Relating olfactory neurotoxicity to altered olfactory-mediated behaviors in rainbow trout exposed to three currently-used pesticides

Odor-evoked neurophysiological responses can form the basis for behavioral responses. Here we first characterized olfactory-mediated behavioral and neurophysiological responses of juvenile rainbow trout to the amino acid l-histidine, then looked at whether there were similar responses to the carbamate antisapstain IPBC and the herbicides atrazine and Roundup®, and lastly explored how exposures to these pesticides modified the l-histidine responses. Trout were behaviorally attracted to 10−7 M l-histidine (as assayed in a counter-current olfactometer), but this preference behavior switched to indifference with higher histidine concentrations. Neurophysiologically, the summed electrical responses of peripheral olfactory neurons, as measured using electro-olfactogram (EOG), was 0.843 ± 0.252 mV to 10−7 M l-histidine. Of the pesticides, only Roundup® evoked EOGs, indicating the amino acid-based pesticide may have acted as an odorant, and generated a behavioral response: it was avoided at active ingredient [AI; glyphosate isopropyl amine] concentrations ≥ 10 mg/l. With 30 min pesticide exposures, 10−7 M l-histidine preference behavior was eliminated following exposure to 1 μg/l IPBC and atrazine, and 100 μg/l AI Roundup®. Similarly, 10−7 M l-histidine-evoked EOGs were significantly reduced by exposure to 1 μg/l IPBC, 10 μg/l atrazine, and 100 μg/l AI Roundup®. When combined together, the results demonstrate that typical preference behavior can be abolished when neurophysiological responses are reduced by >60% of control. This asymmetry in response thresholds suggests that behavioral responses may be more sensitive toxicological endpoints than neurophysiological responses.