Knockdown of Gonadotropin-Releasing Hormone II Receptor Impairs Ovulation Rate, Corpus Luteum Development, and Progesterone Production in Gilts.

Abstract

Reproduction is classically controlled by gonadotropin-releasing hormone (GnRH-I) and its receptor (GnRHR-I) within the brain. In pigs, a second form (GnRH-II) and its specific receptor (GnRHR-II) are also produced, with greater abundance in peripheral vs. central reproductive tissues. The binding of GnRH-II to GnRHR-II has been implicated in the autocrine/paracrine regulation of gonadal steroidogenesis rather than gonadotropin secretion. Blood samples were collected from transgenic gilts, with the ubiquitous knockdown of GnRHR-II (GnRHR-II KD; n = 8) and littermate controls (n = 7) at the onset of estrus (follicular) and 10 days later (luteal); serum concentrations of 16 steroid hormones were quantified by high-performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS). Upon euthanasia, ovarian weight (OWT), ovulation rate (OR), and the weight of each excised Corpus luteum (CLWT) were recorded; HPLC-MS/MS was performed on CL homogenates. During the luteal phase, serum progesterone concentration was reduced by 18% in GnRHR-II KD versus control gilts (p = 0.0329). Age and weight at puberty, estrous cycle length, and OWT were similar between lines (p > 0.05). Interestingly, OR was reduced (p = 0.0123), and total CLWT tended to be reduced (p = 0.0958) in GnRHR-II KD compared with control females. Luteal cells in CL sections from GnRHR-II KD gilts were hypotrophic (p < 0.0001). Therefore, GnRH-II and its receptor may help regulate OR, CL development, and progesterone production in gilts.