Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome

The deleterious effects of ethanol an the developing human brain are poorly understood. Here it is reported that ethanol, acting by a dual mechanism [ blockade of N-methyl-D-aspartate (NMDA) glutamate receptors and excessive a ctivation of GABA, receptors], triggers widespread apoptotic neurodegenerat ion in the developing rat forebrain. Vulnerability coincides with the perio d of synaptogenesis, which in humans extends from the sixth month of gestat ion to several years after birth. During this period, transient ethanol exp osure can delete millions of neurons from the developing brain. This can ex plain the reduced brain mass and neurobehavioral disturbances associated wi th human fetal alcohol syndrome.