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Wiley InterScience | ||||
  Addiction BiologyVolume 9 Issue 2, Pages 137 - 149 Published Online: 9 Jun 2006 Journal compilation © 2009 Society for the Study of Addiction Published on behalf of the Society for the Study of Addiction
Abstract | References | Full Text: PDF (Size: 771K) | Related Articles | Citation Tracking  Fetal alcohol syndrome at the cellular level Copyright 2004 Society for the Study of Addiction to Alcohol and Other Drugs 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. |  |
