In the US about 10.2% women reports EtOH consumption with 3.1% reporting binge drinking during pregnancy1–3. Individuals with fetal alcohol exposure (FAE) possess developmental delays along with cognitive and behavioral impairments3–6. The most devastating and extreme consequence of fetal EtOH exposure is the neuronal loss due to the exacerbation of selective programmed neuronal death, which is a normal aspect of CNS development during developmental organogenesis. Excessive neuronal death disrupts the development of normal neural networks and may lead to structural changes along with cognitive and behavioral dysfunctions7,8. The behavioral abnormalities associated with excessive neuronal death include generalized impairment in the development of motor competence (cerebellar abnormalities)9,10, learning and memory deficits (hippocampal abnormalities)11–13, and stress hyperresponse and anxiety (hypothalamic abnormalities)14–16. The cellular mechanisms involved in increased neuronal death leading to altered structural changes and behavioral functions in fetal EtOH exposed offspring are not clearly demonstrated.
