Rj. Denver, ENVIRONMENT-NEUROENDOCRINE INTERACTIONS IN THE CONTROL OF AMPHIBIAN METAMORPHOSIS, Netherlands journal of zoology, 45(1-2), 1995, pp. 195-200
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.