Blocking effect of tricyclopinate on nicotinic receptors in cultured sympathetic neurons.

AIM: To investigate the mechanism of tricyclopinate, an antagonist of nicotinic receptor, on neuronal nicotinic acetylcholine receptors (nAChR). METHODS: 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). RESULTS: 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. CONCLUSION: Tricyclopinate inhibits neuronal nAChR by interacting with the allosteric sites rather than the open ionic channels or acetylcholine recognition site of the receptor.