Conclusion
In the present study we found that activation of presynaptic nNAChRs
leads to a decrease in the quantal ACh release from the nerve ending.
This negative feedback mechanism is mediated by modulating of function
of VGCCs of Cav1 type, which leads to an increase in the
entry of Ca2+ into the nerve terminal (Figure 9).
Understanding of peculiarities of action of ACh (nicotine) on the
nNAChR-containing nerve endings (not only in cholinergic synapses (Seth
et al., 2002; Garduño et al., 2012)) has of broad scientific and
clinical significance, since cholinergic nicotinic signaling (in
addition to neuromuscular transmission and synaptic transmission in
ganglia) is involved in the setting of a variety of processes, including
anxiety, depression, arousal, memory, and attention (Hogg et al., 2003;
Picciotto, 2003).