Lasting effects of mild embryonic ethanol exposure on voltage-gated ion channels in adult zebrafish brain.

The zebrafish is increasingly well utilized in alcohol research, particularly in modeling human fetal alcohol spectrum disorders (FASD). FASD results from alcohol reaching the developing fetus intra utero, a completely preventable yet prevalent and devastating life-long disorder. The hope with animal models, including the zebrafish, is to discover the mechanisms underlying this disease, which may aid treatment and diagnosis. In the past, we developed an embryonic alcohol exposure regimen that is aimed at mimicking the milder, and most prevalent, forms of FASD in zebrafish. We have found numerous lasting alterations in behavior, neurochemistry, neuronal markers and glial cell phenotypes in this zebrafish FASD model. Using the same model (2 h long bath immersion of 24 h post-fertilization old zebrafish eggs into 1% vol/vol ethanol), here we conduct a proof of concept analysis of voltage-gated cation channels, investigating potential embryonic alcohol induced changes in L-, T- and N- type Ca++ and the SCN1A Na+ channels using Western blot followed by immunohistochemical analysis of the same channels in the pallium and cerebellum of the zebrafish brain. We report significant reduction of expression in all four channel proteins using both methods. We conclude that reduced voltage-gated cation channel expression induced by short and low dose exposure to alcohol during embryonic development of zebrafish may contribute to the previously demonstrated lasting behavioral and neurobiological changes.