Activation of neuronal nicotinic receptors induces an increase
of calcium level in motor nerve terminal
Since the process of evoked release of a neurotransmitter is triggered
by the entry of calcium ions into the nerve ending (Katz B., 1969;
Crawford, 1974), it was suggested that the inhibitory effect of nicotine
on the ACh release could be related to a decrease in
Ca2+ influx.
The amplitude changes of the optical signal (ΔF/F0) from the calcium dye
loaded into the nerve terminal in response to a single stimulus (with
the same characteristics as during EPP registration) averaged about 30%
(Figure 3). Nicotine application did not lead to a decrease, as
expected, but caused a significant increase in the amplitude of the
calcium transient by 13.7 ± 4.3% (n = 5, 8 NMJs; Figure 4). Thus, in
the presence of a nicotinic receptor agonist, the presynaptic calcium
level in response to nerve stimulation increases more strongly than in
its absence. Is this increase indeed triggered by nNAChRs, which
activation of leads to a decrease in subsequent ACh release? The answer
to this question was obtained in the experiments with an antagonist of
nicotinic receptors, DHβE.
Application of the antagonist alone led to a decrease in the calcium
transient significantly by 12.9 ± 1.5% (n = 5, 15 NMJs; Figure 4),
however, after pretreatment with DHβE, the calcium signal-enhancing
effect of nicotine was completely abolished (100.0 ± 0.8%; n = 5; 15
NMJs; Figure 4).