Fluoxetine enhances reproductive output without affecting spawning-site selection in turquoise killifish

Pharmaceutical contamination of aquatic ecosystems is widespread, with mounting evidence that pollutants such as the antidepressant fluoxetine can boost fish offspring production. But such increases may come at a hidden cost if pharmaceuticals also disrupt key reproductive behaviors-like where fish choose to spawn-that determine whether those offspring ultimately survive. To test this possibility, we exposed turquoise killifish (Nothobranchius furzeri) to a field-realistic concentration of fluoxetine (317 ng/L) in a controlled laboratory experiment. Fish could choose among spawning sites of white, orange, or black sand, both in single pairs and in groups. Fluoxetine-exposed fish produced about 50% more eggs in single pairs, but this effect was not observed in groups. Regardless of social context, fish deposited roughly four times more eggs on black sand than on orange or white sand, and fluoxetine did not alter spawning-site preference. In addition, fluoxetine did not affect habitat preference in a non-mating context, with both control and fluoxetine-treated fish spending more time over darker backgrounds. These results show that environmentally relevant fluoxetine concentrations can enhance reproductive output without necessarily affecting spawning-site selection. The broader ecological significance of such changes will depend on how pharmaceutical-induced shifts in reproduction interact with natural social and habitat dynamics in the wild.