Flashcards in Reproduction (Day 1) Deck (75):
What are the two types of cells?
Germ Cells: ova, sperm
Somatic Cells: everything else
What causes most growth and development?
large numbers of gametes produced continuously from stem cells
begins at puberty until senescence (lowered testosterone production)
release only one gamete at a time from a limited pool of preformed gametes
process repeated at regular monthly intervals
begins in utero - mitotic divisions to increase germ cell number (pauses at birth, resumes at puberty)
timing varies by gender
a. Toward end of gestation, female’s oogonia begin meiosis to produce primary oocytes.
b. The ovaries of a newborn girl have 2 million primary oocytes.
c. By puberty, this number is cut to about 400,000.
d. Only about 400 of these will be ovulated in her lifetime.
Primary oocytes contained within primary follicles--have one layer of cells
a) In response to FSH, some of the primary follicles grow to produce many layers of granulosa cells.
b) Some develop fluid-filled vesicles called secondary follicles.
Continued growth results in fused vesicles to form a single antrum; this is a mature Graafian follicle.
As Graafian follicle grows, the primary oocyte finishes meiosis I to become secondary oocyte (plus a polar body, which soon degenerates).
The secondary oocyte begins meiosis II, but stops at metaphase II.
Meiosis II will complete, only if there is fertilization of the ovum.
Sex determination in embryo
Sperm determines genetic sex of zygote
If zygote contains a Y chromosome....
even if multiple X's
If zygote gets only Y, but no X...
--> lethal (X chromosome is vital for survival)
X-inactivation in females
early in development, after ovaries develop, one X in each body cell inactivates, becomes Barr body
— inactivation is random—some may be sperm-derived, others may be ovum-derived
In a Barr Body: female gets rid of one of X chromosomes so that only one is viable in gametes
—random inactivation of one of the X chromosomes
Chromosomal sex & development of embryonic gonads
Genetic sex is detained by which sex chromosome is carried by the sperm
Key gene (SRY/TDF) is carried on Y chromosome
-if sperm contributes Y: SRY expression stimulates tests differentiation
-if sperm contributes X: lack of SRY allows ovary differentiation
Sex Determining Region
(aka TDF - Testis Determining Region)
no SRY = female
SRY = male
Sex differentiation in early development: internal organs
Regardless of genetic sex, embryo has potential to become phenotypically male or female—female pattern occurs unless humoral signals are released from fetal testis
-Depends upon presence of SRY gene on Y chromosome
If female --> no SRY expression, biopotential gonads --> ovaries
If male --> SRY expression elicits gonads --> testes
Testes produce masculinization factors (testosterone, anti-Müllerian hormone [AMH]
What is required for male external genitalia?
SRY and production of dihydrotestosterone
--> NOT testosterone (which is not produced until testes differentiate)
-due to testosterone
-converted to DHT (dihydroxytestosterone)
-changes occur in brain development
From birth to puberty— period of reproductive senescence
-testes stop producing testosterone by 3rd trimester, ovaries don't produce embryonic sex hormone
-sex hormone secretion does not resume until gonads are stimulated at puberty
-onset of puberty: anterior pituitary begins releasing gonadotropic hormones
Onset of Puberty
-secretion of FSH and LH elevated at birth/stays high for first 6 mo. --> declines to almost 0 until puberty
-puberty begins w/release of LH (pulsatile)
--results in increase in testosterone or estradiol-17 secretion
--these hormones produce secondary sex characteristics
maturation of hypothalamic-pitutacy axis: seems to be associated w/childhood nutrition, age of menarche has decreased in Western societies as energy intake has increased
-pulsatile secretion of GnRH increases --> secretion of LH, FSH
-as energy intake increases --> increased storage of TG in adipose --> increased leptin secretion
Age of the onset of puberty
-depends on activity level/amount of body fat
-leptin secreted by adipose cells: required for onset
-exercise may inhibit GnRH secretion (ex. more active, slimmer girls begin puberty later)
What are the three effects of FSH and LH (produced in the anterior pituitary glands)?
