Recovery of rainbow trout olfactory function following exposure to copper nanoparticles and copper ions.

Abstract

In response to environmental information received by olfactory sensory neurons (OSNs), fish display different behaviors that are crucial for reproduction and survival. Damage to OSNs from direct exposure to environmental contaminants can disrupt fish olfaction. Copper nanoparticles (CuNPs) are neurotoxic contaminants which can impair fish olfactory function. However, it is uncertain if CuNP-induced olfactory dysfunction is reversible. Here, we compared the recovery of rainbow trout olfactory mucosa after being exposed to CuNPs or dissolved copper (Cu2+). Following a 96h exposure to CuNPs or Cu2+, recovery was tested 14min and 7 days after exposure using electro-olfactography (EOG). Results indicated the 14min recovery period was not sufficient to improve the olfactory sensitivity in either Cu treatment. After 7 days of transition to clean water, olfactory mucosa was able to recover from Cu2+-induced dysfunction, while no recovery was observed in the CuNP-exposed OSNs. This olfactory dysfunction in the CuNP treatment was observed when no Cu was significantly accumulated in the olfactory mucosa after the recovery period. The transcript abundances of a subset of genes involved in olfactory signal transduction (OST) were downregulated in the CuNP-exposed fish after the 7-day recovery period. These results revealed that odorant reception through OST cascade remained impaired over the recovery period in the CuNP-treated OSNs. The ion regulation gene transcripts were not dysregulated in either Cu treatment, which suggests that neural ion balance was not affected following the recovery period. Collectively, our findings revealed the CuNP-induced olfactory dysfunction was irreversible after the 7-day recovery period. Given the importance of olfaction in crucial aspects of fish life, it is likely that the CuNP-induced impairment of odorant reception pose risks to the survival of fish.