Influence of maternal corticosterone treatment on incubation length of eggs laid by Japanese quail hens selected for divergent adrenocortical stress responsiveness.

1. Previous studies have shown that more yolk corticosterone is found in the eggs of random bred Japanese quail hens implanted with corticosterone during egg formation; both unstressed and stressed quail hens selected for exaggerated (high stress) rather than reduced (low stress) plasma corticosterone response to brief restraint deposit more corticosterone into their egg yolks. The length of egg incubation is also known to be shorter in eggs laid by high than low stress hens. 2. Here we investigated the interactive effects of quail stress line (low vs. high stress) with maternal corticosterone treatment (empty implant controls vs. corticosterone-implants) during egg formation on length of egg incubation. 3. Mean (+/-SEM) length of egg incubation for high stress control eggs (3973 +/- 04 h) was similarly shorter (by about 4.5 h) than that found for low stress control eggs (3928 +/- 02 h). In addition, on average, the incubation length of eggs laid by corticosterone-implanted hens (3929 +/- 05 h) was nearly 3 h shorter than that found for eggs laid by control hens (3958 +/- 02 h) regardless of stress line. 4. Line x hen-implant treatment effects on mean (+/-SEM) length of egg incubation partitioned in rank order as follows: low stress control (3978 +/- 05 h) > low stress corticosterone-implant (3959 +/- 07 h) > high stress control (3938 +/- 03 h) > high stress corticosterone-implant (3912 +/- 04 h). 5. Our original contention that selection for exaggerated adrenocortical responsiveness is associated with a reduction in the length of egg incubation was supported. Because maternal stress-induced elevations of yolk B are known to occur, the present findings of further shortenings of the hatching times of eggs of corticosterone-treated hens of both stress lines are also important to the poultry industry because they warn producers that unless stress in hens during egg formation is minimised, abbreviated egg incubation periods may result beyond the effects that a hen's genetic predisposition to adrenocortical stress responsiveness has on the length of egg incubation.

Maternal corticosterone reduces egg fertility and hatchability and increases the numbers of early dead embryos in eggs laid by quail hens selected for exaggerated adrenocortical stress responsiveness.

Quail hens selected for exaggerated (HS, high stress) rather than reduced (LS, low stress) plasma corticosterone (B) response to brief restraint deposit more B into their egg yolks than do LS hens. Female progeny of HS hens implanted with B also show reduced egg production when compared with female offspring of LS- and HS-control and LS-B-implanted hens. Herein, LS and HS hens were implanted (s.c.) with empty (controls, CON) or B-filled silastic tubes to assess the interactive influences of maternal B-treatment with quail stress line on egg fertility (FERT), total egg hatchability (TOTHATCH) and fertile egg hatchability, and the percentages of embryonic mortality (early dead, ED; late dead) and pipped eggs. Mean FERT was dramatically reduced in eggs of HS compared with LS hens and B-implanted compared with CON-treated hens (P < 0.0001, both cases). Line x implant treatment FERT outcomes partitioned (P < 0.05) as follows: LS-B = LS-CON > HS-CON > HS-B. In addition, TOTHATCH was also affected by line (LS > HS; P < 0.0001) and implant treatment (CON > B-implant; P < 0.0002) and line x implant treatment TOTHATCH means differed (P < 0.05) as follows: LS-CON = LS-B = HS-CON > HS-B. Fertile egg hatchability was reduced (P < 0.05) in HS-B-treated hen eggs when compared with LS-B and HS-CON hen eggs and more (P < 0.05) ED embryos were found in eggs laid by HS-B-implanted hens than in any other treatment group. Late dead and pipped egg percentages were unaffected by any treatment. The findings are important to avian geneticists because they further emphasize the benefits that selection for reduced adrenocortical responsiveness has on hen reproductive performance. The maternal B findings also warn poultry and hatchery managers that unless hen stress during egg formation is avoided, negative consequences in FERT, TOTHATCH, and ED can result, particularly in hens genetically predisposed toward exaggerated adrenal stress responsiveness.