The stress axis in teleost fish attempts to maintain internal homeostasis in the face of allostatic loading.However,stress axis induction has been associated with a higher predation rate in fish.To date,the physiologi...The stress axis in teleost fish attempts to maintain internal homeostasis in the face of allostatic loading.However,stress axis induction has been associated with a higher predation rate in fish.To date,the physiological and behavioral factors associated with this outcome are poorly understood.The purpose of the present study was to investigate the impact of experimental cortisol elevation on anti-predator behavior and physiological responses to predator presence.We hypothesized that semi-chronic cortisol elevation would increase susceptibility to predation by increasing stress-induced risk-taking behaviors.To test this hypothesis,schoolmaster snapper were given cocoa butter implants without cortisol(sham)or with cortisol(50 mg/kg body weight)and tethered to cover.Fish were exposed to either a lemon shark or control conditions for 15-min.Space use and activity were recorded throughout and fish were terminally sampled for blood.Cortisol implantation,relative to shams,resulted in higher blood glucose and plasma cortisol concentrations with a lower plasma lactate concentration.Shark exposure,relative to controls,elicited higher blood glucose and lactate concentrations but had no effect on plasma cortisol concentration.No interactions were detected between shark exposure and cortisol treatment for any physiological trait.Behavioral metrics,including shelter use and activity,were unaffected by either cortisol implantation or shark exposure.Physiological responses to cortisol implantation likely resulted from enhanced gluconeogenic activity,whereas alterations under predator exposure may have been the product of catecholamine mobilization.Further work should address context-specific influences of stress in mediating behavioral responses to predation.展开更多
基金M.J.Lawrence is supported by an NSERC PGS-D.S.JCooke is supported by NSERC and the Canada Research Chairs Program+3 种基金E.J.Eliason was supported by an NSERC PDFJ.W.Brownscombe is supported by NSERC and The Berkeley Marine Conservation Fellowship from The American Fisheries SocietyK.M.Gilmour is supported by NSERCJ.W.Mandelman is supported by the New England Aquarium.
文摘The stress axis in teleost fish attempts to maintain internal homeostasis in the face of allostatic loading.However,stress axis induction has been associated with a higher predation rate in fish.To date,the physiological and behavioral factors associated with this outcome are poorly understood.The purpose of the present study was to investigate the impact of experimental cortisol elevation on anti-predator behavior and physiological responses to predator presence.We hypothesized that semi-chronic cortisol elevation would increase susceptibility to predation by increasing stress-induced risk-taking behaviors.To test this hypothesis,schoolmaster snapper were given cocoa butter implants without cortisol(sham)or with cortisol(50 mg/kg body weight)and tethered to cover.Fish were exposed to either a lemon shark or control conditions for 15-min.Space use and activity were recorded throughout and fish were terminally sampled for blood.Cortisol implantation,relative to shams,resulted in higher blood glucose and plasma cortisol concentrations with a lower plasma lactate concentration.Shark exposure,relative to controls,elicited higher blood glucose and lactate concentrations but had no effect on plasma cortisol concentration.No interactions were detected between shark exposure and cortisol treatment for any physiological trait.Behavioral metrics,including shelter use and activity,were unaffected by either cortisol implantation or shark exposure.Physiological responses to cortisol implantation likely resulted from enhanced gluconeogenic activity,whereas alterations under predator exposure may have been the product of catecholamine mobilization.Further work should address context-specific influences of stress in mediating behavioral responses to predation.
