W. Haresign et al., EFFECT OF PROGESTERONE PRIMING ON GONADOTROPIN-SECRETION AND LUTEAL FUNCTION IN GNRH-TREATED SEASONALLY ANESTROUS EWES, Animal Science, 62, 1996, pp. 97-103
The main objective of the experiment was to investigate the mechanism
by which progesterone priming eliminates defective luteal function in
anoestrous ewes induced to ovulate with GnRH. Animals in group 1 (no.
= 10) were primed with a single i.m. injection of progesterone in corn
oil 3 days before the start of GnRH treatment, while ewes in group 2
(no. = 10) received corn oil alone and served as untreated controls. E
wes in group 3 (no. = 10), which served as positive controls, were tre
ated with an intra-vaginal progestagen sponge for 7 days, and this was
removed just before the start of GnRH treated. Ewes in all three grou
ps were induced to ovulate by administration of 2-h injections of GnRH
(250 ng per injection) for 54 h. Frequent blood samples for LH, FSH a
nd progesterone analysis were taken around the time of both progestero
ne injection and GnRH treatment, as well as daily thereafter to monito
r luteal function, and laparoscopy was performed 3 and 7 days after Gn
RH treatment. The incidence of ovulation was similar for all the three
groups (8/10, 7/10 and 9/10 for groups 1, 2 and 3 respectively). Howe
ver, both laparoscopic examination and plasma progesterone concentrati
ons revealed that the incidence of normal luteal function was signific
antly higher in progesterone-primed animals group 1: 7/8; group 3: 9/9
) compared with controls (group 2: 0/7), P < 0 . 05) with no differenc
e between groups 1 and 3. Injection of progesterone on day-3 significa
ntly suppressed mean LH concentrations (P < 0 . 05), but mean FSH conc
entrations were not altered. However, there were no significant differ
ences between groups in LH and FSH concentrations over the period of G
nRH treatment, nor in the timing, duration and height of pre-ovulatory
LH and FSH surges. These results suggest that progesterone priming ma
y eliminate defective luteal function either by changing LH concentrat
ions at file time of progesterone administration or through mechanisms
not involving gonadotropin secretion.