School of Biological Sciences, Center for Reproductive Biology, Washington State University, Pullman, WA 99164-4236, USA
Department of Migration, Max Planck Institute of Animal Behavior, 78315 Radolfzell, Germany.
J Exp Biol. 2020 Nov 20;223(Pt 22):jeb220152. doi: 10.1242/jeb.220152.
Developmental exposure of embryos to maternal hormones such as testosterone in the avian egg influences the expression of multiple traits, with certain effects being sex specific and lasting into adulthood. This pleiotropy, sex dependency and persistency may be the consequence of developmental programming of basic systemic processes such as adrenocortical activity or metabolic rate. We investigated whether experimentally increased exposure to testosterone influenced hypothalamus-pituitary-adrenal function, i.e. baseline and stress-induced corticosterone secretion, and resting metabolic rate (RMR) of adult male and female house sparrows (). In previous experiments with this passerine bird we demonstrated effects of embryonic testosterone exposure on adult agonistic and sexual behavior and survival. Here we report that baseline corticosterone levels and the stress secretion profile of corticosterone are modified by testosterone in a sex-specific and life history stage-dependent manner. Compared with controls, males from testosterone-treated eggs had higher baseline corticosterone levels, whereas females from testosterone-treated eggs showed prolonged stress-induced corticosterone secretion during the reproductive but not the non-reproductive phase. Adult RMR was unaffected by testosterone treatment but correlated with integrated corticosterone stress secretion levels. We conclude that exposure of the embryo to testosterone programs the hypothalamus-pituitary-adrenal axis in a sex-specific manner that in females depends, in expression, on reproductive state. The modified baseline corticosterone levels in males and stress-induced corticosterone levels in females may explain some of the long-lasting effects of maternal testosterone in the egg on behavior and could be linked to previously observed reduced mortality of testosterone-treated females.
胚胎在禽类卵中暴露于母体激素（如睾酮）会影响多种性状的表达，某些影响具有性别特异性，并持续到成年。这种多效性、性别依赖性和持久性可能是基本系统过程（如肾上腺皮质活动或代谢率）发育编程的结果。我们研究了实验中增加睾酮暴露是否会影响成年雄性和雌性麻雀的下丘脑-垂体-肾上腺功能，即基础和应激诱导的皮质酮分泌以及静息代谢率（RMR）。在之前用这种雀形目鸟类进行的实验中，我们证明了胚胎期睾酮暴露对成年期争斗和性行为以及生存的影响。在这里，我们报告说，基础皮质酮水平和皮质酮的应激分泌特征以性别特异性和生活史阶段依赖性的方式被睾酮修饰。与对照组相比，来自睾酮处理卵的雄性具有更高的基础皮质酮水平，而来自睾酮处理卵的雌性在繁殖期而非非繁殖期表现出延长的应激诱导的皮质酮分泌。成年 RMR 不受睾酮处理的影响，但与整合的皮质酮应激分泌水平相关。我们得出结论，胚胎暴露于睾酮以性别特异性的方式编程下丘脑-垂体-肾上腺轴，在雌性中，其表达取决于生殖状态。雄性中基础皮质酮水平的升高和雌性中应激诱导的皮质酮水平的升高可能解释了母体睾酮在卵中对行为的一些持久影响，并可能与之前观察到的睾酮处理雌性死亡率降低有关。
