Ammonia-N is a common toxic factor in aquatic environments， which inhibits fish feeding, but its mechanism remains unclear. To investigate the mechanism in inhibiting fish feeding, this study conducted experiments exposing juvenile Siberian sturgeon (Acipenser baerii) to ammonia-N at concentrations of 0, 5, 10, and 15 mg/L for 14 days. The results revealed a significant reduction in both daily and cumulative food intake. Obviously decreased hepatosomatic index (HSI), and viscerosomatic index (VSI) at 15 mg/L. On the 14th day, the serum ammonia concentration significantly increased, while the neurotoxic marker acetylcholinesterase (AchE) significantly increased. Brain tissue demonstrated damage; the activity of superoxide dismutase (SOD) was significantly increased. RNA-seq analysis and qPCR indicated that appetite-promoting factors agouti-related protein (agrp) and neuropeptide Y (npy) were significantly down-regulated, appetite-suppressing factors pro-opiomelanocortin (pomc), cocaine-and amphetamine-regulated transcript peptide (cart), and corticotropin releasing factor (crf) were significantly up-regulated. This study lays the groundwork for deeper understanding of the toxicological mechanism of ammonia-N on aquatic animals, particularly its detrimental effects on fish brain function and feeding behavior.

Acipenser baerii,Ammonia-N,Food intake,Feeding regulation