Taurine modulates behavioral effects of intermittent ethanol exposure without changing brain monoamine oxidase activity in zebrafish: Attenuation of shoal- and anxiety-like responses, and abolishment of memory acquisition deficit.

Prolonged alcohol consumption has been considered as an important risk factor for various diseases. Chronic ethanol (EtOH) intake is associated with deleterious effects on brain functions culminating in robust behavioral changes. Notably, drugs available to treat the effects of EtOH have low therapeutic efficacy so far. Taurine (TAU) appears as a promising neuroprotective molecule due to its pleiotropic action in the brain. Here, we investigated whether TAU plays a beneficial role in different behavioral domains of zebrafish submitted to an intermittent EtOH exposure model, specially focusing on social behavior, anxiety-like responses, and memory. Moreover, since monoamines play a role in EtOH-mediated responses, we also evaluated the influence of both TAU and EtOH exposures on brain monoamine oxidase (Z-MAO) activity. Fish were exposed to non-chlorinated water or 1% EtOH for 8 consecutive days (20 min per day). From the 5th day until the end of the experimental period (8th day), animals were kept in the absence or presence of TAU (42, 150, or 400 mg/L) 1 h per day immediately after EtOH exposure. Behavioral measurements started 24 h after the last EtOH exposure. We observed that TAU showed modest attenuating effects on shoaling behavior and anxiety-like responses, while 42 and 150 mg/L TAU abolished the memory acquisition deficit in the inhibitory avoidance task. Biochemical analysis revealed that TAU did not modulate EtOH-induced increase on brain Z-MAO activity. Collectively, our novel data show a potential beneficial effect of TAU in an intermittent EtOH exposure model in zebrafish. Moreover, these findings foster the growing utility of this aquatic species to investigate the neurobehavioral basis of EtOH- and TAU-mediated responses in vertebrates.
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