Early-life exposure to stressors can shape the phenotype of the offspring resulting in changes that may affect their prehatch and posthatch development. This can be modeled indirectly through maternal exposure to stressors (natural model) or by offspring exposure to stress hormones (pharmacological model). In this study, both models were used to investigate the effects of genetic line on hatchability, late embryonic mortality, sex ratio, and body weight until 17 wk of age. To form the parent stock, fertilized eggs of 4 commercial genetic lines - two brown (brown 1 and 2), two white (white 1 and 2), and a pure line White Leghorn - were incubated, hatched, and housed identically in 4 flocks of 27 birds (24 females and 3 males) per strain. Each strain was equally separated into 2 groups: "maternal stress," where hens were subjected to a series of acute psychological stressors (e.g., physical restraint, transportation) for 8 D before egg collection, and "control," where hens received routine husbandry. At 3 maternal ages, fertile eggs from both treatments were collected, and additional eggs from the control group were injected with corticosterone (10 ng/mL egg content) ("CORT"). A "vehicle" treatment was included to account for effects of egg manipulation. Each maternal age comprised a replicate over time. Eggs were incubated and hatched, and the offspring (N = 1,919) were brooded until 17 wk under identical conditions. The results show that prenatal stress interacted with strain to decrease embryonic survival and growth. Among all strains, brown 2 was consistently the most affected line in both prehatch and posthatch development. Our study shows that embryonic survival and offspring growth are mostly affected by the pharmacological model and that strain differences may increase susceptibility to prenatal stress. Moreover, it suggests that the natural stressor model may be useful for quantifying the response of the mother to stressors, whereas the pharmacological model may be useful for quantifying the response of the embryo to increased levels of corticosterone.

中文翻译：

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产前压力和遗传学对蛋鸡胚胎存活和后代生长的影响。

生命早期暴露于应激源会影响后代的表型，导致可能影响其孵化前和孵化后发育的变化。这可以通过母体暴露于应激源（自然模型）或后代暴露于应激激素（药理模型）来间接建模。在这项研究中，两个模型都被用来研究遗传系对直到17周龄的孵化率，后期胚胎死亡率，性别比和体重的影响。为了形成母本，将4种商业遗传系的受精卵-两个棕色（棕1和2），两个白色（白1和2）和纯白色来格霍恩-进行孵化，孵化，并以相同的方式放在4个鸡群中每个品系27只鸟（雌24头，雄3头）。每个品系均分为2组：“母体压力” 在收集鸡蛋之前，母鸡要经受一系列剧烈的心理压力（例如身体约束，运输），持续8天；在“控制”条件下，母鸡要接受常规饲养。在3个产妇年龄，收集两种处理的可育卵，并向对照组的另外卵中注射皮质酮（10 ng / mL卵含量）（“ CORT”）。包括“车辆”处理以说明鸡蛋操纵的影响。每个产妇年龄都随时间重复。将卵孵化并孵化，在相同条件下将后代（N = 1,919）孵化到17周。结果表明，产前应激与品系相互作用降低了胚胎的存活和生长。在所有菌株中 棕色2始终是孵化前和孵化后发育中受影响最大的品系。我们的研究表明，胚胎存活和后代生长主要受药理模型影响，并且菌株差异可能会增加对产前压力的敏感性。此外，这表明自然应激模型可用于量化母亲对应激的反应，而药理模型可用于量化胚胎对皮质酮水平升高的反应。