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Both presynaptic and postsynaptic blockade of ganglionic transmission during the period of naturally occurring ganglion cell death reduced the number of surviving neurons in the sympathetic ganglia (SG) and ciliary ganglion (CG). The CG was chosen for analysis because there was a temporal separation between cell proliferation and death in the CG but not in the SG. Ganglion cell proliferation and migration were unaffected by ganglionic blockade. The increased ganglion cell loss that followed ganglionic blockade was accompanied by an increased number of degenerating cells. These results indicate that the decreased number of healthy ganglion cells that followed ganglionic blockade was the result of enhanced naturally occurring cell death.

We have found a selective inhibition of nicotine-induced antinociception in mice by neosurugatoxin (NSTX, 0.4-3.8 nmol/kg), a neurotoxin with a high affinity for ganglionic nicotinic receptors (ED50 = 0.65 nmol/kg). The toxin also reduced specific [3H]nicotine binding in mouse brain membranes (IC50 = 95 nM). The anti-nicotinic activity of NSTX was markedly greater than that of mecamylamine and pempidine. These data indicate that NSTX may block functional nicotinic cholinoceptors possibly in the central nervous system.