No evidence of increased growth or mortality in fish exposed to oxazepam in semi-natural ecosystems.

An increasing number of short-term laboratory studies on fish reports behavioral effects from exposure to aquatic contaminants or raised carbon dioxide levels affecting the GABA A receptor. However, how such GABAergic behavioral modifications (GBMs) impact populations in more complex natural systems is not known. In this study, we induced GBMs in European perch ( Perca fluviatilis ) via exposure to a GABA agonist (oxazepam) and followed the effects on growth and survival over one summer (70 days) in replicated pond ecosystems. We hypothesized that anticipated GBMs, expressed as anti-anxiety like behaviors (higher activity and boldness levels), that increase feeding rates in laboratory assays, would; i) increase growth and ii) increase mortality from predation. To test our hypotheses, 480 PIT tagged perch of known individual weights, and 12 predators (northern pike, Esox lucius ) were evenly distributed in 12 ponds; six control (no oxazepam) and six spiked (15.5 ± 4 μg l − 1 oxazepam [mean ± 1 S.E.]) ponds. Contrary to our hypotheses, even though perch grew on average 16% more when exposed to oxazepam, we found no significant difference between exposed and control fish in growth (exposed: 3.9 ± 1.2 g, control: 2.9 ± 1 g [mean ± 1 S.E.], respectively) or mortality (exposed: 26.5 ± 1.8 individuals pond − 1 , control: 24.5 ± 2.6 individuals pond − 1 , respectively). In addition, we show that reduced prey capture efficiency in exposed pike may explain the lack of significant differences in predation. Hence, our results suggest that GBMs, which in laboratory studies impact fish behavior, and subsequently also feeding rates, do not seem to generate strong effects on growth and predation-risk in more complex and resource limited natural environments. [ABSTRACT FROM AUTHOR]