A model to explain the timing of seasonal breeding in birds is presented. It is assumed that, despite the wide range in egg-laying seasons, there are common physiological mechanisms which underlie seasonality in birds and that most, if not all, birds are photoperiodic. Birds are considered to possess an internal rhythm of reproduction which is synchronized with seasonal changes in the environment by external factors, particularly the annual cycle of daylength. The rhythm consists, at least in part, of regular changes in the photoperiodic response between states of photosensitivity and photorefractoriness. Avian breeding seasons effectively start in autumn when birds become photosensitive, regardless of when egg-laying occurs. The timing of breeding is then influenced by the rate of increase of hypothalamic 'drive' and by the sensitivity of the hypothalamus and pituitary gland to inhibitory feedback from gonadal steroids. If sensitivity is high, gonadal growth will not occur until the threshold daylength for photostimulation is exceeded after the winter solstice. Egg-laying then starts in late winter, spring or summer. Alternatively, steroid feedback may be relatively low and gonadal growth may be sufficiently rapid once the birds become photosensitive that breeding occurs in late autumn or winter. The time of egg-laying in birds may also be strongly influenced by supplementary information, such as social cues, food availability, temperature and rainfall and, in some species, this information is more important than daylength in determining the timing of breeding. The review also includes the first summary of the breeding seasons of New Zealand birds. The pattern of egg-laying is exactly the same in native birds, in birds introduced to New Zealand and in other Southern hemisphere birds from similar latitudes, with a broad peak of egg-laying occurring from September to December. In addition, annual cycles of steroid hormone concentrations in the North Island brown kiwi, the yellow-eyed penguin and the kakapo are consistent with results from many studies on Northern hemisphere birds. This model for the timing of breeding in birds can be applied to New Zealand birds and it is concluded that the physiological control mechanisms for the timing of seasonal breeding in New Zealand birds are similar to those of other birds.
Melatonin was measured by radioimmunoassay in homogenates of pineal glands from quail (Coturnix coturnix japonica) kept under different photoperiods and in darkness. Under 8-, 12- and 16-h daylengths melatonin levels were increased during the dark period, the duration of the increase depending on the duration of the dark period. As the daylength was increased the peak occurred closer to lights-off, reflecting the more rapid melatonin rise under the longer photoperiods. The pineal melatonin rhythm continued in darkness with an amplitude relative to that seen under a light/dark cycle of slightly less than one-half after 2 days in darkness and one-third after 6 days in darkness. The corresponding average periods of the rhythm were 25.5 h and 25.7 h. These results show that there is a circadian rhythm of melatonin in the pineal gland of the quail which is entrained by light/dark cycles and which continues in darkness.
Twenty-one-hour melatonin plasma profiles were studied in 15 normal elderly volunteers from the community, and eight who had been in hospital for more than six weeks and who had not been exposed to strong natural lighting. The hospital group had significantly higher daytime plasma melatonin levels, an earlier nocturnal rise, and the timing of their secretory profiles was more variable. These results suggest that currently used artificial and supplementary natural lighting may not be sufficient to suppress melatonin secretion adequately during daylight hours nor act efficiently to entrain day/night secretion of melatonin in a physiological circadian manner. Raised melatonin levels by day and variable secretory profiles at night may account for certain mood and sleep disorders observed in institutionalized people.
In cows without a CL present on day 0 of an oestrus synchronisation program, removal of the day 0 GnRH treatment led to reduced CL development; however, no effect of adding progesterone was found. In contrast, in cows with a CL present on day 0 inclusion of a progesterone device led to a higher CL volume, but removal of the first GnRH injection had no effect. Response to the treatment was affected by plasma concentrations of insulin, IGF-I and NEFA.
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