Prey reconfigure their physiology to avoid costs of prolonged predator pressure. However, these changes might not occur under periodic predation risk, with repeating acute phases. To test the effect of predation risk continuity on changes in prey physiology, we exposed amphipods: Dikerogammarus villosus and Gammarus jazdzewskii to periodic and constant predation cue. After one week, we measured: cellular defence systems: total antioxidant status (TAS), heat shock proteins (Hsp70); intracellular damage marker: lipid peroxidation (TBARS); condition index: glycogen concentration. Predator presence reduced TAS level in G. jazdzewskii independent of its continuity and in D. villosus after periodic exposure. Amphipods showed downregulation of Hsp70 when exposed to periodic (D. villosus) or constant (G. jazdzewskii) predation risk. Exposure to predators reduced TBARS level in D. villosus (irrespective of the continuity) and G. jazdzewskii (periodic exposure). Glycogen concentration in both species was not affected by predator presence. Thus, the continuity of the predator cue shaped prey physiology reconfiguration, optimizing costs of physiological adjustments under challenging conditions. Nevertheless, the lack of negative consequences of the prolonged exposure to the predator cue, whether constant or periodic, shows that amphipods can thrive under chronic predation risk, which is a constant part of the wild environment.
One of the options to reduce predation risk is reallocation of energy into locomotion system. The higher aerobic capacity, the more energy can be partitioned into an escape. Thus, increase in aerobic capacity can increase prey escape abilities. We investigated prey (freshwater crustaceans: Dikerogammarus villosus and Gammarus jazdzewskii) ability to improve their locomotor performance through an increase in aerobic capacity under chronic predation risk. We forced gammarids (pre-exposed to the predation cue or control) to long-distance swimming in the presence or absence of predation cues to obtain: control (pre-exposure and test in control conditions), acute (pre-exposure to control conditions, test in the presence of the predation cue) and chronic (pre-exposure and test in the presence of the cue) risk treatments. After this forced swimming effort, we measured various swimming parameters, glycogen content, and lactate concentration of the experimental amphipods. Exposure to predation cues made G. jazdzewskii reduce its speed after prolonged forced swimming in the presence of predation cues, whereas D. villosus never changed its swimming performance due to predation risk. In both species, post-effort lactate concentration was higher under the acute predation risk than in risk-free conditions. However, only D. villosus demonstrated lower lactate concentration when exposed to chronic vs. acute predation risk. Moreover, pre-exposure of both species to predation cues caused reduction in glycogen content. We showed that under chronic predation risk some prey species can modify their physiology to increase aerobic capacity and sustain high efficiency of escape performance. However, this phenomenon is species-specific and costly.
Oxygen free radicals have been implicated in brain damage after neonatal asphyxia. In the early phase of asphyxia/reoxygenation, changes in antioxidant enzyme activity play a pivotal role in switching on and off the cascade of events that can kill the neurons. Hypoxia/ischemia (H/I) forces the brain to activate endogenous mechanisms (e.g., antioxidant enzymes) to compensate for the lost or broken neural circuits. It is important to evaluate therapies to enhance the self-protective capacity of the brain. In animal models, decreased body temperature during neonatal asphyxia has been shown to increase cerebral antioxidant capacity. However, in preterm or severely asphyxiated newborns this therapy, rather than beneficial seems to be harmful. Thus, seeking new therapeutic approaches to prevent anoxia-induced complications is crucial. Pharmacotherapy with deferoxamine (DFO) is commonly recognized as a beneficial regimen for H/I insult. DFO, via iron chelation, reduces oxidative stress. It also assures an optimal antioxidant protection minimizing depletion of the antioxidant enzymes as well as low molecular antioxidants. In the present review, some aspects of recently acquired insight into the therapeutic effects of hypothermia and DFO in promoting neuronal survival after H/I are discussed.
Introduction: Low-frequency electromagnetic field (50 Hz) (EMF) can modify crucial neuronal processes. Existing data indicate that exposure to EMF may represent a mild stressor and contribute to disturbances of hypothalamic-pituitary-adrenal (HPA) axis. The important regulatory pathways controlling HPA axis activity include two types of corticosteroid receptors: mineralocorticoid (MR) and glucocorticoid (GR) receptors. There are particularly abundant in the hippocampus, a key locus of HPA axis feedback control. The research aimed at determining whether 1) EMF exhibits hormesis, it means bidirectional action depending on EMF intensity (1 or 7 mT), and 2) repeated EMF exposure changes stress response to subsequent stress factors. Methods: The exposure (7-day, 1h/day) of adult rats to EMF (1 mT and 7 mT) was repeated 3 times. HPA axis hormones and their receptors were analysed after each following exposure. Moreover, the impact of EMF exposure on hormonal and behavioural responses to subsequent stress factor - open-field test was evaluated. Results/Discussion: Our data suggest that exposure to EMF can establish a new “set-point” for HPA axis activity. The direction and dynamics of this process depend on the intensity of EMF and the number of exposures. EMF of 1 mT induced an adaptive stress response, but 7 mT EMF caused sensitization. Consequently, EMF changed the vulnerability of the organism to a subsequent stress factor. We have also shown the increase of MR mRNA abundance in hippocampus of 1 mT EMF exposed rats, which can represent the possible neuroprotective response and suggest therapeutic properties of electromagnetic fields.
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