A role for the nicotinic alpha-bungarotoxin receptor in neurite outgrowth in PC12 cells.

The addition of nicotine decreased neuritic outgrowth in PC12 cells in culture. This effect occurs as early as one day after addition of nicotine to the culture medium in a concentration-dependent manner. The nicotine-induced decline in neurite outgrowth was prevented by d-tubocurarine (10(-4) M) indicating that the effect was mediated through a nicotinic receptor. alpha-Bungarotoxin (10(-8) M) was also able to inhibit the nicotine-induced decrease in process formation in a dose-dependent manner. The concentrations of alpha-bungarotoxin required to affect process outgrowth correlated with those required to inhibit radiolabelled alpha-bungarotoxin binding. alpha-Bungarotoxin had no effect on [3H]noradrenaline release, a functional response mediated through the alpha-bungarotoxin-insensitive neuronal nicotinic acetylcholine receptor, suggesting that alpha-bungarotoxin specifically interacts with the neuronal alpha-bungarotoxin receptor. The present results suggest a functional role for the neuronal nicotinic alpha-bungarotoxin receptor in neurite outgrowth.