Journal
SCIENCE
Volume 287, Issue 5455, Pages 1056-1060Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.287.5455.1056
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Funding
- NIA NIH HHS [AG 11355] Funding Source: Medline
- NIDA NIH HHS [DA 05072] Funding Source: Medline
- NIMH NIH HHS [MH 38894] Funding Source: Medline
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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 activation of GABA, receptors], triggers widespread apoptotic neurodegeneration in the developing rat forebrain. Vulnerability coincides with the period of synaptogenesis, which in humans extends from the sixth month of gestation to several years after birth. During this period, transient ethanol exposure can delete millions of neurons from the developing brain. This can explain the reduced brain mass and neurobehavioral disturbances associated with human fetal alcohol syndrome.
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