Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis
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In: Integrative Organismal Biology, Vol. 5, No. 1, obad021, 2023, p. obad021.
Research output: Contribution to journal › Article › peer-review
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T1 - Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis
AU - Üveges, Bálint
AU - Kalina, Csenge
AU - Szabó, Krisztina
AU - Móricz, Ágnes M.
AU - Holly, Dóra
AU - Gabor, Caitlin R.
AU - Hettyey, Attila
AU - Bókony, Veronika
N1 - © The Author(s) 2023. Published by Oxford University Press on behalf of the Society for Integrative and Comparative Biology.
PY - 2023
Y1 - 2023
N2 - Chemical defense is a crucial component of fitness in many organisms, yet the physiological regulation of defensive toxin synthesis is poorly understood, especially in vertebrates. Bufadienolides, the main defensive compounds of toads, are toxic to many predators and other natural enemies, and their synthesis can be upregulated by stressors, including predation risk, high conspecific density, and pollutants. Thus, higher toxin content may be the consequence of a general endocrine stress response in toads. Therefore, we hypothesized that bufadienolide synthesis may be stimulated by elevated levels of corticosterone (CORT), the main glucocorticoid hormone of amphibians, or by upstream regulators that stimulate CORT production. To test these alternatives, we treated common toad tadpoles with exogenous CORT (exoCORT) or metyrapone (MTP, a CORT-synthesis inhibitor that stimulates upstream regulators of CORT by negative feedback) in the presence or absence of predation cues for 2 or 6 days, and subsequently measured their CORT release rates and bufadienolide content. We found that CORT release rates were elevated by exoCORT, and to a lesser extent also by MTP, regardless of treatment length. Bufadienolide content was significantly decreased by treatment with exoCORT for 6 days but was unaffected by exposure to exoCORT for 2 days or to MTP for either 6 or 2 days. The presence or absence of predation cues affected neither CORT release rate nor bufadienolide content. Our results suggest that changes in bufadienolide synthesis in response to environmental challenges are not driven by CORT but may rather be regulated by upstream hormones of the stress response.
AB - Chemical defense is a crucial component of fitness in many organisms, yet the physiological regulation of defensive toxin synthesis is poorly understood, especially in vertebrates. Bufadienolides, the main defensive compounds of toads, are toxic to many predators and other natural enemies, and their synthesis can be upregulated by stressors, including predation risk, high conspecific density, and pollutants. Thus, higher toxin content may be the consequence of a general endocrine stress response in toads. Therefore, we hypothesized that bufadienolide synthesis may be stimulated by elevated levels of corticosterone (CORT), the main glucocorticoid hormone of amphibians, or by upstream regulators that stimulate CORT production. To test these alternatives, we treated common toad tadpoles with exogenous CORT (exoCORT) or metyrapone (MTP, a CORT-synthesis inhibitor that stimulates upstream regulators of CORT by negative feedback) in the presence or absence of predation cues for 2 or 6 days, and subsequently measured their CORT release rates and bufadienolide content. We found that CORT release rates were elevated by exoCORT, and to a lesser extent also by MTP, regardless of treatment length. Bufadienolide content was significantly decreased by treatment with exoCORT for 6 days but was unaffected by exposure to exoCORT for 2 days or to MTP for either 6 or 2 days. The presence or absence of predation cues affected neither CORT release rate nor bufadienolide content. Our results suggest that changes in bufadienolide synthesis in response to environmental challenges are not driven by CORT but may rather be regulated by upstream hormones of the stress response.
KW - stress response
KW - poison
KW - phenotypic plasticity
KW - corticosterone
KW - ELISA
KW - HPA axis
U2 - 10.1093/iob/obad021
DO - 10.1093/iob/obad021
M3 - Article
C2 - 37435008
VL - 5
SP - obad021
JO - Integrative Organismal Biology
JF - Integrative Organismal Biology
SN - 2517-4843
IS - 1
M1 - obad021
ER -