Effects of nicotine on ACh release
The results of our study demonstrate that in the mouse neuromuscular
preparation of m.LAL, nicotine at concentrations up to 1 μM has no
effect either on the processes of ACh release from the nerve terminal,
or on the processes of its interaction with the postsynaptic membrane.
At the concentration of 5 μM, the presynaptic effect of nicotine appears
to become detectable (inhibition of the spontaneous release of ACh due
to the activation of presynaptic cholinergic receptors). An increase in
concentration to 10 μM enhances the presynaptic effect of the alkaloid
(suppression of not only spontaneous, but also of the evoked ACh
release) and leads to a weak postsynaptic effect (decrease in RMP due to
activation of postsynaptic cholinergic receptors). With an increase in
nicotine concentration to 50 μM, dramatic changes become evident in all
recorded parameters of neurotransmission.
Thus, nicotine at a concentration of 10 μM exerts both postsynaptic and
presynaptic inhibitory effects on the neuromuscular synapse, in
particular, causing a decrease in the number of ACh quanta released in
response to action potential. Similar decrease in the QC during
activation of cholinergic receptors has been noted earlier (Tian et al.,
1994; Prior & Singh, 2000; Balezina et al., 2006; Khaziev et al.,
2016), however, these results were obtained on other preparations and in
conditions of initially reduced QC, or in cut fiber preparations.