172 G.E. Mann, G.E. Lamming Animal Reproduction Science 64 2000 171–180
inhibition of oxytocin receptors allowing increased PGF
2a
release. © 2000 Elsevier Science B.V. All rights reserved.
Keywords: Cattle-endocrinology; Oestradiol; Luteolysis; Corpus luteum
1. Introduction
In cattle, luteolysis results from the release of luteolytic episodes of uterine prostaglandin F
2
a
PGF
2
a
in response to the binding of oxytocin to newly developed receptors on the uterine endometrium for review see Mann et al., 1999. During the normal luteal phase,
progesterone inhibits the development of these oxytocin receptors until the appropriate time around day 16–17. However, at puberty, and following post partum and seasonal
anoestrus, the basic mechanisms regulating cycle length do not function normally. During these periods of transition from a state of acyclicity to one of cyclicity, the first oestrous cycle
is often of short duration for reviews see Lauderdale, 1986; Hunter, 1991; Garverick et al., 1992. Numerous studies have demonstrated that the occurrence of short-lived corpora lutea
is a function of a lack of prior exposure to progesterone as pre-treatment with progesterone results in the formation of corpora lutea of normal life span. However, the mechanism by
which this lack of prior exposure to progesterone results in premature luteal regression is far from clear.
A number of studies have failed to demonstrate any consistent differences in the charac- teristics of normal and short-lived corpora lutea prior to the initiation of premature luteolysis
in the short-lived group for review see Hunter, 1991; Garverick et al., 1992. This suggests no innate inadequacy of the short-lived corpus luteum. There is, however, strong evidence to
suggest that a premature triggering of the luteolytic mechanism, early in the luteal phase, is responsible for the premature demise of short-lived corpora lutea. The premature luteolytic
signal in animals with short-lived corpora lutea is associated with an increased level of both endogenous Peter et al., 1989; Cooper et al., 1991 and oxytocin-induced Zollers et al.,
1989 PGF
2
a
release. Furthermore, treatment with indomethacin to block prostaglandin synthesis prevents premature luteolysis Troxel and Kesler, 1984, as does removal of the
uterus, the principle source of luteolytic PGF
2
a
release Copelin et al., 1987. A number of authors have reported sub-optimal levels of preovulatory oestradiol secretion
preceding the formation of short-lived corpora lutea Garcia-Winder et al., 1986; Garverick et al., 1988; Braden et al., 1989a,b. During the normal cycle, high levels of preovulatory
oestradiol secretion result in the eventual disappearance of endometrial oxytocin receptors Lamming and Mann, 1995a,b, producing a situation early in the luteal phase of low oxy-
tocin receptor and no oxytocin stimulated luteolytic PGF
2
a
episodes. However, premature luteolysis in animals exhibiting short cycles is accompanied, early in the luteal phase, by
elevated levels of oxytocin receptor Zollers et al., 1991 and increased oxytocin-induced release of PGF
2
a
Zollers et al., 1989. The hypothesis examined in the present study is that inadequate preovulatory oestradiol
production leads to an inadequate inhibition of oxytocin receptors in the uterus, resulting in the premature secretion of luteolytic PGF
2
a
. To test this, we have investigated the direct
G.E. Mann, G.E. Lamming Animal Reproduction Science 64 2000 171–180 173
effects of the level of preovulatory oestradiol on subsequent oxytocin receptor concentra- tions and activity using a hormone treated ovariectomised cow model.
2. Materials and methods
