We sought to determine the effects of alcohol on genetic programs of embryonic neurogenesis using our moderate prenatal alcohol exposure (PAE) paradigm (Brady, Allan, & Caldwell, 2012). This “drinking in the dark” model results in blood alcohol content of 20 mM 4 h after consumption, similar to slightly more than one drink per day (Valenzuela, Morton, Diaz, & Topper, 2012); dams consume alcohol chronically, during preconception and gestation up to embryonic (E) days 15–17. Neurogenesis was chosen as a mechanism for investigation based on our previous publications demonstrating that alcohol elicits long-lasting effects seen in adulthood on neural progenitor cells (NPC) left over from development, including alterations in cell fate (Kajimoto, Allan, & Cunningham, 2013) and the neurogenic capacity to respond to environmental cues (Choi, Allan, & Cunningham, 2005). Ex vivo proliferating and differentiated cell cultures comprised of NPC from E15–E17 tissue exposed to alcohol in vivo were used for transcriptome analysis of neurogenesis-related genes. To our knowledge, we are the first to report that embryonic neurogenesis under both proliferating and differentiating conditions is altered by in vivo moderate alcohol exposure.
