The membrane disordering effect of ethanol on neural crest cells in vitro and the protective role of GM1 ganglioside.

The teratogenic effect of ethanol appears to be related to excessive cell death in selected cell populations including craniofacial neural crest. Because there is a large body of evidence suggesting that a primary site of action of ethanol is at the membrane level, the current study was designed to examine and attempt to ameliorate ethanol-induced neural crest cell membrane changes that proceed cell death. To this end, neural crest cells were grown as primary cultures from mouse cranial neural tube be explants. In these cultured cells, the relationships between changes in membrane lipid lateral mobility (a measure of membrane fluidity) as determined using the technique of fluorescence recovery after photobleaching (FRAP), ethanol-induced cell death, and the protective role of GM1 ganglioside were examined. A dose-response study showed that treatment with 50, 100, 150, or 200 mM ethanol respectively, for 24 h was positively correlated with membrane lipid lateral mobility and negatively correlated with cell viability. Pre- or co-treatment of the cells with GM1 ganglioside diminished the ethanol-induced increases in membrane fluidity and decreases in cell viability. The results of this study suggest that change in membrane fluidity can account, in part, for ethanol-induced neural crest cell death and that the protection conferred by GM1 ganglioside may result from membrane stabilization and subsequent preservation of the biophysical properties and biological function of the ethanol-exposed cell membranes.