ADHD, a widely diagnosed disorder in the school-aged population, is correlated with a variety of causes, but its etiology remains a mystery. Alcohol exposure during pregnancy has been correlated with the occurrence of ADHD in childhood. As ADHD may have several subtypes, one of which is the result of hippocampal dysfunction, and alcohol acts primarily on the hippocampus, alcohol-induced damage to the hippocampus may describe a subtype of ADHD. The project is also a further extension of the investigation of the effect of alcohol on the NMDA receptor, a primary receptor in the hippocampus. The project determines the composition of NMDA receptor protein subunits in rats exposed to alcohol during the third trimester equivalent and second and third trimesters combined. The secondary subunits of the NMDA modulate its function by altering Mg2+ affinity to the attached calcium channel, which in specific configurations may promote either excitotoxicity or apoptosis. Differential NMDA receptor function is observed after exposure to EtOH, as well as cell death, but the means by which cells die has not been described. This project seeks to answer whether altered NMDA receptor subunit composition is responsible for the change in NMDA receptor function, whether it causes apoptosis or excitotoxicity, and its subsequent effects on behavior.