The photoperiodic mechanisms underlying seasonal breeding in male Japanese quail change their characteristics annually, with the result that reproduction is terminated in the late summer rather than the autumn. The reproductive cycle was studied in 4 successive years to determine the critical daylengths for reproductive induction in spring, and for its termination in late summer. In spring luteinizing hormone levels first rise when the daylength has reached 11.9 h but in late summer the first signs of a decrease are detectable when the photoperiod has decreased to 14.7 h and levels are basal when it has reached about 14 h. Thus, quail appear to have evolved a refractoriness to daylengths in late summer that were maximally stimulatory earlier in the year. However, quail are not photorefractory in the `classic' sense as they remain continuously in breeding if held on unchanging long days and can be photostimulated at any time of the year by daylengths in excess of 16 h light: 8 h darkness. Their particular form of refractoriness seems to involve a seasonal shift in the critical daylength. Refractoriness can be induced in quail held in the laboratory under a simulated annual photocycle, and, more importantly, it develops in birds exposed to long daylengths of a fixed duration. For example, quail exposed to 20 h light: 4 h darkness show a shift in the critical daylength from approximately 12 to 15 h over a period of about 2 months. The time course over which the shift occurs is intriguing and can explain the responses under natural photoperiods. Under fixed daylengths the critical daylength that induces regression depends upon the duration of the stimulatory photoperiod. Female quail also develop refractoriness. The evolution of refractoriness does not depend upon the activity of the hypothalamo-pituitary axis and develops in castrated quail as well as in birds implanted with androgens. Castrated quail show annual cycles in gonadotrophin secretion indistinguishable in timing from those in intact birds. Such results suggest that the physiological basis of refractoriness lies either in the neural circuits regulating neurohormone secretion or in the photoperiodic clock mechanism itself.