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.

斑马鱼越来越多地用于酒精研究，特别是在模拟人类胎儿酒精谱系障碍 (FASD) 方面。FASD 是由于酒精到达子宫内发育中的胎儿所致，这是一种完全可预防但普遍且具有破坏性的终生疾病。包括斑马鱼在内的动物模型的希望是发现这种疾病的潜在机制，这可能有助于治疗和诊断。过去，我们开发了一种胚胎酒精暴露方案，旨在模仿斑马鱼中较温和且最普遍的 FASD 形式。我们在这种斑马鱼 FASD 模型中发现了许多行为、神经化学、神经元标记和神经胶质细胞表型的持久变化。使用相同的模型（受精后 24 小时的老斑马鱼卵在 1% vol/vol 乙醇中浸泡 2 小时），⁺⁺和 SCN1A Na ⁺通道使用蛋白质印迹，然后对斑马鱼大脑的苍白和小脑中的相同通道进行免疫组织化学分析。我们报告使用这两种方法显着减少所有四种通道蛋白的表达。我们得出结论，斑马鱼胚胎发育过程中短剂量和低剂量暴露于酒精诱导的电压门控阳离子通道表达降低可能有助于先前证明的持久行为和神经生物学变化。