1. stim of spermatogenesis or oogenesis
2. stim of gonadal hormone secretion
3. maintenance of the structures of the gonads
Interaction between hypothalamus, anterior pituitary, and gonads
Release of FSH and LH controlled by the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus.
Regulated by negative-feedback loop where rising levels of gonadal hormone:
1) Inhibit GnRH release
2) Inhibit pituitary response to GnRH
Hormonal Control of Hypothalamus
-GnRH release is pulsatile in both genders (every 1-3 hours): necessary for optimal pituitary sensitivity to GnRH
-LH, FSH act via feedback inhibition on GnRH release
-release of LH, FSH stim by low levels of gonadal steroids (when steroids increase --> usually get feedback inhibition of LH/FSH)
-But if estrogen increases, you can get stim of gonadotropin (LH) release
Male Reproduction: gross anatomy
glands secrete fluids which lubricate tubular system and nutrients (ex. fructose) to support energy usage by sperm
fluid from seminal vesicles constitutes for about 70% of total semen volume
placement of testis outside of abdominal cavity maintains lower temp (necessary for sperm development)
Testis: Duct of Epididymidis
site of maturation and storage of sperm
FSH receptors (on sertoli cells)
Testis: Seminiferous Tubule
site of sperm production
Testis: smooth muscle contraction
during arousal/ejaculation, contraction of smooth muscles around epidermal duct advance sperm --> vas deferent --> urethra
produce/secrete testosterone in response to LH
active in fetus --> virtually disappear after first 6 mo. until puberty
regulation of sperm development
secrete proteins necessary for sperm development (ex. androgen-binding protein) in response to FSH and testosterone
--> sperm don't have receptors for testosterone (sertoli cells do)
Hormonal Control of Spermatogenesis
-neg feedback effects of testosterone and inhibin maintain relatively consistent secretion of gndtrpns in male
-andrgn secretion decreases slowly in females to hypogonadal state by age 70
-other factors affecting testosterone secretion: physical inactivity, obesity, drugs
partially wrap around ovaries, catch oocyte after ovulation
ciliary action moves egg from ovary toward uterus
dysfunction --> infertility or ectopic pregnancy
normal site of implantation and development of fertilized egg
cervical canal lined with mucus-secreting cells
mucus moms a protective barrier between vagina/uterus
innermost tissue layer of uterus
epithelial thickness and character vary during menstrual cycle: cells progress through monthly cycles of proliferative, secretory, and menses phases coinciding w/ovarian cycle
middle muscle later of uterus
contracts to expel baby at birth
outer connective tissue layer
Follicular Development: Ovarian Cycle
follicle developing under influence of steadily rising levels of estrogen
if no pregnancy, corpus luteum degenerates and cycle resumes
when estrogen levels peak --> induces a surge of LH which induces ovulation
remnant of ruptured follicle - secretes hormones which help prepare for pregnancy
survives only 12 days
What happens if fertilization doesn't occur?
-CL survives 12 days
-no preg: CL undergoes apoptosis (inactive "corpus albicans")
-as luteal cells die, secretion of estrogen/progesterone decrease
-as progesterone levels decrease, blood supply to endometrium is compromised and surface epithelium begins to die
-2 days after CL dies, endometrium begins to slough its surface layer (menstruation)
-as steroids decrease, neg feedback on hypos, pituitary, so GnRH --> FSH, LH increase
Follicular Phase: early
-follicular development begins under influence of FSH
-as follicles mature, FSH/LH stimulate granulose cells an thecal cells to produce androgens
---Granulosa Cells also produce AMH which limits number of follicles developing at a time by decreasing their sensitivity to FSH
---Thecal Cells synthesize androgens --> diffuse to granolas cells --> convert androgens --> estrogens
Follicular Phase: mid-late
-at same time, estrogen stimulates it's own production by granulose cells
-menstruation ends during early phase
-in response to rising estrogen, new endometrium begins to grow (increased cell number, enhanced blood supply)
-as follicles enlarge, granulose cells secrete fluid that collects in a cavity in the follicle (antrum). fluid contains factors ended for ovulation
