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 nic otine to the culture medium in a concentration-dependent manner. The n icotine-induced decline in neurite outgrowth was prevented by d-tubocu rarine (10(-4) M) indicating that the effect was mediated through a ni cotinic receptor. Alpha-Bungarotoxin (10(-8) M) was also able to inhib it the nicotine-induced decrease in process formation in a dose-depend ent manner. The concentrations of alpha-bungarotoxin required to affec t process outgrowth correlated with those required to inhibit radiolab elled alpha-bungarotoxin binding. Alpha-Bungarotoxin had no effect on [H-3]noradrenaline release, a functional response mediated through the alpha-bungarotoxin-insensitive neuronal nicotinic acetylcholine recep tor, suggesting that alpha-bungarotoxin specifically interacts with th e neuronal alpha-bungarotoxin receptor. The present results suggest a functional role for the neuronal nicotinic alpha-bungarotoxin receptor in neurite outgrowth.