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 / 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 synchronised 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 (TSH) 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 sensitisation 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.