BDNF and NGF afford in vitro neuroprotection against ethanol combined withacute ischemia and chronic hypoglycemia

Consumption of alcohol during pregnancy can result in central nervous syste m deficits in infants ranging from fetal alcohol effects to fetal alcohol s yndrome. Changes in cerebral metabolism causing ischemic in utero condition s can also result from ethanol (EtOH). Growth factors have been shown to am eliorate ischemic damage and EtOH-induced neurotoxicity. However, using an in vitro model system of fetal alcohol effects/fetal alcohol syndrome, this study examines the neuroprotective effects of nerve growth factor, brain-d erived neurotrophic factor, or glial cell line derived neurotrophic factor against EtOH treatment (0, 200, 400, 800, or 1,600 mg/dl) combined with acu te ischemia (2-hour hypoxia in EtOH-containing glucose-free media) followed by chronic hypoglycemia (16-hour glucose deprivation in EtOH-containing me dia). 3-(4,5-Dimethylthiazol-2-yl)-2,5-dipheny tetrazolium bromide assays a ssessed relative neurotoxicity. Glial cell derived neurotrophic factor was not neuroprotective. Nerve growth factor protected against ischemia/hypogly cemia combined with 0-1,600 mg/dl EtOH. Brain-derived neurotrophic factor p rotected against ischemia/hypoglycemia combined with 0-800 mg/dl EtOH. Thes e studies demonstrate marked growth factor neuroprotection against a myriad of conditions encountered by developing EtOH-exposed fetuses.