Effects of extracellular Ca(2+) influx and intracellular Ca(2+) release on ethanol-induced cytoplasmic Ca(2+) overload in cultured superior cervical ganglion neurons.

The present research was designed to investigate the interference of Ca(2+) homeostasis by ethanol on the primary cultured superior cervical ganglion (SCG) neurons. (1) Using the whole cell patch clamp recording, the amplitudes of voltage-dependent Ca(2+) channel (VDCC) currents could be reduced by ethanol in a concentration-dependent manner. Ethanol (100mM) inhibited about 25% of Ca(2+) channel current. However, the activation of Ca(2+) channel was not affected by ethanol at those concentrations. (2) The similar extent inhibitions of 100mM ethanol on the increments of intracellular Ca(2+) concentration ([Ca(2+)](i)) induced by 40 mM KCl and 1 microM A23187 were also observed in the fluo-3-AM loaded superior cervical ganglia (SCG) via detecting the change of [Ca(2+)](i) with a laser scanning confocal microscopy. In contrast, the basal [Ca(2+)](i) was significantly increased by ethanol alone in a concentration-dependent manner. These phenomena were also observed even under Ca(2+) free bath solution or the solution added 300 microM cadmium chloride conditions. Together with above results, our data suggest that ethanol increases basal [Ca(2+)](i), but it also inhibits the extracellular Ca(2+) influx through VDCC and ionophore channel. And the augment of basal [Ca(2+)](i) induced by ethanol might attribute to the Ca(2+) releasing from intracellular Ca(2+) pools.