Stress hormones mediate environment-genotype interactions during amphibian development.

Environments experienced by organisms during early development shape the character and timing of developmental processes, leading to different probabilities of survival in the developmental habitat, and often profound effects on phenotypic expression later in life. Amphibian larvae have immense capacity for plasticity in behavior, morphology, growth and development rate. This creates the potential for extreme variation in the timing of, and size at metamorphosis, and subsequent phenotype in the juvenile and adult stage. Hormones of the neuroendocrine stress axis play pivotal roles in mediating environmental effects on animal development. Corticotropin-releasing factor, whose secretion by hypothalamic neurons is induced by environmental stress, influences the timing of amphibian metamorphosis by controlling the activity of the thyroid and interrenal (adrenal; corticosteroids) glands. At target tissues, corticosteroids synergize with thyroid hormone to promote metamorphosis. Thus, environmental stress acts centrally to increase the activity of the two principle endocrine axes controlling metamorphosis, and the effectors of these axes synergize at the level of target tissues to promote morphogenesis. While stress hormones can promote survival in a deteriorating larval habitat, costs may be incurred such as reduced tadpole growth and size at metamorphosis. Furthermore, exposure to elevated corticosteroids early in life can cause permanent changes in the expression of genes of the neuroendocrine stress axis, leading to altered physiology and behavior in the juvenile/adult stage. Persistent effects of stress hormone actions early in life may have important fitness consequences.