Suppression of ovarian activity in the gilt and reversal by exogenous gonadotrophin administration

The aim of the current experiment was to study the regulation of follicle development in the pig using a potent GnRH agonist (GnRH-A) to initially suppress follicle development. Large–White hybrid gilts (n=8) were treated during the luteal phase with GnRH-A. Four of these GnRH-A treated gilts and four control gilts were given a GnRH bolus on days 14 and 28 after GnRH-A administration or during the luteal phase in control gilts. Blood samples were collected for 10 h for FSH and LH, after which 1500 IU PMSG were administered and the ovaries and uteri recovered 72 h later. A further four GnRH-A treated gilts and four control gilts were slaughtered either 28 days after GnRH-A administration or during the luteal phase respectively, and all follicles ≥1 mm diameter were dissected. The mean basal plasma FSH level was lower (P<0.01) in GnRH-A treated than control gilts and showed no response to the GnRH challenge although levels increased (P<0.01) in control gilts. The mean basal plasma LH levels were similar (P>0.1) in GnRH-A treated and control gilts. Whilst in GnRH-A treated gilts plasma LH levels showed no response to the GnRH challenge, plasma LH levels were increased (P<0.01) in control gilts. Pulsatile LH secretion was abolished in GnRH-A treated but not in control gilts. Plasma oestradiol levels were lower (P<0.001) in GnRH-A treated gilts than in control gilts, but nevertheless both GnRH-A treated and control gilts responded to PMSG with increased plasma oestradiol levels. Treatment with GnRH-A reduced both the mean (2.1 vs. 2.7 mm; P<0.01) and the maximal follicle diameter (4 vs. 6 mm) and reduced (P<0.01) the total number of follicles ≥2 mm diameter compared with control gilts. Administration of PMSG increased both mean follicle diameter (5.1 vs. 4.4 mm; P<0.01) and maximal follicle diameter (7 vs. 9 mm) and caused a reduction (P<0.001) in the total number of follicles ≥2 mm diameter in both GnRH-A treated and control gilts. In summary, this study has demonstrated, for the first time in the pig, that the inhibition of follicle development as a result of pituitary down regulation/desensitisation can be reversed by exogenous gonadotrophin treatment. This model will be a powerful tool with which to investigate the precise regulation of follicle development in the pig.