ENVIRONMENTAL-STRESS AS A DEVELOPMENTAL CUE - CORTICOTROPIN-RELEASINGHORMONE IS A PROXIMATE MEDIATOR OF ADAPTIVE PHENOTYPIC PLASTICITY IN AMPHIBIAN METAMORPHOSIS

Environmentally induced phenotypic plasticity allows developing organi sms to respond adaptively to changes in their habitat. Desert amphibia ns have evolved traits which allow successful development in unpredict able environments. Tadpoles of these species can accelerate metamorpho sis as their pond dries, thus escaping mortality in the larval habitat . This developmental response can be replicated in the laboratory, whi ch allows elucidation of the underlying physiological mechanisms. Here I demonstrate a link between a classical neurohormonal stress pathway (involving corticotropin-releasing hormone, CRH) and the developmenta l response to habitat desiccation. Injections of CRH-like peptides acc elerated metamorphosis in western spadefoot toad tadpoles. Conversely, treatment with two CRH antagonists, the CRH receptor antagonist alpha -helical CRH(9-41) and anti-CRH serum, attenuated the developmental ac celeration induced by habitat desiccation. Tadpoles subjected to habit at desiccation exhibited elevated hypothalamic CRH content at the time when they responded developmentally to the declining water level. CRH injections elevated whole-body thyroxine, triiodothyronine, and corti costerone content, the primary hormonal regulators of metamorphosis. I n contrast, alpha-helical CRH(9-41) reduced thyroid activity. These re sults support a central role for CRH as a neurohormonal transducer of environmental stimuli into the endocrine response which modulates the rate of metamorphosis. Because in mammals, increased fetal/placental C RH production may initiate parturition, and CRH has been implicated in precipitating preterm birth arising from fetal stress, this neurohorm onal pathway may represent a phylogenetically ancient developmental re gulatory system that allows the organism to escape an unfavorable larv al/fetal habitat. (C) 1997 Academic Press.