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