-Ovarian estrogen rises to a peak, it's effect now changes to strong stimulatory effect on GnRH --> FSH, LH (huge surge of LH)
-increased estrogen also stimulates growth of endometrium to max thickness
-mature follicle secretes enzymes which break down ECM holding follicular cells together
--> breakdown products induce inflammatory response - neutrophils secrete prostaglandins --> interaction of smooth muscle in outer thecal layer, rupturing follicle wall --> egg is extruded
Post-Ovulatory (Luteal) Phase
-LH surge also causes remaining thecal and granulose cells to migrate into antrum --> transform into luteal cells (remaining structure = corpus luteum)
-CL secretes estrogen, increased progesterone and inhibit - neg feedback on hypothalamus and pituitary (gonadotropin secretion shut down)
-progesterone promotes further development of endometrium to support pregnancy, also promotes thickening of cervical mucus to protect uterus
-progesterone elicits increase in basal body temp which lasts until onset of menstruation
sexual response varies between genders/individuals
increased muscle tone
vasocongestion of sexual organs
contraction of uterus/vagina and male ejaculatory organs
body returns to pre-excitation condition
--> men experience refractory period: unable to ejaculate
Process of an erection
activated Ca channels stimulate s.m. contraction --> vasoconstriction --> NO erection
blocked Ca entry promotes s.m. relaxation --> vasodilation --> erection
-vas deference cut and tied to prohibit sperm transport
-does not affect testosterone production or ejaculation
-suppressing gonadotropin secretion
-gossypol: interferes w/sperm production
-includes synthetic estradiol and progesterone
-acts like prolonged luteal phase
-produces neg feedback inhibition of GnRH --> no ovulation
-endometrium still proliferates
-placebo pills taken for 1 week to allow menstruation
-newer pills have reduced risk for endometrial and ovarian cancers and reduction of osteoporosis
How long is the egg viable after ovulation?
how long does sperm survive in female reproductive tract?
How many sperm enter the female at ejaculaton?
-only about 100 live to enter fallopian tube
-sperm MUST be capacitated (takes at least 7 hrs)
--> pH increases, hyper activation of the flagellum
-capacitated sperm guided to the oocyte by chemotaxis and thermotaxis
Where does fertilization occur?
in distal part of fallopian tube
sperm penetrates outer layers via enzymatically-mediated acrosomal reaction
When sperm enters the oocytes, Ca is released from ER
-Ca wave travels through oocyte to oppose side from entry of sperm
-Ca has several effects:
1. prevents other sperm from entering the oocyte (polyspermy)
2. activates oocyte to finish meiosis to become haploid ovum
12 hours after sperm enters oocyte, the nuclear envelope around the ovum disappears and chromosomes join to form a diploid zygote
-monozygotic twins: single ovum splits
-disygotic twins: 2 eggs are fertilized by 2 sperm
-sperm contributes 1/2 chromosomes, centrosome
-egg contributes 1/2 chromosomes, cytoplasm, all other organelles
Why are mitochondria materially inherited?
autophagy is cellular process whereby worn-out/damaged proteins and organelles are degraded and their components recycled
there is a type of autophagy that is mitochondrial-specific: mitophagy
Zygote begins dividing in Fallopian tube....
implants in uterus as a blastocyst 7-10 days post-fertilization
--> high level sou progesterone limit muscular contractions, so movement through fallopian tube to uterus is slow
Cleavage begins 30-36 hours after fertilization
Division continues, forms hollow ball of cells (blastocyst)
1. inner cell mass --> fetus
2. trophoblast --> chorion --> placenta
6 days post-fertilization trophoblast cells secrete enzyme that allows blastocyst to "eat" into the endometrium
7-10 days blastocyst completely implanted
rapid mitosis, which forms ball of cells (morula), enters uterus about 3 days post-fertilization
portion of trophoblast layer which becomes embryonic portion of placenta
between 7-12 days, chorion splits into:
1. cytotrophoblast (inner)
2. syncytiotrophoblast (outer)
developing cytotrophoblast and inner cell mass separated by amniotic cavity
Extra embryonic Membrane
• Syncytiotrophoblast secretes protein-digesting enzymes and creates blood-filled cavities in endometrium.
