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Fetal alcohol syndrome at the cellular level
Author(s) -
Olney John
Publication year - 2004
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1080/13556210410001717006
Subject(s) - synaptogenesis , neuroscience , glutamate receptor , gabaa receptor , nmda receptor , fetal alcohol syndrome , fetus , biology , receptor , ethanol , medicine , pregnancy , biochemistry , genetics
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.