Journal
PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
Volume 280, Issue 1758, Pages -Publisher
ROYAL SOC
DOI: 10.1098/rspb.2012.3075
Keywords
anti-predator response; stress; tadpole; corticosterone; phenotypic plasticity
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Funding
- University of Michigan Department of Ecology and Evolutionary Biology Block
- NSF [IOS 0909703, IBN 0235401, IOS 0641587]
- NSF LTREB [DEB 0454519]
- Direct For Biological Sciences [0922583] Funding Source: National Science Foundation
- Division Of Integrative Organismal Systems [0922583] Funding Source: National Science Foundation
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Amphibian tadpoles display extensive anti-predator phenotypic plasticity, reducing locomotory activity and, with chronic predator exposure, developing relatively smaller trunks and larger tails. In many vertebrates, predator exposure alters activity of the neuroendocrine stress axis. We investigated predator-induced effects on stress hormone production and the mechanistic link to anti-predator defences in Rana sylvatica tadpoles. Whole-body corticosterone (CORT) content was positively correlated with predator biomass in natural ponds. Exposure to caged predators in mesocosms caused a reduction in CORT by 4 hours, but increased CORT after 4 days. Tadpoles chronically exposed to exogenous CORT developed larger tails relative to their trunks, matching morphological changes induced by predator chemical cue; this predator effect was blocked by the corticosteroid biosynthesis inhibitor metyrapone. Tadpole tail explants treated in vitro with CORT increased tissue weight, suggesting that CORT acts directly on the tail. Short-term treatment of tadpoles with CORT increased predation mortality, likely due to increased locomotory activity. However, long-term CORT treatment enhanced survivorship, likely due to induced morphology. Our findings support the hypothesis that tadpole physiological and behavioural/morphological responses to predation are causally interrelated. Tadpoles initially suppress CORT and behaviour to avoid capture, but increase CORT with longer exposure, inducing adaptive phenotypic changes.
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