Studies utilizing the zebrafish or clawed frog as models for PNEE have shown that ethanol exposure during development can cause growth retardation including reduced body length, microcephaly, skeletal deficits, and eye malformation (48, 149–154) as well as cognitive dysfunction in simple behavioral tasks such as visual acuity tests (149), associative learning (54), and social behavior (155), which were apparent even in the absence of physical malformations (54, 155). These deficits were also accompanied by changes in gene expression (151, 153, 154). These effects were dependent on the dose of ethanol used and the developmental timing and length (chronic vs. acute) of exposure, with the blastula, gastrulation, and somitogenesis periods being particularly sensitive to the effects of ethanol (48, 150).
