Imidacloprid poses a significant threat to aquatic ecosystems. In this study, we investigated the visual toxicity of imidacloprid and the underlying molecular mechanisms in adult zebrafish. After exposure to imidacloprid at environmental relevant concentrations (10 and 100μg/L) for 21 days, the detectable contents of imidacloprid were 23.0 ± 0.80 and 121 ± 1.56 ng/mg in eyes of adult zebrafish, respectively. The visual behavior of adult zebrafish was impaired including a reduced ability to track smoothly visual stimuli and visually guided self-motion. The immunofluorescence experiment showed that the content of Rhodopsin (Rho) in the retina of zebrafish was changed significantly. The expression rhythm of genes played key roles in capturing photons in dim (rho) and bright (opn1mw3, opn1lw2 and opn1sw2) light, and in phototransduction (gnb3b, arr3a and rpe65a), was disrupted significantly throughout a 24-h period in adult zebrafish. Targeted metabolomics analysis showed that the content of 16 metabolites associated with neurotransmitter function changed significantly, and were enriched in top three metabolism pathways including Arginine biosynthesis, Alanine, aspartate and glutamate metabolism, and Tryptophan metabolism. These results indicated that imidacloprid exposure at environmentally relevant concentrations could cause optical toxicity through disturbing the expression of opsins and affecting the phototransduction in the retina of zebrafish adults.
Keywords: Neurotransmitters; Opsins; Optokinetic response; Optomotor response; Retina.
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