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Final

11:067:327 Study Guide - Final Guide: Vas Deferens, Bicornuate Uterus, Zona Pellucida


Department
Animal Science
Course Code
11:067:327
Professor
T Roepke
Study Guide
Final

This preview shows pages 1-3. to view the full 13 pages of the document.
Leydig cells- produce testosterone
Sertoli cells- forms blood testis barrier
Smooth muscle cells- move spermatozoa
Short cells- absorb water
Spermatic cord- cremaster muscle, ductus deferens, pampiniform plexus,
testicular artery
Testicular tubules house sertoli cells and all germ cells
Efferent ducts→ epididymis→ ductus deferens→ ampulla→ urethra
Loss of tubule immune privilege(blood/testis barrier) results in loss of meiotic and
post-meiotic germ cells
Loss of hormone signaling results in loss of post-meiotic germ cells
Caput – sperm membrane modification
Corpus- able to swim
Cauda – gain fertilization (capacitation) ability
Pampiniform plexus and scrotum- temperature control of testis
Loss of temp homeostasis results in loss of all germ cells
Efferent ducts- concentration of spermatozoa
Testis- site of gamete and hormone production
Theriogenology- study of agricultural animal repro organs
The secretory layer of the uterine wall is the endometrium.
Medulla doesn’t have CL
Avian birds- fertilization occurs in infundibulum- no CL
Primordial follicles- most immature, squamous cells, stimulate cell division in
genital ridge
Primary follicles- growing pool, cuboidal cells
Secondary follicles- zona pellucida, no antrum
tertiary/antral- theca externa and interna
Granulosa cells direct oocyte development, are avascular, and perform
steroidogenesis
Mesometrium provides connective tissue support for the uterus
ampulla→ ciliated columnar
Isthmus- nonciliated columnar
Duplex uterus
2 everything, no uterine body- marsupials, forked penis
2 cervix and uterine horn, 1 vagina- rabbits
Bicornuate uterus-
2 uterine horns
Small uterine body- poor to moderately formed
Highly developed- bitch, queen, sow

Only pages 1-3 are available for preview. Some parts have been intentionally blurred.

1 cervix
Peritoneum- lines abdominal cavity, forms broad ligaments which houses
vascular supply and nerves
Avain oocyte- germinal disk(sperm enters), yolk(energy) and vitelline
membrane(zona pellucida)
Mesoderm- gonads
Anterior pituitary- derived from ectoderm in roof of the mouth, rathke’s pouch
Roof of mouth, releasing hormone
Posterior pituitary- from neural tissue, goes towards embryonic mouth, turkish
saddle protects
Comes from brain
In the absence of AMH, the paramesonepheric ducts form the structures of the
female reproductive system
In a male insulin-like factor 3 ‘knock out’ mouse, predict the phenotype- The mice
will be bilaterally cryptorchid
Add sugar or sulfate to steroids to make it water soluble and get discarded
LH- Leydig , FSH- sertoli
RU-486 binds to progesterone receptor and prevents it from binding→ no
pregnancy
Plan B- prevents ovulation in negative feedback
Surge center- MPOA/AVPV
Flush gnrh leading to ovulation
Positive feedback
High E2
End with ovulation and begin with regress of corpus luteum
Tonic center- Arc/VMH
Bleap of gnrh
Negative feedback
High P4
Kisspeptin don’t control release of anything in both negative and positive
feedback
Steroid hormones- growth and control of repro
Prostaglandin have shortest half life
Posterior pituitary don’t produce any hormones!!!!!!! Oxytocin from hypothalamus
Hormonal control- slower acting and longer duration
FSH bind to membrane receptor- Gs-Adenylate cyclase-cAMP production
Suckling reflex- oxytocin
Releasing hormones are produced in the hypothalamus and target the anterior
pituitary

Only pages 1-3 are available for preview. Some parts have been intentionally blurred.

Prostaglandin- contractions, follicle rupture at ovulation, luteolysis
Inhibin suppress FSH!!!
The pattern of steroid hormone secretion observed during negative feedback
control of GnRH is sustained
Male brain→ aromatase estrogen into testosterone→ no surge center
Before puberty, gnrh amplitude and frequency same in male and female
After puberty, female high amplitude in surge center
After puberty, males high frequency in tonic
Fatty acids and leptin positively control pulsatile GNRH - surge - estrogen
Hypothalamus is the limiting factor
Proestrus- estradiol starts to increase
Ewe- seasonally polyestrous- short days
Difference b/w long day and short day seasonal breeders is how kisspeptin
respond to RFRP-3
Rats and mice don’t have metestrus phase
Silent ovulation→ progesterone primes brain for estrogen to facilitate estrous
behavior
No CL without ovulation
Follicular phase→ estrogen
Luteal phase→ P4
LH surge induces ovulation
One month after “surgical menopause”- elevated LH, FSH, low E2 and P4
One month after oral contraception- low LH, FSH and inihin but high E2 and P4
FSH- follicular recruitment
LH- follicular dominance
In antral follicle, granulosa cells produce estradiol in response to FSH binding to
membrane receptor
Menopause- ovarian follicles depleted
Ecg- increase circulating estradiol levels
Spay-vac- target zona pellucida to block sperm binding and fertilization
Gonacon- triggers production of antibodies that bind to and inactivate GNRH
Induced ovulators need LH surge and mechanical stimulator
Block PGF2- no follicular pressure
EAZI-breed- leep P4 elevated and delay estrus
PKA-CAMP- signaling cascade that control P4 in luteal cells
Large luteal cells- granulosa- hypertrophy, oxytocin, relaxin
Small luteal cells- Theca interna- hyperplasia, P4
Mitochondria, cholesterol, protein kinase, camp
CL vigor- vascularization and number and volume of luteal cells
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