Аннотация:ATP is known as a comediator of acetylcholine (ACh) in cholinergic neuromuscular junctions. Being released along with ACh, ATP is able to modulate synaptic transmission and then undergoes fast hydrolysis by ectonucleotidases in synaptic cleft. Modulatory action of ATP is realized via purinergic receptors, which are widely present in motor synapses. The most well-known effect of ATP is the autoregulatory supression of ACh release via presynaptic metabotropic P2Y receptors, also involving retrograde action of muscle-derived reactive oxygen species, synthesized under influence of postsynaptic ATP action.
Whether these complex inhibitory ATP effects remain the same and/or become more pronounced during prolonged ATP presence in synaptic cleft remained unknown. In this study ATP effects were examined in mouse neuromuscular junctions under conditions of ATP accumulation in synaptic cleft using ectonucleotidase inhibition, tetanic nerve stimulation or tonic application of exogenous non-hydrolysable ATP.