• Cytotrophoblast sends villi into these pools of maternal blood, forming chorion frondosum.
• Placental structures are “immunologically privileged site”—barrier preventing direct contact between maternal blood and fetal antigens
• Fetal part of the blastocyst becomes:
-- Endoderm --> gut organs
-- Ectoderm --> skin & nervous system
• Mesoderm develops later --> muscles, bones & connective tissues
Placenta and Amniotic Sac Formation
As blastocyst develops, endometrium also changes to form decidua basalis
-this joins with the chorion frondosum to form placenta
Part of chorion envelops the growing embryo
1. fluid-filled space between becomes the amniotic sac
2. amniotic fluid comes from isotonic secretion, urine from fetus, and sloughed cells
Circulation of blood in placenta
• Umbilical arteries deliver fetal blood to placental vessels.
• Blood circulates within placenta & returns to fetus via umbilical vein.
• Maternal blood is also delivered to/from placenta.
• Thus, maternal and fetal blood do not mix; are separated by only two cell layers.
• Molecules (oxygen & nutrients) diffuse across tissues of the placenta for exchange, from maternal blood to fetal blood.
• Carbon dioxide and wastes diffuse from fetal blood to maternal blood.
• Placenta degrades maternal molecules that may harm fetus.
Human Chorionic Gonadotropin (hCG)
secreted from chorionic villi and placenta
-Binds to LH receptors on corpus luteum
-Maintains viability of C.L., which continues to produce progesterone
-By roughly 2-3 months, placenta takes over production of hormones
Progesterone: supports endometrium, inhibits uterine contractions
Estrogen: supports endometrium, development of milk glands
Human Placental Lactogen (hPL)
• Secreted by placenta in proportion to placental development
• Main function: induce metabolic shift in favor of fetus
• ↓ maternal insulin sensitivityà↑ maternal blood glucose
• ↓ maternal glucose utilization --> spares glucose for fetus
• ↑ lipolysis --> ↑ FFA for use by mother; glucose and ketone bodies used by fetus
**Supports fetal nutrition even under conditions of maternal malnutrition
Labor and Delivery
• Precise initial trigger not clear, but probably due to combination of various factors:
--secretion of CRH by placenta --> uterine production of prostaglandins -->
--stretch of cervix induced by baby’s head --> central reflex --> oxytocin
secretion --> uterine contractions
--decrease of progesterone secretion by placenta --> removes inhibition of uterine contractions
Mammary Gland Structure and Lactation
-composed of 15-20 lobes separated by adipose tissue
-each lobe made up of lobules composed of glandular alveoli that secrete milk
Milk: secondary tubule --> mammary ducts --> lactiferous duct --> nipple
-during pregnancy cortisol, thyroxine, and insulin make mammary glands more sensitive to rising progesterone/estradiol (progesterone --> alveoli growth, estradiol --> tubule/duct growth)
Control of lactation
-prolactin from pituitary gland --> production of milk proteins, casein, and lactalbumin
-prolactin is inhibited by PIH (dopamine) from pituitary, but stimulated by estradiol secretion
-->when placenta is shed at birth, estradiol levels drop lifting inhibition on prolactin
What does the hypothalamus control?
1. posterior pituitary --> oxytocin --> milk ejection
2. anterior pituitary --> prolactin --> milk production
Breast Feeding and Immunity
-IgG antibodies are passed from mom --> baby in utero
-IgA antibodies are passed to baby in breast milk
1. provide passive immunity for first months
2. also promotes development of baby's own active immunity
-cessation of reproduction-competetent phase of life: ovulation, menstrual cycles taper off
-appears to be due to development of insensitivity to FSH, LH in ovaries --> decreased production of estrogen
Symptoms of menopause
Due to lack of estradiol
-hot flashes: by vasomotor disturbances
-walls of urethra/vagina atrophy, and vaginal glands no longer produce lubrication
-after menopause, risk for atherosclerosis/osteoporosis increase
--> estradiol needed for bone deposition (increased risk for osteoporosis...)
--> adipose tissue does make a weak form of estradiol called estrone (heaver women have reduced risk of osteoporosis)