The chronic consumption of alcohol, especially during key growth stages such as pregnancy or adolescence, can lead to neurological damage (Miller 2006). This is believed to occur through alterations in DNA methylation of genes encoding controllers of cell cycle checkpoints such as cyclins, cyclin-dependent kinases (cdks), and their associated inhibitors. To emulate fetal alcohol exposure and understand this dynamic, symmetrically dividing NSC derived from embryonic stem cells were used as a model (Hicks et al. 2010). An ethanol concentration of 400 mg/dL (88 mM) was used due to the finding of in vitro effects similar to those previously observed with rat fetuses in vivo treated with 300 mg/dL (33 mM) ethanol. Concentrations greater than 400 mg/dL affected NSC proliferation and cell death (Cheema et al. 2000). Lower concentrations (100-320 mg/dL; 22-69 mM) had no significant effects.
