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).