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Altered characteristics of catecholamine release from rat cortical slices and bovine adrenal chromaffin cells in culture after chronic exposure to ethanol and the effect of the dihydropyridine drugs on these systems.

The depolarisation-induced release of dopamine from control rat striatal slices is inhibited by ethanol in vitro. The same parameter is enhanced in preparations from ethanol-treated rats. Under conditions of superfusion with normal physiological solutions we were unable to see similar results in noradrenaline (NA) release from cortical slices. Since we believed altered intracellular Ca2+ metabolism might underlie changes induced by ethanol in dopamine neurones, we superfused cortical slices with low K+ solutions which raise intracellular Ca2+. Under these conditions, ethanol in vitro inhibited depolarisation-induced NA release in control preparations. In preparations from ethanol tolerant animals, ethanol enhanced depolarisation-induced release. In cultures of adrenal chromaffin cells, similar alterations in coupling between Ca2+ and catecholamine release can be seen. Some of these changes may be a consequence of increased functional activity of dihydropyridine-sensitive Ca2+ channels.