The mechanism of action of tonically applied choline, the agonist of α7
nicotinic acetylcholine receptors (nAChRs), to the spontaneous and evoked
release of a neurotransmitter in mouse motor synapses in diaphragm
neuromuscular preparations using intracellular microelectrode recordings of
miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) was
studied. Exogenous choline was shown to exhibit a presynaptic inhibitory effect
on the amplitude and quantal content of EPPs for the activity of neuromuscular
junction evoked by single and rhythmic stimuli. This effect was inhibited
either by antagonists of α7-nAChRs, such as methyllycaconitine and
α-cobratoxin, or by blocking SK-type calcium-activated potassium (KCa)
channels with apamin or blocking intraterminal ryanodine receptors with
ryanodine. A hypothesis was put forward that choline in mouse motoneuron nerve
terminals can activate presynaptic α7-nAChRs, followed by the release of
the stored calcium through ryanodine receptors and activation of SK-type KCa
channels, resulting in sustained decay of the quantal content of the evoked
neurotransmitter release.