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Tonic center
continuous pulsatile releases of hormone from hypothalamus
Surge center
hormones released all at once from hypothalamus
not developed in male
Adenohypophysis (anterior pituitary)
hormones released from hypothalamus into portal system
Neurohypophysis (posterior pituitary)
neuropeptides travel along neurons, released directly into capillaries
Protein hormones
bind to membrane receptors on outside of cell & activate signaling cascade
ex: GnRH, LH, FSH, PRL, oxytocin
Steroid hormones
directly cross plasma membrane to bind nuclear receptors & activate transcription
derived from cholesterol, final form determined by packaging of enzymes
metabolized by liver, excreted in urine or feces
ex: progesterone, estradiol, testosterone
HPG in male
GnRH stimulate LH + FSH
LH stimulates Leydig cells to produce testosterone
testosterone gives negative feedback to LH via blood & supports spermatogenesis in Sertoli cells
FSH stimulates Sertoli cells to mature sperm & produce ABP + inhibin
ABP secreted into lumen of seminiferous tubules & concentrates testosterone
inhibin gives negative feedback to FSH via blood
HPG in female
follicular phase: FSH + LH stimulate pre-ovulatory follicles to produce estradiol
high estradiol triggers LH surge, causing ovulation
luteal phase: FSH + LH stimulate corpus luteum to produce progesterone
progesterone gives negative feedback to GnRH + LH
LH stimulates theca cells to produce androgens, which diffuse into granulosa cells
FSH stimulates conversion of androgens to estradiol & secretion of inhibin (negative feedback to FSH)
estradiol has positive feedback effect w/low progesterone, negative feedback w/high progesterone
Y chromosome
smallest chromosome, dozens of genes
SRY required for male development, encodes testis determining factor
Genital ducts
paramesonephric/Mullerian = female
fallopian tubes, uterus, cervix, cranial vagina
mesonephric/Wolffian = male
epididymis, ductus deferens, seminal vesicles, ejaculatory duct
differentiation requires hormones
anti-Mullerian hormone from Sertoli cells
Wolffian duct regresses without testosterone
External genitalia differentiation (males)
testosterone in circulation converted to dihydrotestosterone in Anlage tissues
DHT stimulates tissues to develop
External genitalia differentiation (female)
differentiation occurs in absence of hormone but estrogen required to grow to normal size
exogenous androgens can cause masculinization
External genitalia features
genital tubercle = glans penis/clitoris
genital swelling = scrotum/labia majora
urethral folds = penile urethra + corpus spongiosum/labia minora
urogenital sinus = prostate gland/caudal vagina & vestibule
Sexual differentiation of brain
caused by estrogen
males have constant gonadotropin release, females have cyclic release
A-FetoProtein binds estradiol in female (can’t cross BBB), does not bind testosterone in males (can cross BBB)
testosterone converted to estradiol in brain by aromatase, surge center defeminized
Sperm capacitation
physiological changes spermatozoa must undergo to be able to penetrate & fertilize an egg
removal of adherent seminal plasma proteins
reorganization of plasma membrane lipids & proteins
influx of extracellular calcium
increased cAMP
decreased intracellular pH
occurs while in the female reproductive tract
display hyperactive motility, able to bind zona pellucida, & undergo acrosome reaction
Acrosome reaction
release of digestive enzymes that help sperm penetrate upon binding to zona pellucida
Oocyte maturation
nuclear & cytoplasmic maturational events that result in acquisition of capacity for fertilization & development
LH surge triggers meiosis resumption/nuclear maturation & cortical granule migration/cytoplasmic maturation
first polar body released
ovulation of secondary oocyte
Fertilization
union of two haploid gametes to form zygote-1, requires gamete transport to site of fertilization (ampulla of oviduct)
secondary binding of sperm activates oocyte to resume meiosis & release second polar body
male & female pronucleus form, fuse, & start mitotic divisions
Steps of fertilization
capacitated sperm bind zona pellucida (primary) & undergo acrosome reaction
sperm penetrates zona pellucida into perivitelline space
sperm bind to ooplasma (secondary)
secondary binding induces meiosis resumption & cortical granule exocytosis
cortical granules harden zona pellucida & block polyspermy
Polyestrus
come into heat every 21-28 days
ex: cattle, pigs, rodents
Seasonally polyestrus
come into heat every 21-28 days during a specific season
based on photoperiod
ex: horses, goats, sheep
Photoperiod
pineal gland makes more melatonin during dark periods
melatonin promotes or inhibits reproduction
long day breeder: melatonin inhibits cyclcity (GnRH)
short day breeder: melatonin promotes cyclicity (GnRH)
Monoestrus
come into heat once a year
ex: dog, wolves, bears
Follicular phase (estrus)
20% of cycle, follicles are dominant ovarian structure, ends with ovulation
primary hormone is estradiol
GnRH causes release of LH + FSH (primarily FSH), which causes follicle to start growing & releasing estradiol
estradiol has positive feedback on FSH
inhibin released when follicle reaches dominance to suppress FSH & allow LH surge
dominant follicles acquire receptor for LH
theca cells secrete testosterone, converted to estradiol in granulosa cells, stimulates heat
standing heat, sexually receptive
Proestrus
transition from period of progesterone dominance to period of estrogen dominance
Estrus
period of sexual receptivity & mating
Metestrus
transition from estrogen dominance to progesterone dominance
Diestrus
period of maximal luteal function
Anestrus
condition when female no longer exhibits regular cycles
ex: pregnancy, lactation, presence of offspring, season, stress, disease
Luteal phase (diestrus)
80% of estrus cycle, period from ovulation to corpus luteum regression
primary hormone is progesterone from large + small luteal cells, blocks hormonal cascade
if pregnancy doesn’t occur, prostaglandin lyses corpus luteum & continues cyclicity
Ovulation
occurs due to LH surge
basement membrane of follicle ruptures and creates corpus hemorrhagica
theca cells become small luteal cells, granulosa cells become large luteal cells