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 96 h exposure to CuNPs or Cu²⁺, recovery was tested 14 min and 7 days after exposure using electro-olfactography (EOG). Results indicated the 14 min 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.

为了响应嗅觉感觉神经元 (OSN) 接收到的环境信息，鱼会表现出对繁殖和生存至关重要的不同行为。直接暴露于环境污染物对 OSN 的损害会破坏鱼类的嗅觉。铜纳米粒子 (CuNPs) 是神经毒性污染物，会损害鱼类的嗅觉功能。然而，尚不确定 CuNP 诱导的嗅觉功能障碍是否可逆。在这里，我们比较了虹鳟鱼在暴露于 CuNPs 或溶解的铜 (Cu ²⁺ ) 后嗅觉黏膜的恢复情况。暴露于 CuNPs 或 Cu ^{2+ 96 小时后}，在暴露后 14 分钟和 7 天使用电子嗅觉仪 (EOG) 测试恢复。结果表明 14 分钟的恢复期不足以提高任一铜处理中的嗅觉敏感性。过渡到清洁水 7 天后，嗅觉黏膜能够从 Cu ^2+中恢复-诱导的功能障碍，而在暴露于 CuNP 的 OSN 中没有观察到恢复。当恢复期后嗅觉粘膜中没有明显积累铜时，观察到这种在 CuNP 处理中的嗅觉功能障碍。在 7 天的恢复期后，暴露于 CuNP 的鱼中与嗅觉信号转导 (OST) 相关的基因子集的转录丰度被下调。这些结果表明，在 CuNP 处理的 OSN 的恢复期间，通过 OST 级联的气味接收仍然受损。离子调节基因转录本在任何一种铜处理中都没有失调，这表明神经离子平衡在恢复期后没有受到影响。总的来说，我们的研究结果表明，CuNP 诱导的嗅觉功能障碍在 7 天的恢复期后是不可逆的。