• Decapeptide.
• Released from the hypothalamus.
• Estrogen surge causes its release.
• Currently thought to cause the release of the both gonadotropins, Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH), but there may actually be an LH releasing hormone (LHRH) and an FSH releasing hormone FSHRH.

• Gonadotropins (they affect the gonads - 'trope the gonads').
• Released from same cells in anterior pituitary (may even be in the same granules within the cell).
• Glycoprotein structure (carbohydrate and protein). This means they are antigenic and will degrade.
  • Structure: 2 subunits
    •  Alpha - same within species i.e. LH, FSH, TSH have same alpha unit within a species.
    •  Beta - same between species i.e. LH in all species have same beta unit.
• Mechanism of action: 
  • Bind cell membrane and cause cAMP production
  • Causes phosphorylation in cell. 
  • Fast action results.

• Causes growth of follicles past antral stage.
• Causes stimulation of granulosa cells in the ovary.
• Stimulates establishment of LH receptors on granulosa cells.
• Suppressed by inhibin which is produced by the large follicles.
• The pulse frequency probably initiates subsequent events in the cycle.
• Half life of 60 minutes
• Secreted at same time as LH, but other peaks during cycle may choose follicle for next cycle in polyestrous species.

• Binds to receptor on follicles and corpus luteum.
• Causes ovulation and luteinization of follicle about 24-48 hrs after release. (May cause ovulation by causing collagenase release that breaks down the follicle and then stimulates progesterone release to actually cause ovulation.)
• Stimulates progesterone production by corpus luteum.
• Half life 22 minutes.
• Involved in puberty and seasonal cyclicity.
  • Anestrus - hi freq., low amp.
  • Cycling - hi amp., lo freq.
• Inhibited by low concentrations of estrogens and progesterone during diestrus.
• hCG (Human Chorionic Gonadotropin) has similar action and is used clinically to induce ovulation in mares.

• Basic steroid ring
• Non-antigenic
• Two cell steroid production theory: 
  • Cholesterol to androstenedione in thecal cell
  • Transfer to granulosa cell. 

• Androstenedione to estradiol in granulosa cell.

• Mechanism of action:
  • Bind cytosol receptor. 
  • Transferred to nucleus. 
  • mRNA produced . 
  • Changes cellular machinery. 
  • A slower process than gonadotropins.

• Oocyte is arrested at the end of prophase in meiosis.
• LH is needed to restart oocyte development.
• FSH starts follicular growth past antral stage.

• From granulosa cells in follicles.
• Causes LH and FSH surges via GnRH release.
• 'Primes' uterus.
• Causes estrous behavior.

• From the ovulated follicle.
• Composed of transformed thecal cells and granulosa cells.
  • Thecal cells become small luteal cells.
  • Granulosa cells become large luteal cells.
• Produces progesterone.

• Steroid.
• Two compartment theory of production.
• Stimulate uterine secretions.
• Stimulates estrogen receptors
• Inhibit uterine motility
• Decrease uterine immunity
• Inhibit LH and FSH
• Needed to maintain pregnancy

• Peptide produced by granulosa cells in growing follicle.
• Inhibits FSH release and possibly FSH binding to granulosa cells.
  • Alpha-1 + beta-A or beta - B - inhibits FSH.
  • Beta -A + beta-B cause FSH stimulation.

• Mostly released from posterior pituitary.
• Causes uterine contractions.
• Released from bovine corpus luteum.
• Causes prostaglandin release and luteolysis.

• 20 carbon acid.
• Secreted by uterus in some animals to cause luteolysis.