Abstract
Ethanol caused a concentration-dependent loss of PC12 cells over a 24 h interval, accompanied by an increase in intracellular calcium. The specific α7 nicotinic receptor partial agonist DMXB attenuated both of these ethanol-induced actions at a concentration (3 μM) found previously to protect against apoptotic and necrotic cell loss. The α7 nicotinic receptor antagonist methylylaconitine blocked the neuroprotective action of DMXB when applied with but not 30 min after the agonist. These results indicate that activation of α7 nicotinic receptors may be therapeutically useful in preventing ethanol-neurotoxicity.
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