Effect of exogenous melatonin and extending the dark period at dusk before the summer solstice on the onset of oestrus in Romney Marsh ewes

Abstract

Groups of Romney Marsh ewes (n = 24) were injected with exogenous melatonin or subjected to extended darkness or a combination of both at dusk from the winter to the summer solstice before being re-exposed to the natural photoperiod at 35 degrees S. The animals were at all times exposed to natural dawn. The onset of subsequent oestrus was delayed when compared with controls subjected to the natural photoperiod. Either melatonin or darkness or a combination were equally effective at delaying oestrus. The results are consistent with a hypothesis based on an external coincidence model of seasonal breeding involving the coincidence of a light-sensitive phase set close to dusk that, when exposed to light in spring and summer, prepares the reproductive axis to respond correctly to the direct effects of the inductive photoperoid in autumn. The offset of the time of oestrus was not affected by the experimental treatments nor was the timing of the subsequent reproductive season. Since melatonin was as effective as darkness at influencing the assumed photosensitive signal, even in the presence of natural light, melatonin may act through the light reception system.

Is a Critical Interval of the Circadian Pacemaker at Dusk Responsive to Light and Melatonin Responsible for the Timing of Estrus in the Romney Marsh Ewe?

“…Several pieces of evidence suggest in the sheep that the photoperiodic response consists of two cues: a &dquo;long-day&dquo; signal, which serves to prepare or sensitize the reproductive neural centers to a second signal, namely, the short days of autumn Malpaux et al, 1989). An important element in the long-day signal appears to be the reception of light at dusk before the summer solstice because when natural dusk light is precluded at this time, the breeding season is delayed Guerin et al, 1994). If, however, dusk light is precluded after the summer solstice, the breeding season is advanced Dunstan, 1977).…”

“…This signal is considered central to the precise timing of estrus because melatonin-free (pinealectomized) animals fail both to interpret photoperiod accurately and to synchronize the breeding season to the correct time of year (Bittman, Karsch, and Hopkins, 1983;Kennaway et al, 1987). Exogenous melatonin appears to interfere with the reception of the dusk light signal and mimics darkness when administered at dusk before the summer solstice, and the breeding season is delayed (Guerin et al, 1994); when it is similarly administered after the summer solstice, however, the breeding season is advanced (Kennaway et al, 1982;Nett and Niswender, 1982;Arendt et al, 1983).…”

“…This may be the basis of the long-day signal required for estrus timing. This hypothesis was initially tested by either precluding dusk light or administering melatonin at dusk before the summer solstice, and both protocols were associated with a delay in the timing of the subsequent breeding season (Guerin et al,1994).…”

“…Experiment 1 repeats the administration of melatonin at dusk before the summer solstice to confirm a delay in the subsequent breeding season (Guerin et al, 1994) but with regular monitoring of endogenous melatonin secretion both under the treatment conditions and under acutely extended darkness throughout the treatment period. This experiment's particular aim is to examine the effect of melatonin at dusk on the timing of the unmasked onset of melatonin secretion, which may reflect a critical interval of the endogenous circadian pacemaker.…”

“…In Experiment 2, exogenous melatonin or the preclusion of light at dawn is examined before the summer solstice to investigate the effect on the timing of the subsequent breeding season. These treatments at dawn were complementary to the dusk treatments reported by Guerin et al (1994). Again, the secretion of endogenous melatonin both under treatment conditions and under acutely extended darkness was monitored regularly during the treatment phase as a marker of the impact of treatment on the phase of the circadian pacemaker.…”