Effects of gonadotropin-releasing hormone agonist and antagonist on ovarian activity in a mouse model for polycystic ovary

PCOS is a major cause of anovulatory infertility in women in their reproductive age. However, its etiology and pathophysiology remain uncertain. The immature mice chronically injected with DHEA, termed as PCO-mice, develop numerous large cystic follicles, high circulating androgen and anovulation similar to PCOS in women. Although PCO-mice show decreased ovarian GnRH I-receptor in immunoblot but show increased immunostaining for GnRH I-receptor in oocytes of cystic follicles. PCO-mice show reduced ovarian LH receptor expression, circulating estradiol and progesterone level compared to normal mice injected with vehicle only. The treatment with low dose of GnRH-Agonist in PCO-mice restores ovarian LH receptor expression to the level of normal mice and promote ovulation and formation of functional corpus luteum. GnRH-Antagonist although cause ovulation in PCO-mice but does not restore LH receptor expression to the level of normal mice, and they show low circulating progesterone and hypertrophied vacuolated corpus luteum. Our study suggests that GnRH-agonist restores ovulation in PCO-mice and produces biphasic and beneficial effect over the use of GnRH-Antagonist.