Hormones translate environmental information to time amphibian metamorphosis

DENVER, Robert/J*; CRESPI, Erica/J; University of Michigan; University of Michigan: Hormones translate environmental information to time amphibian metamorphosis

Metamorphic timing in amphibians is highly dependent on environmental conditions. Hormones, in particular those of the neuroendocrine stress axis, play central roles in linking sensory information about the external environment with changes in development and growth. Neuropeptides of the corticotropin-releasing factor (CRF) family play critical roles in behavioral, physiological and developmental responses to stress. Hypothalamic corticotropin-releasing factor (CRF) neurons respond to environmental stressors, and CRF peptides stimulate the secretion of both thyroid hormone and corticosterone, two hormones that control metamorphosis. Also, CRF peptides are potent anorexigens, and the reduced foraging seen in tadpoles after exposure to an acute stressor and just prior to metamorphic climax is mediated, at least in part, by these peptides. Thus, in response to adverse environmental conditions, the stress neurohormone CRF simultaneously reduces growth rate through a central anorectic action, and induces morphological changes associated with metamorphosis through its hypophysiotropic actions. Resource restriction of late prometamorphic tadpoles accelerates metamorphosis, elevates brain CRF content, and whole body corticosterone and thyroid hormone content, suggesting that CRF production is influenced by energy balance in tadpoles. In mammals the activation of the neuroendocrine stress axis in the fetus or neonate leads to long term phenotypic changes in the adult; e.g., profound effects on growth, behavior and the basal activity and reactivity of the stress axis. Our recent findings show that, in addition to playing an essential role in timing metamorphosis, exposure to stress hormones during early development can have important organizing effects in the amphibian, leading to long-term, permanent alterations in phenotypic expression. (supported by NSF grant IBN 0235401 to R.J.D.)

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