When neuronal activity is abnormally suppressed during the developmental period of synaptogenesis, the timing and sequence of synaptic connections are disrupted. This causes nerve cells to receive an internal signal to commit suicide, a form of cell death known as 'apoptosis'. By altering glutamate and GABA transmission (thereby suppressing neuronal activity), alcohol causes millions of nerve cells in the developing brain to commit suicide. This provides a likely explanation for the clinical observation that in utero exposure of human fetuses to alcohol leads to diminished brain size and lifelong neurobehavioral disturbances [called fetal alcohol syndrome (FAS)]. These findings have public health significance in relation to FAS and many other drugs, including drugs used in obstetric and pediatric medicine that can act by this same mechanism to drive developing neurons to commit suicide.