Taurine-mediated aggression is abolished via 5-HT1A antagonism and serotonin depletion in zebrafish

Abstract

Taurine is one of the most abundant amino acids in vertebrates involved in important physiological functions, including osmoregulation, membrane stability, and neuronal activity. The pleiotropic effects of taurine support the existence of different mechanisms of action (e.g., modulation of GABAA, strychnine-sensitive glycine, and NMDA receptors), which can play a role in aggressive-related responses. However, the mechanisms underlying the effects of taurine on aggression are still poorly understood. Because aggression has been associated with diverse central mechanisms, especially serotonergic activity, we aimed to investigate the involvement of this system in taurine-induced aggression in zebrafish. We treated adult zebrafish with ρ-chlorophenylalanine (ρCPA), an inhibitor of the serotonin synthesis, as well as 5-HT1A receptor antagonist and agonist (WAY100135 and buspirone, respectively). Taurine effects were tested individually at three concentrations (42, 150, and 400 mg/L) for 60 min. We further analyzed the effects on aggression and locomotion using the mirror-induced aggression test. Taurine concentration that changed behavioral responses was selected to the succeeding pharmacological experiments using ρCPA, WAY100135, and buspirone. We found that buspirone did not alter the aggression. Yet, 42 mg/L taurine increased aggression, which was abolished by ρCPA and WAY100135, indicating the involvement of 5-HT1A receptors in taurine-mediated aggression. These set of data support an indirect mechanism mediating taurine-induced aggression via serotonin release and activation of 5-HT1A receptors in zebrafish. While the exact mechanisms underlying aggression are still unclear, our novel findings reveal a key role of the serotonergic system in the effects of taurine, supporting the use of zebrafish models to understand the neural basis of aggression in vertebrates.