From the viewpoints of presynaptic autoreceptors, it should be taken into consideration that the mechanism underlying the interplay between presynaptic muscarinic and adenosine receptors controls ACh release in mammalian motor nerve terminals depending on the nerve stimulation paradigm; the A2A adenosine receptor (operating Ca2+ influx via L-type channels) plays a key role during long-lasting and/or high-frequency nerve activity [79,80,81,82,83,84], a situation that is impaired in toxin-induced myasthenia gravis and dysfunctional in experimental autoimmune myasthenia gravis [85,86]. Here, ADORA2A is linked to myasthenia gravis.