Ancient origins of human developmental plasticity.
Animals have the ability to alter development, physiology, growth, and behavior in response to different environmental conditions. These responses represent critical assessments of both external and internal factors. For example, the timing of metamorphosis, hatching, or birth depends on the trade-offs between growth opportunity and mortality risk in the developmental habitat. Physiological sensors compute these trade-offs as a function of energy balance and environmental stress, and effectors initiate physiological, developmental, and behavioral responses to these determinations. The neuroendocrine stress axis provides a means for animals to integrate information from multiple sources and to respond accordingly. Considerable evidence now supports the view that the secretion of hormones critical to development (corticosteroid and thyroid hormones) is controlled by a common neuroendocrine stress pathway involving corticotropin-releasing factor (CRF) and related peptides. CRF produced in the hypothalamus stimulates the biosynthesis and secretion of both thyroid and corticosteroid hormones, leading to accelerated tadpole metamorphosis. Similarly, in mammals CRF of fetal and placental origin has been shown to influence the timing of birth. Studies in several experimental animal models and in humans show that early life experience can have long-term phenotypic consequences. Furthermore, there is evidence that phenotypic expression is strongly influenced by the actions of stress hormones produced during development. The integrated neuroendocrine response to stress, and its role in timing critical life history transitions and establishing long-term phenotypic expression, arose early in the evolution of vertebrates.
Crespi
Erica J
EJ
Department of Molecular, Cellular and Developmental Biology, The University of Michigan, Ann Arbor, Michigan 48109, USA.
Denver
Robert J
RJ
D000222:Adaptation, Physiological / Q000235:genetics*; D000305:Adrenal Cortex Hormones / Q000378:metabolism*; D000818:Animals; D005075:Biological Evolution; D002395:Catecholamines / Q000378:metabolism; D015509:Developmental Biology; D004777:Environment; D005260:Female; D047109:Fetal Development / Q000235:genetics / Q000502:physiology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000254:growth & development* / Q000378:metabolism; D007231:Infant, Newborn; D008675:Metamorphosis, Biological / Q000235:genetics / Q000502:physiology; D023421:Models, Animal; D009473:Neuronal Plasticity / Q000235:genetics*; D009490:Neurosecretory Systems / Q000254:growth & development* / Q000378:metabolism; D010641:Phenotype; D010802:Phylogeny; D010913:Pituitary-Adrenal System / Q000254:growth & development* / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013312:Stress, Physiological / Q000378:metabolism
D000305:Adrenal Cortex Hormones; D002395:Catecholamines