Environmental stress as a developmental cue: Corticotropin-releasing hormone is a proximate mediator of adaptive phenotypic plasticity in amphibian metamorphosis
Environmental stress as a developmental cue: Corticotropin-releasing hormone is a proximate mediator of adaptive phenotypic plasticity in amphibian metamorphosis
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DOI：
10.1006/hbeh.1997.1383
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发表时间：
1997-04-01
影响因子：
3.5
通讯作者：
Denver, RJ
中科院分区：
文献类型：
--
作者：
Denver, RJ
环境诱导的表型可塑性使发育中的生物体能够适应其栖息地的变化。沙漠两栖动物已经进化出了在不可预测的环境中成功发展的特征。这些物种的蝌蚪可以加速变态，因为他们的池塘干涸，从而逃避死亡的幼虫栖息地。这种发育反应可以在实验室中复制，从而可以阐明潜在的生理机制。在这里，我展示了一个经典的神经激素应激途径（包括促肾上腺皮质激素释放激素，CRH）和栖息地干燥的发展反应之间的联系。注射CRH样肽加速西方铲足蟾蜍蝌蚪的变态。相反，用两种CRH拮抗剂，CRH受体拮抗剂α-螺旋CRH（9-41）和抗CRH血清处理，减弱了由栖息地干燥诱导的发育加速。栖息地干燥的蝌蚪表现出升高的下丘脑CRH含量的时候，他们对水位下降的发展作出反应。CRH注射升高全身甲状腺素，三碘甲状腺原氨酸，皮质酮含量，主要的激素调节器的变态。相反，α-螺旋CRH（9-41）降低甲状腺活性。这些结果支持CRH作为环境刺激的神经激素换能器到内分泌反应，调节变态率的核心作用。因为在哺乳动物中，增加的胎儿/胎盘CRH产生可能会引发分娩，并且CRH与胎儿应激引起的早产有关，这种神经激素途径可能代表了一种遗传学上古老的发育调节系统，该系统允许生物体逃离不利的幼虫/胎儿栖息地。(C)北京：科学出版社.
Environmentally induced phenotypic plasticity allows developing organisms to respond adaptively to changes in their habitat. Desert amphibians have evolved traits which allow successful development in unpredictable environments. Tadpoles of these species can accelerate metamorphosis as their pond dries, thus escaping mortality in the larval habitat. This developmental response can be replicated in the laboratory, which 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 developmental response to habitat desiccation. Injections of CRH-like peptides accelerated 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 acceleration induced by habitat desiccation. Tadpoles subjected to habitat 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 corticosterone content, the primary hormonal regulators of metamorphosis. In contrast, alpha-helical CRH(9-41) reduced thyroid activity. These results 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 CRH production may initiate parturition, and CRH has been implicated in precipitating preterm birth arising from fetal stress, this neurohormonal pathway may represent a phylogenetically ancient developmental regulatory system that allows the organism to escape an unfavorable larval/fetal habitat. (C) 1997 Academic Press.