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Redefining the Limits of Day Length Responsiveness in a Seasonal Mammal

School of Biological Sciences (G.C.W., D.G.H.), University of Aberdeen, Aberdeen AB24 2TZ, United Kingdom; School of Biomedical and Molecular Sciences (J.D.J.), University of Surrey, Guildford GU2 7XH, United Kingdom; Department of Physiology (I.J.C.), Monash University, Victoria 3880, Australia; and School of Biomedical Sciences (G.A.L.), University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh EH8 9JZ, United Kingdom

Address all correspondence and requests for reprints to: Dr. David G. Hazlerigg, School of Biological Sciences, University of Aberdeen, Zoology Building, Tillydrone Avenue, Aberdeen AB24 2TZ, United Kingdom. E-mail: d.hazlerigg{at}abdn.ac.uk.

At temperate latitudes, increases in day length in the spring promote the summer phenotype. In mammals, this long-day response is mediated by decreasing nightly duration of melatonin secretion by the pineal gland. This affects adenylate cyclase signal transduction and clock gene expression in melatonin-responsive cells in the pars tuberalis of the pituitary, which control seasonal prolactin secretion. To define the photoperiodic limits of the mammalian long day response, we transferred short day (8 h light per 24 h) acclimated Soay sheep to various longer photoperiods, simulating those occurring from spring to summer in their northerly habitat (57°N). Locomotor activity and plasma melatonin rhythms remained synchronized to the light-dark cycle in all photoperiods. Surprisingly, transfer to 16-h light/day had a greater effect on prolactin secretion and oestrus activity than shorter (12 h) or longer (20 and 22 h) photoperiods. The 16-h photoperiod also had the largest effect on expression of circadian (per1) and neuroendocrine output (βTSH) genes in the pars tuberalis and on kisspeptin gene expression in the arcuate nucleus of the hypothalamus, which modulates reproductive activity. This critical photoperiodic window of responsiveness to long days in mammals is predicted by a model wherein adenylate cyclase sensitization and clock gene phasing effects of melatonin combine to control neuroendocrine output. This adaptive mechanism may be related to the latitude of origin and the timing of the seasonal transitions.

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