Abstract

The hypothalamic-pituitary-interrenal (HPI) axis, through corticosteroid secretion, is an integral mechanism regulating internal homeostasis when vertebrates are faced with a stressor. However, continued HPI-axis stimulation can produce homeostatic overload, where corticosteroids are detrimental to organismal function. This overload condition may play an important role in mediating predator-prey interactions, because chronically/previously stressed animals may have higher rates of predator-induced mortality. However, the mechanism(s) underlying this observation are unknown. Using fish as models, we hypothesized that chronic stress would increase predation susceptibility owing to a poor physiological state (e.g. homeostatic overload) with corresponding sub-optimal changes in predator-avoidance behaviour. As cortisol is also required in low quantities to help regulate basic metabolic functions in fish, we expected that a glucocorticoid receptor antagonist (GR; e.g. homeostatic failure) may produce similar effects. Schoolmaster snapper (Lutjanus apodus) were given intraperitoneal implants of cocoa butter impregnated with nothing (sham; 5ml/kg body weight (BW)), cortisol (50mg/kg BW) or the GR antagonist RU486 (100mg/kg BW). At 24-h post-implantation, fish were tethered to the seafloor and observed for behavioural metrics associated with predation. Blood samples were collected from a subset of fish to assess the physiological consequences of the implants. Cortisol- and RU486-implanted fish both had significantly higher plasma cortisol concentrations than sham fish, with blood glucose and plasma urea being elevated only in the former. Further, anti-predator behaviours and predation mortality did not differ significantly among treatments. Despite changes in physiological state, predation susceptibility was unaffected, a finding that may reflect the complex relationships linking the physiology and behaviour of an organism as well as potential tethering artefacts.

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