Suelen Baggio
Background: Fetal Alcohol Spectrum Disorder (FASD) is a syndrome related to ethanol (EtOH) exposure during development with neurological impairment. Glutamatergic neurotransmission is modulated by EtOH exposure, which affects synaptic plasticity and cognitive processes. Adult zebrafish is a known model to evaluate long-lasting impairments of milder forms of FASD, also used to investigate the glutamatergic system. Aim: Evaluate brain glutamatergic system of adult zebrafish exposed to ethanol during development. Methods: zebrafish larvae (24 h post-fertilization), were exposure to EtOH (0.0%, 0.1%, 0.25%, 0.5% and 1%) for 2 hours. After 4 months, the animals were euthanized and their role brain was used to access: glutamate transport uptake activity; glutamate binding in enriched membrane fraction; glutamine synthetase (GS) activity; Na+/K+ ATPase activity; and high-resolution respirometry. Results: Animals exposed to EtOH 0.5% and 1% presented a 50% reduction of brain glutamate uptake compared to control (p < 0,001). Ceftriaxone, a positive modulator of glutamate uptake, rescued 50% of this drop (p < 0,0001). Both groups presented reduced levels of glutamate binding compared to control (43% and 60%, respectively, p = 0,0041). Both groups presented 32% reduction in Na+/K+ ATPase activity compared to control (p = 0,0003). One-fifth of GS activity was reduced on EtOH 1% group compared to control (p = 0,0032). No alterations were observed in high-resolution respirometry. Conclusion: Embryonic alcohol exposure disrupts adult zebrafish glutamatergic neurotransmitter system
