Abstract
As acute stress induced by predation risk can generate significant oxidative damage, prey organisms are forced to balance their defence reaction and the cost of activating the cellular defence system. Stress tolerance differs significantly among species; therefore predator pressure indirectly shapes the community structure. To test adaptation abilities of amphipod crustaceans (Dikerogammarus villosus and Gammarus jazdzewskii) we exposed them to acute (35 min.) and chronic (1 or 7 days) predation risk (the Eurasian perch). We measured respiration (related to metabolic rate), cellular defence systems (antioxidant enzyme (catalase) activity and heat shock protein (Hsp70) concentration), and the level of oxidative damage (thiobarbituric acid reactive substances (TBARS) concentration). Both amphipods increased their respiration rate in the presence of predation cues, irrespective of the duration of their pre-exposure to danger. This increase in D. villosus was initiated more quickly (immediately vs. after 10 min. of the test) and lasted for a longer time (20 vs. 10 min.) than in G. jazdzewskii. However, only G. jazdzewskii after a short exposure to predation risk exhibited an increase in its catalase activity, Hsp70 concentration and oxidative damage. No changes in these parameters were exhibited by D. villosus or after a chronic exposure of G. jazdzewskii to predation cues. Our results show that prey organisms are able to reconfigure their physiology to maintain increased metabolic rate under prolonged predator pressure and, at the same time, reduce oxidative damage as well as costs related to anti-oxidant defence.
Highlights
Predator pressure is a crucial evolutionary force, driving a number of adaptations in prey species (Yoshida et al 2003; Bollache et al 2006; Engel and Tollrian 2009; Naddafi and Rudstam 2013)
We evaluated the heat shock protein 70 (Hsp 70) level, which is often increased in stress conditions (Sørensen et al 2003), including predator presence (Slos and Stoks 2008)
Only D. villosus responded to the predation cue, doubling its oxygen consumption compared to the control treatment (Fig. 1a)
Summary
Predator pressure is a crucial evolutionary force, driving a number of adaptations in prey species (Yoshida et al 2003; Bollache et al 2006; Engel and Tollrian 2009; Naddafi and Rudstam 2013). In response to predation risk, prey individuals reallocate available energy from growth and reproduction to defence mechanisms, expressed as changes in behaviour, morphology and life history (Creel et al 2007; Strobbe et al 2010; Hawlena et al 2011). At the same time prey individuals limit food acquisition, intensifying negative non-consumptive predator effects (Jermacz and Kobak 2017; Beermann et al 2018). It was experimentally demonstrated that changes in prey physiology could be responsible for the lower growth (Slos and Stoks 2008; Hawlena and Schmitz 2010; Janssens and Stoks 2013; Jermacz and Kobak 2017) or even death (McCauley et al 2011) of prey under predation risk
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