one or more large preovulatory follicles exerting a major inhibitory effect on other antra follicles from the recruited and selected cohort
low FSH + high LH pulse frequency + high inhibin
atresia
degeneration
degeneration of follicles
selection
low FSH + moderate LH + low inhibin
recuitment (emergence)
phase of follicular development in which a cohort (group) of small antral follicles begin to grow and secrete estradiol
high FSH + low LH pulse frequency + low inhibin + low estradiol
monotosous (give birth to single offspring)
polytocous (litter bearers): multiple dominant follicles
atresia: involves more follicles than does the process of dominance
follicular dynamics be subdivided
initial recruitment phase
cyclic recruitment
FSH and LH exert different effects on follicles
LH: promote final growth and maturation of dominant follicles and to stimulate ovulation
FSH controlled vy estrogen and inhibin
LH regulated by GnRH pulses that control the pulse frequency LH
ovlation results from a cascade of events starting with the LH surge
hyperemia (local elevated blood flow) cntrolled at the tissue level by hustamine and prostaglandin E2
ovulation happens by
breakdown of connective tissue
elevated blood flow
ovarian contractions
dominant follicles being to secrete progesterone before ovualtion
local elevation of progesterone is essential for ovulation because progesterone stimulates synthesis off an enzyme called collagenase by the theca interna cells
collagenase is "digesting" the collagen of the tunica albugunea, follicular fluid volume inside the follicle increases
the apex of the follicle (called the stigma) begins to push outward and weaken
some species require copulation before ovulation can occur
two types of ovulators
spontaneous ovulators
reflex (induced) ovulators
requires stimulation of the vagina and/or cervix for ovulation to occur
some spontaneous ovulators apparently have some residual neural input from the reproductive tract that can alter the timing if the LH surge
camelids appear to be modified induced ovulators
presence of seminal plasma in the female reproductive tract appears to be more important for inducing ovulation than lactive stimulation
folliculogenisis and ovulation can be induced artificially using various hormones
superovulation
decline in blod progesterone
allows endogenous GnRH to be released, stimulating the release of FSH and LH from anterior lobe of pituitary
due to an abnormally high number of follicles that are selected followed by ovilation
oocyte maturation is not limited to the follicular phase, but occurs throughout the lifetime of the female conceptus
four phases of oocyte maturation
resumption of meiosis
cytoplasmic growth
nuclear arrest (dicytotene)
mitotic division of primordial germ cells (prenatal)
oocyte growth involves formation of a large cytoplasm and the zona pellucida
some primary oocytes begin to accumulate larger volumes of cytoplasm
juctional complexes
gap junctions
help with cell contacts are important for communications
mediated primarly by granulosal cell of the follicle
final maturation of resumption of meiosis occur near the time of ovulation
nucelar arrest must be interrupted to permit final oocyte maturation
cAMP proposed as the primary inhibitor of meiotic from the cytoplasm of the oocyte, cAMP is no longer available to inhibit the oocyte
oocyte meiotic inhibitor (OMI)
controlling the resumption of meiosis, but this substance has not been purified and its exact role remains uncertain
once inhibitors have been removed oocyte is free to proceed with the first miotic division