Amplitude Modulation of the Nightly Melatonin Rise in the Neonatal Lamb and the Subsequent Timing of Puberty1

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Abstract
Spring-born female lambs require a decrease in day length for the normal timing of puberty the following autumn. If this decrease occurs early in postnatal life (i.e. 0–10 weeks), puberty is delayed. This study tested the hypothesis that failure of the neonatal lamb to respond to the critical long-day to short-day signal is due to inadequate nocturnal melatonin secretion. The approach was to artificially increase, to adult levels, the low nighttime rises of melatonin during the early postnatal period. Eight female lambs served as controls; they were raised on short days until 17 wk of age, and then exposed to 5 wk of long days, after which they were returned to short days. This alternating sequence of photoperiods during mid-development would be expected to induce normal puberty. Sixteen experimental females were exposed to the critical block of long days much earlier; they were placed in long days between 2 and 7 wk of age and in short days thereafter. Half (n = 8) received no further treatment. The other half (n = 8) were infused nightly with melatonin during the 8-h dark phase of the 5-wk, long-day photoperiod. This increased the amplitude of the natural nighttime melatonin rises 3- to 4-fold, well into the adult range. In most uninfused lambs exposed to long days as neonates, puberty was delayed relative to controls (33 ± 1 wk, n = 7 of 8) that experienced the 5 wk of long days at an older age, only 2 of 8 lambs treated neonatally with long days exhibited repetitive reproductive cycles by the end of the study at 44 wk. Supplementation of the neonatal nocturnal melatonin rises was without effect; only 1 of 8 melatonin-infused lambs attained puberty. The inference from these results is that the low-amplitude melatonin rhythm of the neonatal lamb does not limit the induction of puberty by seasonal light cues. Rather, the failure of early long-day exposure to induce puberty several weeks later is probably due to a postpineal gland deficiency related to immaturity of the reproductive axis itself or to growth-related signals indicating that somatic development is inadequate.