Figure 8.
The GABAergic system contributes extrinsic mechanisms that are altered with ethanol exposure in utero. Crossing index of isotypic slice cocultures obtained from GFP β-actin embryos demonstrates that blocking the GABAA receptor with bicuculline (Bicu) or sequestering ambient GABA with a GABA-specific antibody blocks the effect of ethanol. Addition of 2 μm GABA, similar to the ambient level of GABA observed in ethanol-exposed embryos increases the crossing index to levels that are indistinguishable from that of ethanol-treated slice cocultures. Data are expressed as mean ± SEM. Asterisks denote a significant difference (***different from control, ethanol + Bicu, ethanol + GABA; **different from control and ethanol + Bicu only; ANOVA and Holm–Sidak Method, p < 0.05). EtOH, Ethanol.