Abstract

We studied the relationship between progesterone (P 4) concentrations early in the estrus cycle and follicular dynamics in dairy goats. We used seven untreated goats (control group) and six progesterone treated goats (P group) with a controlled internal drug release device from Days 0 to 5 (Day 0: day of ovulation). We performed daily ultrasonograph during the interovulatory interval to determine ovarian change and took daily blood samples to determine serum estradiol 17β (E 2) and P 4 concentrations by RIA. We divided the control goats into 3- ( n=4) and 4-wave goats ( n=3), according to the number of follicular waves recorded during the ovulatory cycle. Mean progesterone concentrations between Days 1 and 5 were higher and mean estradiol concentrations between Days 3 and 5 were lower in 4-wave goats (P 4: 3.8±0.2 ng/ml; E 2: 1.6±0.2 pg/ml) than in 3-wave goats (P 4: 2.0±0.5 ng/ml, P≤0.05; E 2: 4.4±0.9 pg/ml, P≤0.05). Wave 2 emerged earlier in 4-wave (Day 4.2±0.3) than in 3-wave goats (Day 7.3±0.3, P≤0.05). Three out of six of the progesterone-treated goats had short cycles (mean 8.0±0.0 days) and ovulated from Wave 1. The other three goats had shorter cycles (mean 18.3±0.3 days) than the control group (20.0±0.2 days; P≤0.05), although they were within the normal range of control cycles (shortened cycles). In the three treated goats with shortened cycles (two with four waves, one with three waves), mean progesterone concentrations between Days 1 and 5 were higher (4.7±0.6 ng/ml) than in the 3-wave control goats. In these goats, Wave 2 emerged at Day 4.3±0.3, similar to the time observed in 4-wave goats but earlier ( P≤0.05) than in 3-wave control goats. Overall results confirm a relationship between the progesterone levels and the follicular wave turnover during the early luteal phase in the goat. Higher progesterone concentrations may accelerate follicular turnover probably by an early decline of the negative feedback action of the largest follicle of Wave 1. This is followed by an early emergence of Wave 2.

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