Abstract
Regulation of steroid production by the corpus luteum (CL) is largely dependent on pituitary-derived LH acting through the cAMP/protein kinase A (PKA) pathway. Administration of GnRH antagonist, which binds in a competitive manner to the GnRH receptor, results in the acute suppression of gonadotrophin secretion, particularly LH. We recently demonstrated in vivo (JCEM, 88,3421yr–30, 2003) that GnRH antagonist administration in the mid-luteal phase dramatically reduces the plasma level of P4 within 4 h and the expression of the Steroidogenic Acute regulatory protein (StAR) 24 h after administration, respectively.
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