ENVIRONMENT-NEUROENDOCRINE INTERACTIONS IN THE CONTROL OF AMPHIBIAN METAMORPHOSIS

The profound morphological changes which occur during amphibian metamo rphosis are controlled by thyroid hormone, the production of which is regulated by the neuroendocrine system. Attempts to identify neurohorm ones which control the tadpole thyroid axis have focussed on the tripe ptide thyrotropin-releasing hormone (TRH). However, exogenous TRH does not influence the rate of metamorphosis or stimulate the release of t hyrotropic activity (TSH) by tadpole pituitaries in vitro. We found th at corticotropin-releasing hormone (CRH) is a potent stimulator of the thyroid asis in tadpoles and this led us to hypothesize that CRH may function as a common neuroregulator of thyroid and interrenal activity during metamorphosis (DENVER & LIGHT, 1989). We and others have since demonstrated that injection of CRH-like peptides accelerates metamorp hosis in several amphibian species and elevates whole body concentrati ons of corticosterone, thyroxine and triiodothyronine. Conversely, tre atment with anti-CRH serum ora CRH receptor antagonist blocks or slows metamorphosis. Expression of the CRH gene is correlated with thyroid hormone production and morphogenesis. The activity of CRH neurons is e xtremely sensitive to fluctuations in the environment, and changes in the larval habitat can influence the rate of morphogennesis. We have e vidence that CRH is involved in the acceleration of metamorphosis in a toad which rapid development in response to habitat desiccation. This undergoes response can be replicated in the laboratory, and treatment of tadpoles with CRI-I receptor antagonist blocks this response. The CRH neuron may function as a transducer of environmental information ( e.g., environmental 'stress') during development and allow tadpoles to assess habitat quality and alter their rate of development accordingl y.