PHOTOPERIODIC CONTROL OF REPRODUCTION IN JAPANESE QUAIL: CHANGES IN GONADOTROPHIN SECRETION ON THE FIRST DAY OF INDUCTION AND THEIR PHARMACOLOGICAL BLOCKADE

Abstract

SUMMARY Photoperiodic processes often seem rather slow because the induced developmental changes, such as gonadal growth in a seasonally breeding bird, may take many weeks to reach completion. This is rather deceptive, however, as initial changes occur rapidly. Following the transfer of sexually immature Japanese quail to a photoperiod of 20 h light:4 h darkness (20L:4D), plasma levels of both LH and FSH remained low on the first day of treatment until 18 h after the onset of light when they both rose significantly. Over the next few hours the levels of both hormones rose three- to fourfold. In a more detailed experiment in which blood samples were collected every 2 h, the mean LH concentration showed no increase before hour 20 but rose significantly from 0·92± 0·09 (s.e.m.) to 1·67± 0·19 ng/ml (n = 6) between hours 20 and 22. By hour 26 the mean LH level had reached 2·68 ± 0·25 ng/ml. To determine the light-sensitive period on the first day of photostimulation, immature quail were transferred from short days (8L: 16D) to one of the following photoperiods: 12L: 12D, 13·3L: 10·7D, 14·7L: 9·3D, 16L: 8D, 20L: 4D or to continuous light. Blood samples were collected at hours 12, 19 and 25 after the onset of light. The concentration of LH did not change in the groups exposed to 12L:12D or to 13·3L:10·7D. In all other groups, however, it increased significantly between hours 19 and 25 regardless of whether the quail were in darkness or light, or whether a light/dark transition occurred. The magnitude of the rise was similar in the four stimulatory photoperiods. These results indicate that light before the twelfth hour is not photoperiodically effective but that further exposure to 3 h or more light from hour 12 causes induction after a lag of some hours, and an increase in LH at the end of the first day. When the LH rise was observed over 2 consecutive long days the response seemed to occur earlier on the second than on the first day. To see whether the delay in the rise of LH secretion until hour 20 was due to a change in the sensitivity of the pituitary gland to LH releasing hormone (LH-RH), birds were tested in three experiments. 'Short-day' quail were injected i.m. with two equal doses of synthetic LH-RH, the second dose being given 30, 60 or 90 min after the first. The results indicated that the first dose of LH-RH did not enhance the amount of LH released by the second dose. In fact, the response to the second dose was significantly less. Similarly, an injection of LH-RH at hour 12 did not advance the LH response on the first long day. Finally, the sensitivity of the pituitary gland to exogenous LH-RH was determined at various times on the first long day. No augmented responsiveness was observed at hours 22 and 24. It would appear, therefore, that the lag may not be in the pituitary gland but may exist in neural or neuroendocrine events which occur in the brain of the quail between hours 12 and 16 and which lead to enhanced gonadotrophin secretion beginning at about hour 20 on the first long day.