Post-natal glucocorticoid elevation affects GnRH-induced luteinizing hormone concentration in female house sparrows.
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Most non-mammalian studies investigating the long-term effects of early-life stressor exposure on endocrine regulation have focused on the hypothalamic-pituitaryadrenal (HPA) axis. However, the hypothalamic-pituitary-gonadal (HPG) axis may more directly affect fitness by regulating reproduction. Changes in HPG axis regulation could allow vertebrates to adaptively mitigate negative effects of early-life stressor exposure. However, only a few studies have examined long-term effects of early-life stressor experience on the HPG axis, and these have found mixed results. Here, we evaluate long-term effects of post-natal corticosterone exposure on the HPG axis in adult female house sparrows (Passer domesticus). We elevated circulating corticosterone non-invasively in wild nestling house sparrows between 8 and 11days post-hatching, and then brought birds into captivity at fledging. Early in their first breeding season (ages 285-353d post-hatching), females were given a gonadotropin releasing hormone (GnRH) challenge. We found that early-life corticosterone exposure interacted with current condition such that females exposed to elevated post-natal corticosterone had higher baseline and GnRH-induced luteinizing hormone (LH) concentration than control females, but only if they had a high mass. Our results suggest that female house sparrows may mitigate negative impacts of early-life corticosterone exposure by investing in early reproduction, but only when current energetic condition allows.
