Abstract
The data reported here together with recent reports from other investigations suggest that ethanol may act selectively to alter Ca++ metabolism in nerve cells. Changes in calcium content and binding after acute and chronic exposure to ethanol suggest that nerve cells may adapt to ethanol exposure through increasing endogenous calcium content on the synaptic membranes. Since calcium plays an integral role in neurotransmitter metabolism, it may be suggested that adaptation to ethanol may occur via such Ca++ dependent processes as altered membrane transport capabilities and excitation-secretion coupling mechanisms. Future research in these areas would hopefully be directed toward the role of Ca++ in neurotransmitter release and subsequent activation of cyclic nucleotide metabolism.