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


CONCLUSIONS
Tricyclopinate inhibits neuronal nAChR by interacting with the allosteric sites rather than the open ionic channels or acetylcholine recognition site of the receptor.
Zheng
J Q
JQ
Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China.
He
X P
XP
Yang
A Z
AZ
Liu
C G
CG
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D004594:Electrophysiology; D005260:Female; D006575:Heterocyclic Compounds, 3-Ring / Q000494:pharmacology*; D008297:Male; D009474:Neurons / Q000502:physiology*; D018733:Nicotinic Antagonists / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D017783:Superior Cervical Ganglion / Q000502:physiology*
D006575:Heterocyclic Compounds, 3-Ring; D018733:Nicotinic Antagonists; C437004:tricyclopinate