Manganese is essential for normal development and activity of the nervous tissue. Mn2+ ions are involved in protein synthesis and may prevent free radical damage. Since it is now established that alcohol degradation may produce free radicals, we studied the effect of Mn2+ on ethanol induced alterations using cultured nerve cells as an experimental model of the central nervous system. Neurons and glial cells were cultured from rat brain cortex; a tumoral rat glial cell line (C6) was also examined. We measured enzymatic markers of nerve cell maturation (enolase, glutamine synthetase) and superoxide dismutase, a scavenger of free radicals; all these enzymes being activated by Mn2+ ions. Only for the glial cell types an alcohol antagonizing effect was found when Mn2+ was combined with ethanol. Neurons were not sensitive to that Mn2+ effect.
The effects of physiological concentrations of K+ on Mn2+ accumulation were compared in rat glial cells and neurons in culture. Increasing the K+ concentration in growth medium increased significantly the Mn2+ level of the cultivated cells, with glial cells more affected than neurons. Ethanol markedly increased the Mn2+ accumulation within glia but not within neurons while ouabain caused inhibition of Mn2+ uptake with neurons and glial cells. A modulation of the total protein synthesis by Mn2+ and ethanol level in the growth medium was observed with glial cells. These data suggest that the mechanisms involved in Mn2+ accumulation in glial cells are different from those present in neurons. Moreover, the results are consistent with the hypothesis that Mn2+ plays a regulatory role in glial cell metabolism.
The effect of maternal alcohol exposure on nerve cell development was investigated in neurons and glial cells cultured from foetal rat brain. Neurons were grown for one week from two-week-old cortical brain cells and glial cells were cultured for four weeks from newborn cortical brain cells. Two types of maternal alcohol treatment were performed; either before and during pregnancy or only until the beginning of pregnancy. In both situations, we found a delayed nerve cell maturation assessed by microscopic observations and determination of enzymatic markers of nerve cell development (non-neuronal and neuron-specific enolase for the neuronal cells, non-neuronal enolase and glutamine synthetase for the glial cells). The results confirmed our previous in vivo experiments pointing out long-lasting effects of maternal alcohol exposure in the offspring.
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