Abstract
The principal neuropathological abnormality in fetal alcohol syndrome is a disorder of neuronal migration. This developmental process is directed by radial glial (astrocytic) cells. One potential deleterious effect of ethanol on these cells is an inhibition of proliferation. To address this possibility we utilized primary cultures of dissociated neonatal rat brain, which we and others have shown to consist of >90% astrocytes. Cell proliferation was assessed by measurement of DNA synthesis (from [3H]thymidine) and protein deposition. The effect of ethanol, added on day 3 (the time of first cell attachment), on DNA synthesis on day 7, the time of peak cell proliferation in control cells, and on protein deposition on day 10 is shown in the Table, as percent of control. The activity of glutamine synthetase (an astrocyte specific enzyme) on day 18 is also shown.
The relative specificity of the effect of ethanol was shown by demonstrating no comparable effect on glycoprotein synthesis (from [3H]mannose) or on sterol synthesis (from [14C]acetate). The data thus show a significant decrease in DNA synthesis in developing astrocytes at concentrations of ethanol observable within the range of human intoxication (10-40mM). (NIH-HD-07464)
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Bass, W., Volpe, J. ETHANOL INDUCED DEPRESSION OF DNA SYNTHESIS IN ASTROCYTES. Pediatr Res 21 (Suppl 4), 209 (1987). https://doi.org/10.1203/00006450-198704010-00259
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DOI: https://doi.org/10.1203/00006450-198704010-00259
