In our study, we found that human neural progenitors and immature neurons were highly sensitive to the toxic effects of EtOH. Exposure to EtOH at various concentrations led to a significant reduction in metabolic activity and viability of these cells and resulted in activation of caspase-3 and induction of apoptosis. On the other hand, although a modest but significant reduction in metabolic activity and viability was observed, there was no significant caspase-3 activation in mature neuron cultures isolated from the matching fetal brain suggesting that while neural progenitors and immature neurons are highly sensitive to the toxic effects of EtOH, mature neurons may possess resistance at the same concentrations. These observations are in line with studies where the toxic effects of EtOH were also described on neural stem cells and progenitors during adult neurogenesis in in vitro cell culture and in vivo experimental animal models45–48. In our neuronal culture model, alcohol toxicity assessments by cell viability and apoptosis analysis showed a robust toxicity in neural progenitor cells with only modest effect in neurosphere cultures. This could be due to the
