Key Results:
Nicotine hydrogen tartrate salt (considered as a stable form for
potential therapeutic delivery of nicotine) effects on the parameters of
ACh release from the nerve ending were analyzed. Nicotine application
(10 μM) decrease the amount of evoked ACh release, while calcium
transient increase in the motor nerve terminal. Both of these effects of
nicotine were abolished by the neuronal ACh receptor antagonist
dihydro-beta-erythroidine and Cav1 blockers, verapamil
and nitrendipine.