title: Fetal alcohol syndrome at the cellular level.
abstract: A single exposure of infant rats or mice to ethanol during synaptogenesis (mid to late pregnancy for humans) can cause developing neurons to commit suicide (die by apoptosis) on a massive scale. The neuronal loss demonstrated in recent studies is more severe and much more widely distributed (many brain regions, plus spinal cord and retina) than has been documented in prior animal ethanol studies. By suppressing neuronal activity via NMDA glutamate and GABAA receptors, ethanol disrupts synaptogenesis, thereby activating in developing neurons a programmed signal to commit suicide. These recent findings help clarify important aspects of the fetal alcohol syndrome, and demonstrate the usefulness of an in vivo infant rodent model for studying the neurotoxic effects of ethanol on the developing central nervous system.
authors.forename: John W
authors.initials: JW
authors.lastname: Olney
mesh_terms: D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000378:metabolism* / Q000503:physiopathology*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D016202:N-Methylaspartate / Q000378:metabolism; D011247:Pregnancy; D011963:Receptors, GABA-A / Q000502:physiology*
chemical_list: D011963:Receptors, GABA-A; D018698:Glutamic Acid; D016202:N-Methylaspartate