Blocking effect of tricyclopinate on nicotinic receptors in cultured sympathetic neurons

To investigate the mechanism of tricyclopinate, an antagonist of nicotinic receptor, on neuronal nicotinic acetylcholine receptors (nAChR). A tight seal whole-cell recording patch-clamp technique was performed to record nicotine-evoked currents in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG). Tricyclopinate inhibited the nicotine-induced currents competitively and the inhibition was voltage-independent. The decay of the nicotine-induced current was accelerated significantly in the presence of tricyclopinate. Tricyclopinate inhibits neuronal nAChR by interacting with the allosteric sites rather than the open ionic channels or acetylcholine recognition site of the receptor.