Abstract
This experiment was designed to study the effects of different doses and different patterns of change in circulating concentrations of oestradiol on the genesis of the surge release of luteinising hormone (LH) and follicle stimulating hormone (FSH), following progesterone withdrawal, in oestradiol and progesterone treated, long-term ovariectomised ewes. During the breeding season, 60 long-term ovariectomised ewes received progesterone releasing implants on Days 0, 2, 4, 6 and 10 of the study; two, one and two implants were then removed at 09:00 h and 21:00 h on Day 11 and 09:00 h on Day 12, respectively. The ewes were also fitted with 0.5 cm or 6.0 cm oestradiol releasing implants for the duration of the study. The temporal profile of serum concentrations of progesterone closely resembled that of the luteal phase of the oestrous cycle of an intact ewe. With progesterone removal, several supplementary oestradiol treatments were applied, resulting in peak serum concentrations of oestradiol similar to the luteal phase (basal) (6.6±1.2 pg ml −1), follicular phase (17.54±2.6 pg ml −1), or up to two times the peak follicular phase level seen in intact cyclic ewes. The mode of delivery of oestradiol varied from an additional implant or injection (i.m.), to intravenous infusion with increasing doses of oestradiol. Following progesterone withdrawal, gonadotrophin surges were observed in some, but not all of the ewes when serum concentrations of oestradiol were in the follicular phase range. No surges were seen when serum oestradiol concentrations were in the basal range. The pattern of increase in oestradiol following withdrawal of progesterone did not appear critical. Treatments resulting in constant high levels of oestradiol after progesterone withdrawal consistently elicited gonadotrophin surges, but the surge amplitudes were not as high as those resulting from rising serum concentrations of oestradiol. Peak serum oestradiol concentrations (28.7±2.9 pg ml −1) in excess of follicular phase concentrations consistently resulted in surges, increased LH (but not FSH) surge amplitude and decreased latency to the LH surge. Peak serum concentration of oestradiol of 36.4±4.1 pg ml −1 consistently resulted in surges but depressed LH and FSH surge amplitudes. Induction of FSH surges appeared to be less responsive to oestradiol than the induction of LH surges.
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