Gonadotrophin Releasing Hormone (GnRH), Lutenizing hormone (LH), Follicle Stimulating Hormone (FSH)

The fluid filled space called the Antrum begins to form in tertiary follicles.

Rapid transport phase and sustained transport phase. Sustained transport phase will succeed at fertilizing the oocyte.

Yolk sac, amnion, chorion, and allantois.
The chorion and allantois fuse into the chorioallantois or allantochorion.
These 4 fetal membranes connect to the embryo proper and subsequently, the fetus via the umbilical cord.

Protein, minerals, vitamins, and immunoglobulins. Serves as the child's "first" immunization.

Lutenizing Hormone

Progesterone is needed to maintain pregnancy and if lost, it induces abortion or starts parturition.

The testes shrink, there will be no spermatogenesis, leydig cells will deteriorate (decreasing testosterone production), and testosterone output falls.

Muscle cells contract and shorten but do not regain their original length and relaxation. These muscles go from long thin uterine muscle cells and contract into short fat muscle cells. • They’ll biochemically relax but morphologically remain contracted. In subsequent contractions, they’ll continuously get shorter and fatter, pulling back muscle layers at the point of the cervix this is why contractions are painful.

Mammogenesis: development of mammary tissue
Lactogenesis: onset of milk secretion
Galactopoesis: maintenance of lactation - continual milk production and requires removal of milk from breast.

1. Stimulate grown and activity of mammary gland and endometrium.
2. Prepare uterus for spermatozoal transport by increasing contractile activity of the uterus (OPPOSITE OF PROGESTERONE)
3. Prepare endometrium for progestagen action (induce progesterone receptors)
4. Increase vascular permeability and tissue edema
5. Regulate secretion of gonadotrophins (negative and positive feedback).
6. Associated with sexual behavior in some species.
7. Stimulate secondary sex characters of females.

Nurtures the fetus by acting as an attachment site for the placenta. The caruncles attach to the fetal cotyledons which transmit fetal blood to mom and allow exchange of oxygen and nutrients with mom.

If you take testosterone to bulk up, you’ll down-regulate your levels of GnRH, which stops the pituitary gland from functioning. This will stop Leydig cells from producing their own testosterone and stops spermatogenesis, causing cells of testes to shrivel.
If testosterone can’t be produced, dihydrotestosterone can’t

1. The fetus pushes down on the cervix
2. Mechanoreceptors detect pushing of fetus on cervix and these receptors are stimulated to send a signal to the hypothalamus.
3. Hypothalamus releases oxytocin.
4. Oxytocin travels down via neurons into the posterior pituitary, where it enters the blood.
5. Oxytocin enters the blood and it’s transported from the posterior pituitary gland down into the myometrial muscles to lower the excitation threshold, causing a contraction. This contraction stimulates the fetus to push down more on the cervix, releasing more oxytocin and causing a positive feedback loop.

Lactogenesis is triggered following the expulsion of the placenta by a fall in progesterone and estrogen levels and continued presence of prolactin.

1. Induce and maintain differentiation of male somatic tissues (Induce secondary sex characters of males (deep voice, body hair, penile growth) and body hair of females; Induce and maintain some secondary sex characters of males (accessory sex organs))
2. Promote protein anabolism/ metabolism and somatic growth
3. Support spermatogenesis.
4. Influence sexual and aggressive behavior.
5. Regulate secretion of gonadotrophins (testosterone).

1. Capture and transport of oocytes and convey sperm in ascent (make way up through vagina).
2. Site of fertilization (ampulla-isthmus junction).
3. Nutrition of gametes and zygotes.
4. Timed transport of developing zygote in uterus.

Capacitation: takes place in the uterus
Hyperactivation: takes place in the oviduct
Acrosome Reaction: takes place in the oviduct

1. Exchange nutrients and waste
2. Changes metabolism of mother
3. Protection from trauma and teratogens (chemicals)
4. Immunological protection
5. Hormone secretion
6. Influence developmental vital organs

Entry via 2 external pudic arteries, which branch into the caudal mammary artery and the cranial mammary artery.
Branched from the aorta.

Exit: external pudic veins - when animal is sitting; SQ abdominal veins when animal is standing.
Both drain blood back to the heart

1. Budding: an offspring grows out of the body of the parent. Ex: Hydra genus (brine shrimp)
2. Gemmules (internal buds): a parent releases a specialized mass of cells that can develop into an offspring. Ex: sponges
3. Fragmentation: the body of the parent breaks into distinct pieces, each with can produce and offspring. Ex: flatworms.
4. Regeneration: if a piece of a parent is detached, it can grow and develop into a completely new individual. Ex: echinoderms, such as starfish, sea urchin.

1. Proestrus - estrogen dominant phase
2. Estrus - estrogen dominant phase (secondarily, LH will surge due to positive feedback from estradiol)
3. Metestrus - progesterone becomes dominant hormone
4. Diestrus - progestrone is the dominant hormone.

Spermatogenesis consists of 3 stages:
1. Mitotic proliferation: takes immature gonocytes sitting on the basement membrane of the seminiferous tubule and making them undergo multiple rounds of mitosis, causing proliferation.
-This produces large number of cells (spermatogonia).
-Developing sperm produced by proliferation. At this stage, they’re genetically identical but are also all diploid (consisting of same chromosomes).
-The sperm are genetically and morphologically immature.
2. Meiotic division: this occurs in 2 rounds.
-Generates genetic diversity (chromatids exchange genetic material)
-The chromosome number splits in half haploid.
-Spermatocytes become spermatids (haploid).
3. Cytodifferentiation (spermiogenesis)
-Packages genes for delivery to oocyte.
-Elongating round spermatids into spermatozoa (with tails).

1. Primary uterine inertia
-Failure to initiate contractions at start of parturition.
-Lack of oxytocin/ lack of oxytocin receptors in uterus
-Lack of induction of contractions by a small fetus. (a small fetus isn’t pressing down on the cervix and not producing those signs to produce the oxytocin in the first place via Fergusson reflex).

2. Secondary uterine inertia
Good uterine contractions at start of parturition
-Large size of fetus or multiple lambs and prolonged labor.
-Dystocia (obstructed labor) due to abnormal fetal presentation.
-Uterus fatigue and overstretched – contraction stop

Oxytocin is used to stimulate uterine contractions if they are weak, absent, or if they stop.

MER is sometimes called “let – down”. It’s the reflex that causes the alveoli to release the milk they have made.

1. When a newborn suckles, a neural pulse travels through neural loop into the hypothalamus. Hypothalamus produces oxytocin.
2. Nerve cells transfer oxytocin to the posterior pituitary gland for release into the circulation.
3. Oxytocin causes smooth muscle cells (myoepithelia) to contract, pushing the milk into ducts.