Time-lapse analysis of ethanol's effects on axon growth in vitro.

The cortical abnormalities found in animal models of fetal alcohol syndrome (FAS) suggest a disruption of axon growth. After emerging from the cell body, axons exhibit saltatory growth, cycling between periods of extension and periods of retraction. The timing of neuronal process outgrowth an the balance between extension and retraction together determine the net rate of axon elongation, and may be independently regulated.

Morphologic and neurotoxic effects of ethanol vary with timing of exposure in vitro.

Results of investigations with animal models of fetal alcohol syndrome (FAS) seem to indicate that neuronal vulnerability to ethanol-induced cell death may be correlated with specific developmental events. In the present study, we sought to test this observation in a cell culture model of neuronal development in which morphogenesis as well as survival could be assessed. Using embryonic rat hippocampal pyramidal neurons in primary cultures, we compared the sensitivity of neurons to ethanol added, at 400 mg/dl, to the medium at different times relative to the development of axons and dendrites.

Astrocyte-derived factors modulate the inhibitory effect of ethanol on dendritic development.

Numerous studies in vivo and in vitro have demonstrated that ethanol disrupts neuromorphogenesis. However, it has not been determined what role, if any, is played by non-neuronal cells in mediating this effect. We recently reported that ethanol inhibits dendritic development in low-density cultures of fetal rat hippocampal pyramidal neurons (Yanni and Lindsley, 2000: Dev Brain Res 120:233-243).