Chlorpyrifos is a common organophosphate insecticide that has been widely detected in surface waters that provide habitat for Pacific salmon in the western United States. Although chlorpyrifos is known to inhibit acetylcholinesterase (AChE) in the brain and muscle of salmonids, the relationship between sublethal AChE inhibition and more integrative indicators of neuro-behavioral impairment are poorly understood. This is particularly true for exposures that reflect the typical range of pesticide concentrations in the aquatic environment. To directly compare the effects of chlorpyrifos on AChE activity and salmon behavior, we exposed juvenile coho salmon (Oncorhynchus kisutch) to chlorpyrifos (0-2.5 microg/L) for 96 h. A computer-assisted, three-dimensional video imaging system was used to measure spontaneous swimming and feeding behaviors in control and chlorpyrifos-exposed fish. After the behavioral trials, brain and muscle tissues were collected and analyzed for AChE activity. Chlorpyrifos inhibited tissue AChE activity and all behaviors in a dose-dependent manner. Moreover, brain AChE inhibition and reductions in spontaneous swimming and feeding activity were significantly correlated. Benchmark concentrations for sublethal neurotoxicity (statistical departure values) were <0.5 microg/L and were similar for both neurochemical and behavioral endpoints. Collectively, these results indicate a close relationship between brain AChE inhibition and behavioral impairment in juvenile coho exposed to chlorpyrifos at environmentally realistic concentrations.
Motor vehicles are a major source of toxic contaminants such as copper, a metal that originates from vehicle exhaust and brake pad wear. Copper and other pollutants are deposited on roads and other impervious surfaces and then transported to aquatic habitats via stormwater runoff. In the western United States, exposure to non-point source pollutants such as copper is an emerging concern for many populations of threatened and endangered Pacific salmon (Oncorhynchus spp.) that spawn and rear in coastal watersheds and estuaries. To address this concern, we used conventional neurophysiological recordings to investigate the impact of ecologically relevant copper exposures (0-20 microg/L for 3 h) on the olfactory system of juvenile coho salmon (O. kisutch). These recordings were combined with computer-assisted video analyses of behavior to evaluate the sensitivity and responsiveness of copper-exposed coho to a chemical predation cue (conspecific alarm pheromone). The sensory physiology and predator avoidance behaviors of juvenile coho were both significantly impaired by copper at concentrations as low as 2 microg/L. Therefore, copper-containing stormwater runoff from urban landscapes has the potential to cause chemosensory deprivation and increased predation mortality in exposed salmon.
The sublethal effects of copper on the sensory physiology of juvenile coho salmon (Oncorhynchus kisutch) were evaluated. In vivo field potential recordings from the olfactory epithelium (electro-olfactograms) were used to measure the impacts of copper on the responses of olfactory receptor neurons to natural odorants (L-serine and taurocholic acid) and an odorant mixture (L-arginine, L-aspartic acid, L-leucine, and L-serine) over a range of stimulus concentrations. Increases in copper impaired the neurophysiological response to all odorants within 10 min of exposure. The inhibitory effects of copper (1.0-20.0 micrograms/L) were dose-dependent and they were not influenced by water hardness. Toxicity thresholds for the different receptor pathways were determined by using the benchmark dose method and found to be similar (a 2.3-3.0 micrograms/L increase in total dissolved copper over background). Collectively, examination of these data indicates that copper is broadly toxic to the salmon olfactory nervous system. Consequently, short-term influxes of copper to surface waters may interfere with olfactory-mediated behaviors that are critical for the survival and migratory success of wild salmonids.
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