Abstract

In Exp. 1, 10 quiescent non-lactating tammars were exposed to 15L:9D (Days -41 to -1), 24L:0D (Days 0 to 14), 15L:9D (Days 15 to 34) and then to ambient increasing daylength from 13L:11D on Day 35. From Days 0 to 22 they received a s.c. injection of melatonin (400 ng/kg, N -5) on the arachis oil vehicle (N = 5) in the evening (19:30 h) 2.5 h before dark. Exposure to 24L:0D abolished the nocturnal plasma melatonin rise but this was reinstated by subsequent exposure to 15L:9D. Of 5 melatonin-treated tammars, 4 gave birth on Day 45, so had failed to respond to the melatonin injection alone but reactivated when this was combined with the endogenous melatonin rise during exposure to 15L:9D. Of 5 control tammars, 4 remained quiescent until reactivated by the decrease in daylength to 13L:11D, and gave birth significantly later (Day 63.7 +/- 2.2, mean +/- s.e.m., P less than 0.05). In Exp. 2, 6 tammars were exposed to 15L:9D (Days -15 to -1) and then to 12L:12D (Days 0 to 15) by extending the dark phase by 3 h in the morning. This extended the nocturnal melatonin rise by 2-3 h in the morning and all 6 tammars gave birth on Day 31.2 +/- 1.0. A transient pulse of peripheral plasma prolactin (81.5 +/- 31.0 ng/ml) was detected at dawn during 15L:9D in all 6 tammars but was not observed in any of them 5 days after exposure to 12L:12D. Together these results do not support the time of day hypothesis but indicate that increase in duration of the nocturnal melatonin rise mediates the effects of decreased daylength on reactivation of the corpus luteum, and that the first detectable result of this may be the abolition of a transient prolactin pulse at the end of the dark phase.

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