Conclusion and Implications:
Neuronal nicotinic ACh receptors activation decreases the number of ACh
quanta released by boosting calcium influx through Cav1
channels. Understanding of mechanisms of autoregulation of ACh release
is important for the searching new approaches treat diseases associated
with cholinergic dysfunction.
Keywords: neuromuscular junction, neurotransmitter release,
acetylcholine, nicotinic receptor, calcium channel, calcium transient.
Abbreviations: ACh, acetylcholine; CaM, Calmodulin; CaMKII,
Ca2+/calmodulin-dependent protein kinase II; CNS,
central nervous system; DHβE, dihydro-β-erythroidine hydrobromide; DMSO,
dimethylsulfoxide; EPP, evoked endplate potentials; LAL, levator auris
longus; mEPP, miniature endplate potentials; NMJ, neuromuscular
junction; nNAChRs, neuronal nicotinic acetylcholine receptors; PNS,
peripheral nervous system; QC, quantal content; VGCCs, voltage-gated
calcium channels