This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Many of the drugs that target human brain chemistry, such as antidepressants, are still biologically active when they leave the body. These substances and their metabolites can persist in wastewater and eventually end up in the sea, rivers or other aquatic environments.
Because fish also use the same neurotransmitters as humans, including serotonin, dopamine and norepinephrine, pharmaceuticals designed to interact with these chemical signals in humans can also interfere with fish's biological processes, potentially affecting both behavior and physiology. However, observing behavioral changes in exposed fish does not by itself reveal how a given drug caused that effect. Antidepressants often act on proteins called monoamine transporters, which help clear serotonin, dopamine and norepinephrine from the synaptic cleft.
The three main transporters are known as SERT for serotonin, DAT for dopamine and NET for norepinephrine. Although fish possess versions of these proteins, it remains unclear whether they respond to human-targeted pharmaceuticals in a similar way to their human counterparts. Moreover, most mechanistic research has focused on a small number of fish species, so scientists are not sure whether pharmaceutical sensitivity is broadly shared across fish.
To address these questions, a research team led by Professor Shinichi Miyagawa of the Department of Biological Science and Technology, Faculty of Advanced Engineering at Tokyo University of Science, Japan, characterized monoamine transporters from two evolutionarily distinct fish species: medaka (Oryzias latipes) and ayu (Plecoglossus altivelis). The study, published in Environmental Science & Technology on Aug. 24, 2026, was co-authored by Professor Masaru Ihara of the Faculty of Agriculture and Marine Science at Kochi University, Japan. The researchers first identified and cloned genes encoding DAT, NET and two types of SERT (SERTa and SERTb) from both fish species.
The team produced these transporters in the laboratory by culturing genetically engineered human cells and then exposed them to a range of commonly used antidepressants. By measuring how effectively the transporters took up a fluorescent marker, the researchers could determine how strongly each drug inhibited transporter activity. The results showed that SERTa was consistently much more sensitive to antidepressants than SERTb in both fish species.
This is consistent with the team's genetic analysis, as human SERT belongs to the SERTa lineage, whereas SERTb is absent in mammalian species. SERTb also contains substitutions at several residues associated with antidepressant interactions. Surprisingly, when the researchers compared fish SERTa with human SERT, the fish transporter often responded at lower drug concentrations, sometimes more than 10 times lower than those affecting the human transporter.
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