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.