Vulnerability of the developing brain to the toxic effects of alcohol is a crucial factor leading to fetal alcohol spectrum disorder (FASD). Among various animal models for FASD, neonatal mice exposed to ethanol, which display acute apoptotic neurodegeneration and the following long-lasting behavioral and physiological abnormalities, have been widely used for elucidating mechanisms behind FASD. Using this animal model, it was observed that various bioactive lipid molecules changed their metabolism. Recently, it was revealed that signaling lipid molecules regulate biological functions of neural cells and affect their survival. It appears that some toxic lipid metabolites are linked to ethanol neurotoxicity in neonatal mice. Changes in the brain lipid metabolism associated with FASD are examined.